HX00044083 r— ------- " MB |H m ■ llllii EnB" hBRhS : '•■"■-'■"■-■" '■"■"■" tliEfl _ fnffia **, flnr flnii'i7iTT Columbia ntoersrttp mtfjeCttpofj^etollodi ^ g>cfjool of Bental anb <^ral gmrgerp Reference ILtbrarp ' A < \ -. <. . / /in wn < GENERAL AND DENTAL PATHOLOGY Digitized by the Internet Archive in 2010 with funding from Columbia University Libraries http://www.archive.org/details/generaldentalpatOOende GENERAL AND DENTAL PATHOLOGY With Special Reference to Etiology and Pathologic Anatomy A Treatise for Students and Practitioners BY JULIO ENDELMAN, M.S., D.D.S. Professor of Special Dental Pathology, College of Dentistry, University of Southern California; Editor of the Pacific Dental Gazette; Member of the Southern Cali- fornia Dental Association, the California State Dental Association, and the National Dental Association; Corresponding Member of the Societe Odontologique de Fiance. Honorary Member of the Sociedad Odontologica de Chile, S. A., etc. AND A. F. WAGNER, A.M., M.D. Professor of General Pathology, College of Dentistry, University of Southern California; Pathologist and Autopsy Surgeon of the County and City of Los Angeles; Mem- ber of L,os Angeles County Medical Society, California State Medical Association, American Medical Association, etc. WITH 440 ILLUSTRATIONS, OF WRICK 340 IN THE SECTION ON DENTAL PATHOLOGY ARE ORIGINAL, AND FOUR COLORED PLATES ST. LOUIS THE C. V. MOSBY CO. 1920 Copyright, 1920, By C. V. Mosby Company (All rights reserved) Press of C. V. Mosby Company St. Louis TO EDWARD C. KIRK, D.D.S., Sc.D., LL.D. Scientist, Teacher, Author From Whom the Authors Eeceived the Instruction in Dental Pathology Which Constitutes the Foundation op the Section of This Book Devoted to That Purpose, and in Appreciation of His Contributions to Dental Science, This Book is Gratefully Dedicated. P RE FACE It has been the aim of the authors to treat the subject from the standpoint of gross and microscopic pathology, realizing that the needs of the dental student call for just that character of infor- mation. It is, of course, assumed that the object in undertaking the study of pathology is to the effect that the information neces- sary to treat diseases upon a rational basis may be available; there- fore the clinical aspects of the maladies discussed throughout the text have been worked out on the basis of the structural changes in- duced in the tissues by various forms of irritation. The clinic and the laboratory have been made use of extensively in the collection of the data and in their arrangement in sequential order, and an effort has been made to include only tangible information, excluding all statements of more or less speculative character. The book, it is hoped, will be a help to dental students by imparting a founda- tional knowledge of the subject and by rendering less complicated the interpretation of pathologic phenomena in the field of dental diagnosis. The comprehension of dental pathology rests upon a clear conception of those abnormal phenomena which, because they may develop in any organ or tissue of the body, are grouped under the heading of general pathology. Practically all the illustrations in the section on Dental Pathology are original, and this feature of the book, we trust, will greatly assist the student in his analysis of the pathologic anatomy of the diseases with which he concerns himself. We are greatly indebted to Dr. Lewis E. Ford for placing at our disposal the laboratories and clinical material of the College of Dentistry of the University of Southern California and for his friendly encouragement and help. To Dr. A. C. LaTouche we are indebted for many courtesies extended to us during the prepara- tion of the manuscript and illustrations and for the use of the microscopical sections from which Figs. 292, 293, and -105 were made, and for the original photograph of Fig. 401. To Dr. Carroll W. Jones, who greatly aided us in the preparation of the manuscript for the press and in the revision of the proofs, we gratefully acknowledge our appreciation. To Dr. James D. PREFACE McCoy the authors' thanks are due for repeated courtesies and sug- gestions and for his cooperation in gathering the data for the chap- ter on systemic infections ; all the radiographs in that chapter were supplied by Dr. McCoy, without whose assistance its preparation would have been greatly handicapped. To Dr. E. F. Tholen we ex- press our thanks for the originals of Figs. 346, 347, 348, and 349, and to Dr. C. F. Oakman for the use of Fig. 342. Our thanks are also due to Professor Win. J. Gies, of Columbia University, for hav- ing placed at our disposal the literature covering his valuable inves- tigation in the domain of dental science ; from this we have quoted freely, especially in the chapter on dental caries. "We are also in- debted to Dr. H. P. Pickerill for the use of Figs. 93, 94, and 95 from his excellent work ' ' The Prevention of Dental Caries and Oral Sepsis. ' ' Our thanks for the loan of cuts are due to the publishers of the following works: Stengel and Fox's "Pathology," Bailey's "Textbook of Normal Histology," Delafield and Prudden's "Text- book of Pathology," McFarland's "Pathology," McConnell's "Pathology and Bacteriology for Dentists," Black's "Operative Dentistry," Ziegler's "Textbook of General Pathology,." Blair's "Surgery and Diseases of the Mouth and Jaws," "American Text- book of Dentistry, ' ' The Dental Cosmos, The Dental Summary, and others. The courtesy extended by Dr. F. W. Frahm in offering sug- gestions which are incorporated in the chapter on macroscopic deformities is also acknowledged. The authors desire to thank Dr. W. A. Danielson of the Chicago College of Dental Surgery, for valuable suggestions in the text. To Dr. Gordon B. New of the Mayo Clinic, for contributing the chapter on Cystic Odontomas, and to Dr. J. Walter Reeves, for contributing the chapter on Malformations, the authors acknowl- edge their obligation. The authors wish to extend their thanks to the publishers for their hearty cooperation. Julio Endelman A. F. Wagner Los Angeles, Cal. CONTENTS PART I GENERAL PATHOLOGY CHAPTER I PAGE 21 Introductory Pathology, 21; Disease, 21; The Cell, 23; Anatomy of the Cell, 24; The Chemistry of the Cell, 26; The Physics of the Cell, 29; Stain- ing Reactions of the Cell, 30; The Physiology of the Cell, 32; Ori- gin of the Blastodermic Layers, 34. CHAPTER II The Etiology of Diseases 37 Etiology of Disease, 37; Age, 28; Sex, 28; Race, 29; Idiosyncrasy, 39; Traumatisms, 39; Injurious Occupations, 39; Unsanitary Sur- roundings, 40; Habits, 40; Heredity, 4; Specific or Determining Causes, 41; Traumatism, 41; Heat, 41; Cold, 42; Atmospheric Pres- sure, 43; Electricity, 43; Light, 43; X-rays, 44; Chemical Agents, 44; Living Organisms, 44; Autointoxication, 44. CHAPTER III 4.p; Pathologic Processes Retrograde Processes, 45; Atrophy, 45; Degenerations (or Meta- morphoses), 47; Cloudy Swelling, Parenchymatous or Granular De- generation, 48; Fatty Degeneration, 48; Mucoid Degeneration, 50; Colloid Degeneration, 52; Hyaline Degeneration, 54; Amyloid De- generation (Waxy, Baeony, or Lardaceous Degeneration), 56; In- filtrations, 59; Fatty Infiltration, 59; Pigmentary Infiltration, 61; Calcareous Infiltration, 67; Concretions of Concrements, 69; Hy- dropic, Dropsical, or Serous Infiltration, 70; Glycogenic or Glycog- enous Infiltration, 71; Necrosis, 72; Coagulation Neorosis, 73; Liquefaction Necrosis, 75; Cheesy Necrosis, or Caseation, 76; Fat Necrosis, 77; Focal Necrosis, 78; Gangrene, 79. CHAPTER IV The Circulatory Changes 8j Ischemia, or Local Anemia, 82; Hyperemia, 83; Active Hyperemia, Z CONTEK [yperemia, - tatic < _ , 85; Hemorrl . 35; , 87; Throml sis, 87 fcs, 92; Edema, Dropsy or Anasarca. CHAPTEB V Inflammation" Etio _ - Pal gy of A I [nflammation, 98; Edema- tons or Serous, 100; Fibrinous, 100; Diphtheritic or Cron] 'ormation, 1>'<: Hemorrhagic Inflamma- tion, 106; Neerotie or G _ is Inflammation, 106; Prod;, Inflammation. 106; Beg 108; Pathologic Anal Patli' >logic Regeneration, 108; Metaplasia, 11": Heteroplasia, 110. CHAPTEB VI KESsrvx Tissue Changes Ill Hypertrophy, 111; Etiology, 111; G . . 112; Micro- pic Pathology, 112; Pathologic Physiology, 112: L12. CHAPTEB VII Tumors 113 Theories of Origin and Causation, 113; Fibromata, 117: Myxomata, 119: Chondromata, 12"; Chordomata, 121; Osteomata, 121; Odon- tomata, 122; Lipomata, 122: Sarcomata. 123; Bound-celled - comata, 121; Spindle-cel 3 imata, 127: Melanotic Sarcoma, or Melanomata, 127; Giant-celled 8arc ,128; Bhabdomyomata, 130 ; Leiomyomata, 130; Glioma. i:;2: Glioma Ganglionare, or Ganglionic Glioma, or Neuroma, 133; Angiomata, 133; Papillomata, 135; Adenomata, 138; Carcinomata, 139; Epithelioma, 141; Adenocarcin- omata, 143; Scirrhous Carcinoma, 14:: ; Medullary Carcinoma, 14-",; Endotheliomata, 146; Teratomata, 148; Dermoid I sts. 18; Hyper- nephroma, L48 ' •-. 14f». CHAPTEB VIII The Pathology of Infectious Diseases 152 The Pathology of Infectious Diseases, 152; Suppurative Diseases, 154; Epidemic ' spinal Meningitis, 156; Gonorrhea, 157; - Chancre, or Chancroid, 158; Pneumonia, or Pneumonitis, 1~>9; Bron- chopneumonia or Lobular Pneumonia, 161; Tuberculosis, K>4: Lep- 7 - philis, or Lues (or '-Gnat Pox"), 168; Glanders, or E'juinia, 171; The Toxemic Diseases, 172; Tetanus or Lock Jaw, CONTENTS 5 PAGE L72; Diphtheria, 17:'.; Asiatic Cholera, L73; Typhoid Fever, 171; Bacillarv Dysentery, 17"); Malta Fever or Mediterranean Fever, 17'i; Anthrax, 176; Malignanl Edema, 177; Gas s Edema, 177; Bu- bonic Plague, L76; [nfluenza, 178; Epidemic Conjunctivitis, 17!); Whooping Cough or Pertussis, 17!»; Vincent's Angina, 179; Relaps- ing Fever, 179; The Higher Bacteria, 180; (Trichomycetes, Chalam ydobacteriacese) , 180; Leptothrix Infections (Leptotrichoses), 180; Cladothrix and Nocardia [nfections or Mycoses, 180; Actin ycosis, 181; Mycetoma, or Madura Foot of India, 182; Blastomycosis or Saccharomyeosis, 1 SU ; Oidiomycosis, 183; Mycoses due to Molds, or Hyphomycetes, 183; The Protozoan Infect ions, IS."); Amebic Dysen- tery, 185; Trypanosomiasis, 186' ; Leishmaniases, 1 S7 ; Malaria, 187; Coccidiosis, 190; Infectious Diseases Caused by Undetermined Microorganisms, 190; Measles, 190; German Measles, 1!»1 ; Chicken Pox or Varicella, 191; Scarlet Fever or Scarlatine, 191; Mumps, or Acute Epidemic Parotitis, 191; Acute Poliomyelitis, or Infantile Paralysis, 1!>2 ; Acute Articular Rheumatism, 1D2; Dengue, 193; Yellow Fever, or Typhus Ieteroides, 193; Typhus Fever, 194; Small- pox, or Variola, L94; Foot-and-mouth Disease, 194; Rocky Mountain Fever, 195; Metazoa, 195; The Cestodes, or Tapeworms, 198. CHAPTER IX M W. FORMATIONS 208 Malformations by Excess, 208; Malformations by Defect, 209; Hare- lip and Cleft Palate, 211. PART II DENTAL PATHOLOGY CHAPTER X Introduction 213 Predisposing and Exciting Causes, 213; Lowered Vital Resistance, 214; Exciting Causes, 21-1; Predisposing Causes of Dental Disease, 215. CHAPTER XI Enamel, Dentin, and Cementttm 217 Normal Histologic Considerations, 217; Normal Enamel, 217; Dentin, 228; Cementum, 233. 4 CONTEXTS CHAPTEE XII PAGE Development of the Teeth 241 Dentin, 246; Cementum and Peridental Membrane, 248. CHAPTEE XIII Hypoplasia, Microscopic axd Macroscopic 250 Dental Hypoplasia, 251; Enamel, Dentin, and Cementum, 251. CHAPTEE XIV Macroscopic Deformities of the Teeth 264 Abnormalities of Form Affecting the Crowns and Boots of the Per- manent Teeth, 264; Geminated Teeth, 284. CHAPTEE XV Abnormalities ix the Number of Teeth 287 Supernumerary Teeth, 287. CHAPTEE XVI Abnormalities ix the Number of Teeth 291 Absence of Teeth, 291. CHAPTEE XVII Hutchixsox's Teeth axd Other Syphilitic Stigmata 299 Hutchinson's Teeth and Other Syphilitic Stigmata, 299. CHAPTEE XVIII Dental Caries 306 Historical Data, 306. CHAPTEE XIX Dental Caries (Coxt'd ) 311 General Considerations, 311; Predisposing Causes, 317. CHAPTEE XX Pathologic Processes ix Dextal Caries 322 Pathologic Processes in Dental Caries, 322. CHAPTEE XXI Caries of the Examel 331 Etiology and Pathologic Anatomy, 331. CONTENTS CHAPTER XXI] PAGE Gabies of Dentin and Oementxjm 340 Etiology and Pathologic Anatomy, 340 j Transparent Zone or Zone of Tomes, 344; Pigmentation, .".17; The Decay of Cementum, 349. CHAPTER XXIII Rtpercementosis 350 General Considerations, 350; Etiology and Pathologie Anatomy, 352. CHAPTER XXIV Abrasion and Erosion 356 Etiology of Abrasion, 356; Pathologic Anatomy of Abrasion, 357; Etiology of Erosion, 359; Pathologic Anatomy of Erosion, 365. CHAPTER XXV The Saliva 366 Normal and Pathologic Considerations, 366; Color, 367; Odor, 368; Taste, 368; Constituents of the Saliva, 369; Mucin, 369; Ptyalin, 370; Albumin, 371; The Sulphocyanates, 371; Inorganic Constit- uents, 372; Reaction, 373. CHAPTER XXVI The Gums and Gingiva 375 Normal and Pathologic Considerations, 375; Gingiva?, 376; Normal and Pathologic Considerations, 376; Functions, 378. CHAPTER XXVII Calcareous Deposits 381 Etiology, 381; Lesions in the Investing Tissues Caused by Salivary Calculi, 387. CHAPTER XXVIII Subgingival Deposits 390 Etiology, 390; Lesions Produced by Subgingival Deposits: Chronic Gingivitis, 392; Pathologic Anatomy, 392. CHAPTER XXIX Diseases of the Peridental Membrane 402 Horizontal Fibers, 405; Oblique Fibers, 405; Apical Fibers, 406; Alveolar Crest, 406; Free Gingiva, 406; Transseptal Fibers, 406. b CONTEXTS CHAPTER XXX PAGE Xonseptic Pericementitis 408 Nonseptic Pericementitis, 408. CHAPTER XXXI Septic Pericemental Inflammation and Acute and Chronic Dento- alveolar abscess 412 Prophylaxis of Pulp Involvements, 414 ; Etiology of Septic Apical Pericementitis, 415; Periapical Infection by the Hematogenic Route, 421; Recovery from Periapical Infections, Acute and Chronic Proc- esses, 422. CHAPTER XXXII Acute Apical Dentoalveolar Abscess 424 Etiology, 424; Clinical Symptoms, 425; Sinus Formation, 427. CHAPTER XXXIII Pathologic Anatomy of Acute Dentoalveolar Abscess 433 Pathologic Anatomy of Acute Dentoalveolar Abscess, 433. CHAPTER XXXIV Chronic Dentoalveolar Abscess '436 Etiology and Pathologic Anatomy, 436; Difference in the Pathology of Acute and Chronic Dentoalveolar Abscess, 443; Bacteria of Septic Pericementitis and Dentoalveolar Abscess, 4.12. CHAPTER XXXV Bone 455 Normal and Pathologic Considerations, 455 ; Bone Involvement in Dentoalveolar Abscess, 457; Xecrosis, Caries, and Rarefying Ostei- tis of the Alveoli and of the Jaws — Xecrosis of the Apical Areas of Roots, 462. CHAPTER XXXVI Periostitis of the Jaw 467 Periostitis of the Jaw, 467. CHAPTER XXXVII Pyorrhea Alveolaris 471 Historical Sketch, 471; General Considerations, 473; Pyorrhea Al- veolaris Caused by Salivary Calculi, 474; Pyorrhea Alveolaris Caused by Subgingival Deposits, 476; Pyorrhea Alveolaris of Systemic Ori- gin, 487. CONTENTS I CHAPTEB WW III PAGE Pyorrhea Alveolaris and Pericemental Abscess of Gouty Origin . 195 Etiology and Pathologic Anatomy of Pyorrhea Alveolaris and Peri cemental Abscess of Gouty Origin, l'.». Chronic interstitial nephritis 105 27. Loops of blood-vessels in granulation tissue 107 28. Formation of new blood-vessels as seen in the tail of a tadpole . . . 107 29. Fibroblasts forming fibrous tissue 108 30. Eegeneration of epithelium 109 31. Hard fibroma 117 32. Soft fibroma of the subcutaneous tissue 118 33. Section of a myxosarcoma 119 34. Chondroma of the thumb 120 35. Osteoma of the lower jaw 122 8 ILLUSTRATIONS PIG. PAGE Small round-celled sarcoma 125 37. Large round celled sarcoma 126 38. Alveolar sarcoma * 126 39. Spindle-cell sarcoma of the mammary gland 127 40. Large spindle-celled sarcoma 128 II. Melanosarcoma 1 - : ' 42. Giant cell sarcoma of the thigh 129 4:;. Metastatic melanosareoma of lung 130 44. Submucous fibroid in the uterus 131 45. Glioma of the brain 132 46. Cavernous angioma of liver ■ .... 134 17. Papillomata of the vocal cords 137 -. Papilloma of the scalp 137 49. Adenoma of the mammary gland 138 . Squamous epithelioma 142 51. Adenocarcinoma of the body of the uterus 1-4 4 52. Scirrhous carcinoma of breast 145 53. Medullary carcinoma of breast 146 .">4. Endothelioma of the dura mater 147 55. Finer structure of the adenomatous form of hypernephroma . . . 149 50. Chorionepithelioina or syncytioma malignum 150 57. Cyst of the parovarium I' 1 58. Acute urethritis 1**8 59. Acute' lobar pneumonia 160 60. Acute lobar pneumonia. Later stage 161 61. Bronchopneumonia. Child 162 02. Miliary tubercles in the liver 165 63. Miliary tubercle of the human form 165 64. Nodular leprosy 1^8 65. Gummatous meningo-encephalitis 170 66. Typhoid fever, showing necrosis of Peyer's patches and intense con- gestion of the bowel 175 67. Actinomycosis of the tongue 181 68. Blastomycosis I 82 69. Invasion of a human hair by trichophyton 184 70. Trypanosoma gambiense 186 71. The common liver-fluke enlarged to show the anatomic characters . 197 7 2. Head of Taenia solium 198 7:'.. Taenia echinoeoccus, enlarged 200 74. Asearis lumbricoides 201 75. Male Trichocephalus dispar or whipworm 202 76. Cephalic extremity of uncinaria duodenalis 203 77. Duodenum showing attached uncinaria 203 78. Trichina spiralis with its connective-tissue covering 205 7!'. Filaria embryo, alive in the blood 206 10 ILLUSTRATIONS FIG. PAGE SO. Female acarus 207 81. Head of fetus at end of fifth week 210 82. Head of fetus in the seventh week 210 83. Diagram of ordinary harelip 211 84. Almost complete single harelip 211 85. Diagram of median harelip 211 8G. Cleft of the hard and soft palate 212 87. Complete double cleft in an infant 212 88. Area of normal dentin and enamel 218 89. Area of normal dentin and enamel from ground section of area near apex of incisor of man 219 90. Contrast between normal enamel and decalcified enamel .... 220 91. Dentoenamel junction 221 92. Ground section, showing junction of enamel and cementum . . . 222 93. Imbrication lines on lower incisor of sclerotic type 224 94. Imbrication lines on lower incisor of malaeotic type 224 95. Calcarine fissures on the surface of a malaeotic molar 225 90. Decalcified longitudinal section showing butt type of enamel-cemen- tum junction 227 97. Longitudinal section of upper cuspid showing the course and ar- rangement of the dentinal tubuli (Color Plate) 228 98. A field of dentinal tubules 229 99. Transverse section of dentin 229 100. Interglobular spaces of Czcrmack in the dentin 231 101. Longitudinal ground section of tooth showing fields of dentin and enamel 232 102. Transverse ground section at the apical region of a root .... 2.", 1 103. Transverse ground section of tooth at the beginning of apical third of root 235 101. Thick area of cementum in the bifurcation of the roots of a molar . 23G 105. Longitudinal ground section showing hyaline cementum, etc. . . . 237 106. Ground section, longitudinal, showing gingival third of root . . . 238 107. Ground section, longitudinal, showing hyaline cementum devoid of lacunae and canaliculi 238 108. Longitudinal ground section of cementum, showing lacunae in areas near dentin and fibers of pericemental membrane incased in the ce- mentum 239 109. Longitudinal ground section in gingival third 239 110. The cementum in the apical region of the roots of an upper first bicuspid 240 111. First evidence of tooth development 242 112. A slightly later stage than in the preceding illustration 243 113. The four sets of cells of the enamel organ 244 114. Same stage of development as seen in the preceding illustration . . 247 ILLUSTRATIONS 11 FIfi. PAGE 115. Calcification of the deciduous teeth 248 116. Calcification of the permanent teeth 248 117. Hypoplastic defeets of the enamel 251 118. Hypoplastic defect of the enamel 252 119. Hypoplasia of the enamel producing an external macroscopic defect on the labial surface of an incisor 255 120. Hypoplasia of the enamel in the approximal surface of an incisor . 256 121. A case of enamel agenesia 257 122. Decalcified section showing a multitude of interglobular spaces . . 257 123. Hypoplasia of the enamel in the shape of a slight reddish brown discoloration 259 124. Hypoplasia of the enamel in the shape of intense reddish brown dis- coloration 259 125. A case of biown stain affecting the enamel on the labial surfaces of the central and lateral incisors only 259 126. A slight hypoplasia of the enamel on the labial surface of an upper cuspid 260 127. Hypoplasia of the enamel on the labial surface of an upper cuspid 260 128. Hypoplasia of the enamel on the labial surfaces of upper left and upper right lateral incisors, semilunar in shape 260 129. Hypoplasia of the enamel in an upper left central incisor .... 260 130. Hypoplasia of the enamel in an upper right lateral incisor .... 261 131. Hypoplasia in the crown of a lower molar 261 132. Hypoplasia of the crown of an upper molar 261 133. Hypoplasia of the enamel in upper molars 261 134. Hypoplasia of the enamel in lower molars 262 135. Hypoplasia of the enamel in an upper cuspid 262 136. Hypoplasia of the enamel in an upper central 262 137. Overdeveloped cervico-lingual ridge in upper left lateral incisor . 265 138. Hypoplasia of the cervico-lingual ridge of upper incisors .... 265 139. Fissured cervico-lingual ridge in lateral incisor 265 140. Photomicrograph of a central incisor with an over-developed cervico- lingual ridge simulating a cusp 266 141. Severe hypoplasia of upper central incisor 267 142. Severe form of hypoplasia in upper incisor 267 143. Severe form of hypoplasia in upper incisor involving the crown and the root 267 144. Hypoplasia of the root of an upper incisor 267 145. Ground section of specimen shown in Fig. 144 268 146. Hypoplasia of the incisal third of an upper incisor 269 147. Peg-shaped upper lateral incisor 269 148. An upper right lateral incisor mesial view- with a labial defection of its root 269 149. A prong-like process on the lingual surface of the lower lateral in- cisor 269 12 ILLUSTRATIONS FIG. PAGE 150. Lower lateral incisor with two roots 270 151. Severe hypoplasia of upper cuspid 270 152. A marked case of enamel and dentin hypoplasia 270 153. A series of upper cuspids with unusually short roots 271 154. A series of upper cuspids with abnormally long roots 271 355. Distal deflection of an upper right cuspid 272 156. A marked deflection to the mesial in an upper right cuspid . . . 272 157. Lower cuspids with two roots 272 158. Eadiogram of a lower right cuspid with two roots 273 159. Supernumerary root in lower cuspid 273 160. Marked hypoplasia of the crown of a lower cuspid 273 161. Upper first bicuspid with three roots 273 162. Upper right first bicuspid with three roots 273 163. An upper second bicuspid with a bifurcated root 273 164. An upper first bicuspid with marked deflection of the lingual root . 273 165. Bifurcation of the roots of an upper second bicuspid 274 166. An upper bicuspid with three roots 274 167. An upper first bicuspid with an abnormally long root 274 168. A hypoplastic upper bicuspid 274 169. Pronounced deflection of the root of an upper bicuspid 274 170. Upper left second bicuspid; disproportion between the size of the crown and that of the root 275 171. An upper second bicuspid with a disproportionately small root . . 275 172. A lower first bicuspid with two roots 275 173. Lower second bicuspid with two roots 275 174. A lower first bicuspid with a marked deflection of its roots .... 275 175. Distal deflection of the root of the lower right first bicuspid . . . 275 176. Disproportion between the size of the crowns and roots of lower sec- ond bicuspids 276 177. Hooked root in lower bicuspid 276 178. Disproportion between the crown and root of a lower right second bicuspid 276 179. Disproportion between the size of the crown and that of the root and deflections of the root of lower first bicuspids 276 180. Hypoplasia of the lingual cusp of a lower first bicuspid .... 277 181. A hypoplastic lower second bicuspid 277 182. Lower left second bicuspid with six cusps 277 183. The roots of an upper molar united by bands of cementum . . . 278 184. An upper second molar with its three roots fused together by means of cementum 278 185. Upper left third molar with badly deflected, fused, and hyperce- mentosed roots 278 186. An upper first molar with hooked roots 278 187. Deflection to buccal and distal roots of upper first molar .... 279 188. A supernumerary root in upper molar 279 ILLUSTRATIONS 13 FIG. PAGE L89. Lower right first molar with superrfumerary root on the lingual aspect • 280 190. Supernumerary root on distobuccal aspect of a lower first molar . . 280 191. A lower first molar with a supernumerary root between the mesial and distal roots on the lingual aspect 280 192. A lower firsl molar with three roots 280 L93. A lower first molar with three roots; supernumerary root on incisal aspect 280 194. Four well-developed roots iu lower left second molar .... 281 195. A hypoplastic lower third molar 281 196. Dwarfed upper third molar 282 197. Dwarfed lower third molars 282 198. Dwarfed upper third molar 282 199. Hypoplastic upper third molars 283 200. Marked deviation of the roots of an upper third molar .... 283 201. Upper third molars with double deflection of the buccal roots and single deflection of the lingual roots 283 202. Geminated deciduous incisors 285 203. Geminated upper central and lateral incisors 285 204. Geminated molar and bicuspid; possibly two bicuspids .... 285 205. Geminated upper second and third molars 285 206. Geminated upper second and third molars 286 207. Geminated upper second and third molars 286 208. Enamel pearl on upper left second molar located in the concavity on the lingual root which shows a tendency toward bifurcation . . 286 209. Enamel pearl in upper right first molar 286 210. A peg-shaped supernumerary tooth between the upper central incisors 287 211. Two tuberculated supernumerary incisors in the same arch . . . 287 212. A tuberculated supernumerary tooth between the incisors .... 288 213. A peg-shaped supernumerary tooth located lingually to the upper in- cisors 288 214. A supernumerary central in perfect alignment between normal in- cisors 288 2\~>. A supernumerary upper incisor fused to the normal central incisor 289 216. Supernumerary molar between the upper second and third molars . 289 217. A fourth molar in place 289 218. Deciduous upper second molar retained until late in life .... 292 219. A retained lower left second deciduous molar 292 220. Absence of the upper right lateral incisor 293 221. Xoneruption of permanent lower first molar 293 222. Xoneruption of permanent cuspid 294 223. Xoneruption of permanent cuspid 294 224. Impaction of lower third molar 295 225. Impaction of third molar 295 14 ILLUSTRATIONS FIG. PAGE 226. Impaction of lower third molar 296 227. Impaction of second bicuspid and second molar 296 228. Impacted lower third molar 297 229. Hutchinson's teeth. Sulciform erosions of incisors 300 230. Hutchinson teeth. Cuspal erosions of canines and molars .... 300 231. Hutchinson's teeth. Cuspal atrophy of canines and first molars . . 301 232. Multiple sulciform erosions, general, and involving the bicuspids . 301 233. Lingual aspects of preceding illustrations. Hutchinson's teeth . . 301 234. Hutchinson teeth. Honeycomb erosions 302 235. Hutchinson teeth. Mierodontism 303 236. Complete congenital absence of teeth in the upper arch 303 237. Defective fissure in a molar 318 238. Typical conical form of penetration of caries into the dentin . . . 326 239. Microorganisms in the structure of the dentin 327 240. Microorganisms in the structure of the dentin 327 241. Microorganisms in the structure of the dentin 329 242. Microorganisms in the structure of the dentin 329 243. Artificial decalcification of the enamel by one per cent hydrochloric acid simulating caries 332 244. Caries of enamel at the deepest portion of the cavity 333 245. Caries of enamel in proximal surfaces 335 246. Caries of enamel in a proximal surface in which caries lias made con- siderable progress 336 247. Caries of enamel in a pit 337 248. Progress of enamel caries in a molar 338 249. Progress of enamel caries in a molar 339 250. Caries of dentin showing decalcification of the organic constituents and conversion into a soft cartilaginous mass 340 251. Caries of dentin showing decalcification of the inorganic constit- uents and conversion into a soft cartilaginous mass 341 252. Undermining caries; destruction of tooth substance from within . 342 253. Undermining caries; destruction of tooth substance from within . 343 254. Undermining caries of approximal surface; undeeayed enamel cusp about to break away 344 255. Caries of dentin 345 256. Transparent zone of Tomes in dentin 346 257. Caries of enamel and dentin 348 258. Caries of eementum on labial surface of abraded upper left central incisor 348 259. Hypercementosis of lower first bicuspid and deflection of its root . 350 260. Hypercementosis in upper rigid second molar 350 261. Hypercementosis in upper bicuspid 351 L'62. Hypercementosis of root of lower molar, the two roots are united by a band of eementum 351 263. Hypercementosis involving the three roots of an upper molar . . . 351 ILLUSTRATIONS 1 5 FIG. PAGE 264. Hypercementosis involving the apical area of the three roots of an upper molar • 351 265. Excessive hypercementosis in :i lower molar 351 2<>7. Hypercementosis involving the three roots of an upper left first molar .''>-">2 268. Hypercementosis of the posterior rool of the lower first molar . . 352 269. Nodular form of hypercementosis 352 270. 1? sorption of dentin and obliteration of the resorbed area by ce- mentum 353 271. Hypercementosis accompanied by dentin resorption and filling in of the resorbed area of dentin by cementum 354 272. Abrasion— mechanical wearing away of the cusps of a lower molar :!-">7 273. A series of incisors which have suffered from slight abrasion . . 358 274. Abrasion of the incisal edges of two upper central incisors; brown- ish discoloration of exposed dentin 358 275. Photomicrograph of ground section of one of the abraded teeth . 359 27<>. Upper right cuspid 360 277. Upper cuspids which for many years have been the seat of abrasion 360 278. Abrasion of lower third molar. Complete wasting away of the crown 361 279. Abrasion of lower third molar. Complete wasting away of the crown 361 280. Spiral-shaped abrasion in upper left cuspid caused by an ill-fitting clasp 361 £81. A series of abraded lower cuspids 361 282. Abrasion of upper right central incisor 362 283. Abrasion of lingual surface of upper left cuspid 362 2S4. Abrasion of the labial surface of the lower right first bicuspid . . ."!fi2 285. Cup-shaped abrasion in lower molars 362 286. Cup-shaped abrasion in lower first molar 363 287. Cup-shaped abrasion in a lower molar 363 288. Cup-shaped abrasion in lower molar 363 289. Abrasion in a. deciduous molar 363 290. Action of acid calcium phosphate in conjunction with friction . . . 364 291. Tubular calcification in the dentin 364 292. Normal gingiva of sheep 376 293. Gingiva? of sheep 377 294. Human gingiva 378 295. Salivary calculi on the lingual surfaces of the roots of lower cuspids 383 296. Voluminous salivary calculus with shelf -like formation .... 384 297. Salivary calculus with shelf-like formation 384 298. Salivary calculus in lower right incisor 384 299. Salivary calculus which had attained considerable size and had caused exfoliation of the tooth 384 16 ILLUSTRATIONS FIG. PAGE 300. Salivary calculus in lower incisor which had caused the exfoliation of the tooth 385 301. Salivary calculus covering all of the crown and most of the root of the tooth 383 302. Salivary calculus which covered a large area of crown surface and all of one-half the root surface 385 303. Salivary calculus on lower right cuspid involving approximately two- thirds of the root 385 304. Salivary calculus on lingual aspect of the root of a lower central incisor 385 305. Salivary calculus covering portion of the labial surface of lower right central incisor 385 306. Salivary calculus entirely covering the buccal surface of the crown and half the length of the roots of an upper left first molar . . 386 307. Voluminous salivary deposits upon buccal and part of the occlusal surfaces of an upper molar 386 308. Large masses of salivary calculi removed from the teeth to which they were attached 387 309. Large masses of salivary calculi 387 310. An upper lateral incisor with its root covered with subgingival de- posits 390 311. Subgingival deposits in upper right lateral incisor 390 312. Subgingival deposits in upper right cuspid 390 313. Subgingival deposits in upper right second molar 391 314. Subgingival deposits in upper right second molar 391 315. Eoots of a molar covered with subgingival deposits 391 316. Subgingival deposits on the anterior and posterior roots of a lower molar 391 317. Section of human gingiva 393 318. Chronic inflammation of gingiva 394 319. Chronic inflammation of the free gingiva 395 320. Gingivitis, chronic, advanced stage, infection progressing toward peridental membrane 396 321. Gingivitis, chronic, advanced stage, induced by subgingival deposits 397 322. Progressive chronic gingivitis 398 323. Chronic inflammation of gingiva 399 324. Chronic inflammation in the gingiva which has spread to the periden- tal membrane 400 325. Progressive chronic gingivitis 401 326. Normal peridental membrane 403 327. Normal peridental membrane in situ 404 328. Normal peridental membrane and its relation to cementum and al- veolar process 405 329. Chronic dentoalveolar abscess of an upper lateral incisor with a large area of rarefaction 416 [LLUSTRATIONS 17 FIG. PAGE 330. Chronic dentoalveolar abseesa 416 331. Chronic dentoalveolar abscess in upper firsl and second left bicuspids 416 332. Three chronic dentoalveolar abscesses 416 333. Chronic dentoalveolar abscess 117 334. Chronic dentoalveolar abscesses 417 335. Chronii' dentoalveolar abscess 418 336. Chronic dentoalveolar abscess , 418 337. Chronic dentoalveolar abscess (so-caUed dental granuloma) . . . 419 538. Chronic dentoalveolar abscess in the bifurcation of the roots (if the lower right first molar 420 339. Chronic dentoalveolar abscess caused by the perforation of the disto- lingual aspect of an upper second bicuspid 420 340. Chronic dentoalveolor abscess caused by a fragment of a broach broken in the root canal 420 341. Intraalveolar root fracture of an upper right cuspid 420 342. Result of poulticing the face in connection with acute dentoalveolar abscesses 428 343. Submental fistula 430 344. A chronic dentoalveolar abscess (dental granuloma) 437 345. Chronic dentoalveolar abscess 437 346. Dentigerous or root cyst 442 347. Dentigerous or root cyst 442 348. Dentigerous or root cyst 442 349. Dentigerous or root cyst 442 350. Chronic dentoalveolar abscess (so-called dental granuloma) . . . 444 351. Section of a chronic dentoalveolar abscess 445 352. Chronic dentoalveolar abscess 446 353. Chronic dentoalveolar abscess 447 354. Chronic dentoalveolar abscess 448 355. Chronic dentoalveolar abscess 449 356. High power reproduction of cellular elements in the round-cell infil- tration in a chronic dentoalveolar abscess 450 357. Alveolar bone in the periapical region 458 358. Transverse section of tooth 459 359. Arrangement of cancellated bone in region of central incisors . . 460 360. Bone of alveolar process and two cancellated spaces 460 361. Arrangement of bono in incisal region 461 362. Arrangement of bone in bicuspid region 461 363. Arrangement of bone in molar region 461 326. Beginning resorption of the apical third of a root of an upper central 465 365. Resorption of the roots of a lower right first molar 465 366. Beginning resorption of the apical third of a root of an upper central 465 367. A chronic alveolar abscess 465 368. Chronic dentoalveolar abscess 466 18 ILLUSTRATIONS FIG. PAGE 369. Sequestrum that came away attached to a tooth following a chronic dentoalveolar abscess of long standing 468 370. Subgingival deposits on the root surfaces 475 371. Absence of approximal contact accounting for the formation of a pocket between lateral incisor and cuspid 47.1 372. Absence of contact and pyorrhea pocket formation 475 373. Absence of contact and pyorrhea pocket formation 475 .",74. Absence of contact and pyorrhea pocket formation 475 375. Absence of contact and pyorrhea pocket formation 475 376. An area of gingivae from a pyorrhea pocket, the seat of a chronic inflammation 476 377. Gum tissue overlying a pyorrhea pocket decalcified section . . . 477 378. Chronic gingivitis which by process of continuity will spread to the gums and peridental membrane 478 379. Decalcified transverse section of upper incisor 479 3S0. An area of peridental membrane the seat of chronic inflammation in pyorrhea alveolaris 480 381. Chronic inflammation of peridental membrane 481 382. Transverse section showing dentin, cementum, peridental membrane, etc 482 383. An infection from the peridental membrane involving the medullary substance in the cancellated space, an osteomyelitis being the re- sult 483 384. Destruction of alveolar process and pi ridental membrane .... 484 385. Destruction of the alveolar process and peridental membrane in pyorrhea alveolaris 484 386. Absorption of the apical areas of the roots of the upper central in- cisors caused by infection 484 387. Eacliograms showing error in technic of taking 485 S88. Destruction of the alveolar process and peridental membrane ... t85 389. Destruction of the alveolar process and peridental membrane . . 485 390. Destruction of the alveolar process and peridental membrane in pyorrhea alveolaris 486 391. Destruction of alveolar process and peridental membrane in pyorrhea alveolaris 486 392. Destruction of alveolar process and peridental membrane in pyorrhea alveolaris 486 393. Destruction of alveolar process and peridental membrane establishing a pocket distal to the first molar 486 394. Extensive pockets involving all the roots of lower first and second molars 486 :'.9r). Extensive destruction of alveolar process in pyorrhea alveolaris . 1st; 396. Pyorrhea alveolaris 487 ;i97. Pyorrhea alveolaris in the lower teeth 488 398. Pyorrhea alveolaris in the upper right cuspid 488 ILLUSTRATIONS 1!) FIG. • PAGE 399. Pyorrhea alveolaris 489 4(ii). A typical ease of pyorrhea alveolaris 489 101. Destruction of alveolar process in an extensive case of pyorrhea alveolaris 490 402. A longitudinal section of a normal pulp of man 501 103. Longitudinal section of normal pulp 502 104. Section of tooth showing relation of the pulp at the apical foramen to the peridental membrane 503 405. Section ~> 437. Radiograph of case of systemic involvement 556 438. Eadiograph of case of systemic involvement 557 20 ILLUSTRATIONS FIG. PAGE 439. Radiograph of case of systemic involvement 558 440. Eadiograph of case of systemic involvement 558 441. Radiograph of case of systemic involvement 559 442. Radiograph of case of systemic involvement 560 443. Radiograph of case of systemic involvement 560 444. Ulcerative stomatitis (Color Plate) 5G8 GENERAL AND DENTAL PATHOLOGY PART I GENERAL PATHOLOGY CHAPTER I INTRODUCTORY Pathology is the science which treats of the causes, manifesta- tions, and results of disease. Broadly speaking, pathology stud- ies disease in all its phases, but the bulk of the clinical symp- toms and the treatment, which constitute so large a field of in- vestigation, are usually dealt with in other departments of medical science. Disease 1 is any alteration of the structure or the composition of the tissues, which impairs or tends to impair their function. 2 Disease is not an established entity, but a process. It is a continu- ing series of alterations which go on until interrupted by death, or until recovery takes place. The examination of a pathologic specimen shows the changes in structure and composition which have taken place up to the time when the tissue was examined; 'It is often contended that disease can not be accurately or scientifically defined, that there is no clearly marked dividing line between health and disease. This is undoubtedly true, but the same objection obtains against a definition of insanity, abnormality, hys- teria, death and many other terms. Eut few terms could be defined, if an absolutely un- assailable and faultless definition were demanded. A definition that would include all path- ologic manifestations and exclude all normal variations is neither possible nor necessary. It is far more important that the general reader, and particularly the student who is just beginning the study of pathology, should learn the meaning of terms as they are generally used and understood by pathologists, than that our definition should be scientifically flawless. : "Just as physiology is the study of the functions of the body in health, so is pathology the study of the same functions in disease." — Adami. "* * * disease is not a thing, but a process. It is an abnormal performance of cer- tain of the functions of the body." — Delafield snd Prudden. "It is doubtful whether alterations of function can occur without some alteration in structure." — Stengel and Fox. 21 22 GENERAL PATHOLOGY later examinations will reveal furl her alterations, and in many instances additional pathologic processes. Health is that state or condition in which the tissues and organs of the body are enabled to perform all their functions in a normal manner. It is of course impossible, with any great degree of exactitude, to point out where normality ends and abnormality begins, so gradually does the one condition merge into the other. The nearer we approach the boundary line, the more difficult it becomes to determine whether we are face to face with a normal variation of health or incipient disease. This difficulty, how- ever, disappears when a well-marked instance of disease is met with, and the task then resolves itself into a determination of the nature and extent of the morbid process. Health then is the performance of all the functional activities of the body in a normal (i.e., an average, regularly established) manner, and disease is impairment of these activities. In those cases where function is pathologically increased, as in the hy- pertrophies, the increase is at most only temporary and tends toward impairment later; in fact, when considered as a part of the sum total of activities which must act in harmony to con- stitute a state of health, any pathologic increase of functional activity must be regarded as an impairment of health. Life and functional activity are one and the same thing. Let one of the vital organs cease to do its work and death ensues. So far as biological science can determine, life is the result of chemical (more correctly, physicochemical) processes occurring within the tissues. When these processes are so coordinated that all the organs perform their activities in perfect harmony with one another, the individual is said to be healthy; when these processes are stimulated or retarded, by any cause whatsoever, beyond the normal, disease results. These abnormal chemical changes in the tissues can often be demonstrated by means of staining and other reactions before structural changes manifest themselves, and in all cases precede the latter. Chemical and structural changes result in changes of function, that is, disease. The so-called "functional diseases" 3 as for example, epilepsy, are such as exhibit decided functional changes, without discoverable 3 Green's Pathology, p. 5. INTRODUCTORY '2'.) anatomic or chemical changes, bu1 these undoubtedly exisl and have caused the functional disturbance. Pathology therefore studies the morbid side of anatomy, chemis- try, and physiology, and it follows that a comprehensive knowledge of normal anatomy, chemist vy, and physiology is a prerequisite to the study of pathologic conditions. THE CELL The living organism, animal and vegetable, is made up wholly of cells. Although recognized much earlier, the cell was not gen- erally accepted as the structural unit until Virchow founded modern pathology by the publication of his epochal work on Cellular Pathology in 1858. Since then it has also become the basis of chemical and physiologic considerations, and the cell is now the histologic, the chemical and the physiologic or biological unit. All organisms, unicellular and multicellular, are derived from a parent cell ("omnis cellula e cellula"- — Virchow). The uni- cellular organisms, as protozoa and bacteria, are composed of but one cell, which is capable of performing all the essential vital functions. In the multicellular organisms, the cells, after a suffi- cient number have been formed from the parent cell, form groups which become differentiated during the course of the development of the embryo, and destined to perform different functions. Such differentiated or specialized groups of cells with their character- istic intercellular substance (the latter being in all instances a product of the cells themselves) constitute the various tissues; appropriate amounts and kinds of different tissues form organs; and a system of organs with their supporting structures form the individual organism. Protoplasm is a term given to the albuminous material which composes the cell and gives to it its vital properties. It is not synonymous with cytoplasm (q.v.) or any histologic division of the cell. It is the basic substance found in all parts of the cell. Structurally the cell may be divided into two essential parts — the cytoplasm and the nucleus. Given these two essentials, a cell can perform all its physiologic functions, and may there- fore be considered a true cell. In addition to these two parts, the vegetable cells and some of the animal cells have a peripheral 24 GENERAL PATHOLOGY membrane, or cell wall ; and some cells, particularly when in an actively reproducing- state, contain a body called the centrosome. A typical cell, therefore, may be said to consist of the follow- ing structures: Anatomy of the Cell 1. A cell wall, or membrane. 2. Cytoplasm, or cell material exclusive of the nucleus. 3. The nucleus, or karyon (literally, a nut or kernel). 4. Centrosome, lying within its centrophere. The cell wall, or membrane is a condensation and modification of the peripheral cytoplasm, which governs the entrance and Fig. '1. — Diagram of a typical cell. (After Bailey.) /, Cell membrane; 2, metaplasm; .?. karyosome; 4, hyaloplasm; 5, spongioplasm; 6, linin; 7, nucleoplasm; S, attraction sphere; 9, centrosome; 10, plastids; //, chromatin network; 12, nuclear membrane; 13; nucleolus; 14, vacuole. exit of nutritive substances excretory products and other ma- terials. Only a few of the animal cells, such as fat cells, goblet cells, cartilage cells, etc., have a distinct cell wall ; the great majority of animal cells present merely a more or less homo- geneous outer layer of cytoplasm, called ectoplasm or exoplasm, to distinguish it from the inner endoplasm which is usually granu- lar, and the phenomena of diffusion and osmosis indicate that the ectoplasmic zone serves the purposes of a cell wall. Vegetable cells have distinct cell walls, which often contain cellulose or chitin. The former appears as a blue circle on the application of iodine. INTRODUCTORY -•> The cytoplasm, or cell body, is a semifluid substance composed of a network of fibrils (cytoreticulum) called spongioplasm, in the meshes of which is found a clear, glass-like, homogeneous, semi fluid substance called hyaloplasm (also paraplasm). The actual structure of the spongioplasm is still a mooted ques- tion. Altmann believed it to be made up of granules lying in a gelatinous substance, lie believed these granules to be the vital elements of the cell and called them bidblasts. Butchli's "foam" theory considers the reticular appearance of the spongioplasm to be due to a foam-like emulsion produced by the mixture of fluid of different degrees of viscosity, the cut walls of the minute foam spaces resembling a network. Others still believe the spongioplasm to be a felt work of independent fibrils (filar mass or mitome). Within the cytoplasm are often found granules of pigment or secretory products, fat globules, substances in vacuoles, etc., which are collectively called metaplasm or paraplasm (though some writers use the latter term as synonymous with hyaloplasm). These cell inclusions are adventitious bodies and not true con- stituents of the cell. Plastids or protoplasts are bodies often occurring in vegetable cells, less often in animal cells, which are usually regarded as local areas of cytoplasm, specialized for the performance of some function, e.g.. the transformation of starch, etc. The nucleus is a vesicular body, which in general conforms to the shape of the cell, being elongated in muscle and connective tissue cells, flat in epithelial cells, etc. Its morphology, however, may be very irregular, as seen in leucocytes, and the large bone- marrow cells (megakaryocytes) . The typical cell contains but one nucleus, while the osteoclasts and the various giant cells are mul- tinucleated, resulting probably from repeated division of the nucleus without corresponding division of the cytoplasm. The vegetative nucleus (one not in active process of division) has a transparent, faintly staining nuclear wall or membrane (amphipyn nin). The substance of the nucleus, or karyoplasm structurally re- sembles the cytoplasm in being composed of a network of fibrils (nucleoreticulum) and an interfibrillar semifluid material (nucleo- plasm, nuclear matrix). 26 GENERAL PATHOLOGY The nucleoreticulum consists of an achromatic, faintly staining network of fibrils (or linin), which supports in its meshes a deeply staining substance, called chromatin because of its great affinity for basic dyes. At the nodal points of the linin, the accumula- tions of chromatin into conspicuous granules are called karyo- somes (or net knots or false nucleoli). As usually stained the nuclei of many cells appear to be composed almost solidly of chromatin, because the latter stains deeply, while the linin and nucleoplasm stain faintly. The nucleoplasm or matrix is a clear fluid or semifluid sub- stance, lying in the meshes of the nucleoreticulum, probably nu- trient in character, resembling the hyaloplasm of the cytoplasm. The nucleolus, or plasmosome, is a small spherical body, some- times more than one. lying within the nucleus. It does not ap- pear to be attached to the nuclear structures, stains less in- tensely than the chromatin, particularly in fixed tissues, where it elects the acid stains, resembling in this respect the cytoplasm. Its function is not known. Cells without nuclei, as the red blood cells, are no longer true or complete cells, having lost the nuclei which all such cells pos- sessed in their early life history, together with their power of reproduction. In some of the simple forms of life, as bacteria, the nucleus either fills the whole cell, leaving an almost undemonstrably small ring of cytoplasm about the nucleus; but according to the more generally accepted view, the nuclear material, instead of being collected together into a compact nuclear body, is scat- tered throughout the entire cell. Bacterial cells, therefore, re- semble the nuclei of tissue cells in staining solidly and in hav- ing the same affinity for basic dyes. The centrosome is a very minute body of variable staining quality, and often difficult to distinguish from metaplasmic gran- ules. It is usually found in the cytoplasm near the nucleus, and is often surrounded by a clear area, the ccntrosphere, from which radiations into the surrounding cytoplasm may be seen when the cell is about to divide. The Chemistry of the Cell Protoplasm, or bioplasm, is the soft, colorless, jelly-like sub- stance of which living cells or tissues are composed. There is INTR0D1 CTORY 27 no way of chemically analyzing living protoplasm. Chemical reagents cause the death of the cells with coagulation of various constituents, etc., hence the term "protein" (given to the most important constituent of protoplasm) refers necessarily 1o what the chemist finds when he analyzes dead cells, while the term "proteinogen" may be applied to the living material. Thus analyzed, cells are found to he composed essentially of proteins, lipoids, inorganic suits and watt r, often called the primary constituents. Other substances as fats, carbohydrates, secretory granules, pigment granules, enzymes, etc., are food mate- rials and metabolic products, and are not essential chemical com- ponents of the cell. These are often called secondary constit- uents, and it is these secondary constituents that account for the great differences in the histologic appearances of the various types of cells. Proteins are the most complex substances known to the chemist. They will not diffuse through animal membranes or other dif- fusion membranes, and some fail even to pass through fine porce- lain filters, hence their molecules must be very large. Both their structural and molecular formula? are as yet unknown, and even their empiric or percentage formulae have only been approxi- mately determined. For example, the percentage composition of oxyhemoglobin (one of the simplest of the proteins) varies according to different analyses; perhaps the most trustworthy being C 658 H 1181 O 210 N 207 S 2 Fe ; while the molecular weight accord- ing to different reports varies from 15,000 to 17,000. By hydrolysis of the proteins, with acids, alkalies, steam or enzymes, they yield successively, although not wholly synchron- ously, proteoses, peptones and peptides (which still retain certain properties characteristic of proteins) and finally amino acids— the "building stones" or ultimate constituents of the protein molecule. These amino acids are optically active, crystalloid sub- stances, of known chemical structure. Each contains an acid (carboxyl) group and a basic (amin) group, and is therefore am- photeric in reaction. Their type formula is NIL O I " II R— CH— C— O— H 28 GENERAL PATHOLOGY Eighteen of these acids have been identified; all contain the ammo-acid radicle combined with other groups or "nuclei," and the latter may belong to the aliphatic, or open-chain series (as glycocoll), homocyclic (as tyrosin) or heterocyclic (as trypto- phane). All protein food materials are reduced by the digestive enzymes into amino acids, preparatory to assimilation by the cell; after their introduction into the cell, the amino acids are synthesized by the intracellular enzymes into such type of proteins as the cells may need. Proteins have been classified as follows : 4 I. Simple Proteins. Substances which yield only amino acids on hydrolysis. (a) Albumins, as egg albumin, serum albumin, lactalbumin. (b) Globulins, as serum globulin, ovoglobulin (from yolk of c feO ) ' (c) Glutelins, as glutenin from wheat. (d) Prolamins, as hordein from barley. (e) Albuminoids or scleroproteins, as collagen, elastin and keratin, from fibrous tissues, elastic tissues and skin appendages respectively. (f) Histones, as globin from hemoglobin. (g) Protamins, the simplest natural proteins, as salmine. The simple proteins differ among themselves in solubility, coagulability and other properties. II. Conjugated or Compound Proteins. (a) Nucleoproteins. Compounds of protein molecules and nu- cleins. The nueleins yield on further hydrolysis other protein molecules and nucleic acids. Nucleic acids are rich in phosphorus, being composed of phosphoric acid, pyrimidin bases, purin bases ("nuclein bases") and a carbohydrate. The different combina- tions of these various ingredients result in an enormous variety of nucleoproteins, which constitute the most important part of the cell, both of cytoplasm and nucleus. (b) Glycoproteins. Compounds of protein molecules and a car- bohydrate group (other than that present in the molecule of nu- cleic acid), as the mucin of secretory cells, and the mucoid of fibrous tissues. 4 The American Physiological Society and The American Society of Biological Chem- ists. [NTRODUCTOR'S 29 (e) Phosphoproteins. Compounds of protein and phosphorus- containing substances (other than nucleic acid or lecithin), as casein from milk. (d) Hemoglobins. Compounds of protein with hematin or simi- lar substance, as hemoglobin from blood. (e) Lecithoproteins. Compounds of protein with lecithins (see below). Lipoids are substances which resemble fats in certain physical properties but differ chemically; they dissolve in ordinary fat solvents. The chief lipoids (or "fat-like" bodies) are lecithin and cholesterin. Lecithin is a combination of certain fatty acid radicals with phos- phoric acid and cholin, and constitutes the greater part of the lipoids. Lecithin plays a very important part in cell metabolism. Cholesterin, or cholesterol, is an alcohol, related to the terpenes. It is chemically rather inert, and its role is probably a physical one. Inorganic Salts, particularly chlorides, carbonates, phosphates, and sulphates of the alkaline metals and the alkaline earths, ionize in the water of the cell, and their ions unite chemically with the protein groups (ion proteins). It is very probable that proteins and lipoids engage in those chemical reactions, which are essentially the basis of life, only as they form compounds with the ions of inorganic salts. Water in generous amount within the cell is necessary to carry out the vital chemical processes, because it is the medium in which dissociation of the molecules of the salts above mentioned may take place, and the ions which are constantly liberated and reunited during the life of the cell become the electrolytes, bear- ing the electrical charges or energies which represent the fun- damental vital processes. The Physics of the Cell The substances before mentioned as essential or primary chemical constituents of the cell, together with the secondary constituents, are present in different physical states ; viz., as colloids and crystalloids which are in solution, or semisolution, in the water and in each other. 30 GENERAL PATHOLOGY It should be borne iu mind that a solution is a physical condi- tion — a homogeneous mixture of molecules, and that ionization is an additional process whereby the molecules which have undergone solution are to a greater or less degree dissociated into atoms or groups of atoms electrically charged. When acids, bases, and salts "dissolve" in water, there is solution plus ionization. A sus- pension or emulsion is a more or less homogeneous mixture of mi- nute masses of molecules in a fluid. Colloids are substances which do not pass through diffusion mem- branes or do so very slowly. They are usually amorphous, but hemoglobin, egg albumin and certain other proteins crystallize readily. Colloids include all forms of proteins, the carbohy- drates (except the sugars), tannic acid, etc., also various in- organic compounds and metals. The protein colloidal solution is either a true solution of protein molecules, whose size, though undetermined, must be very great; or, as is more generally be- lieved, it is a suspension of minute masses of protein molecules. The colloids within the cell are therefore believed to be in a state of suspension. The foodstuffs of the cells — proteins, car- bohydrates and fats — in colloid form are first reduced to the crystalloid form of amino acids, sugar and diffusible soaps and glycerin respectively, and when these enter the cell through the cell wall, which acts as a diffusion membrane, pervious to water, salts, and crystalloids, but impervious to colloids, they are syn- thesized into colloidal proteins, fats, and carbohydrates again by aid of the intracellular enzymes. Crystalloids are substances which diffuse readily through the usual diffusion membranes, and tend to form crystals under favorable conditions. The cellular crystalloids include inorganic salts, sugars, amino acids, urea, creatinine, etc. The inorganic crystalloids or salts form ions, which carry electric charges and are therefore electrolytes. The organic crystalloids do not ionize and are nonelectrolytes. As Mann had stated, the elec- trolytes put life into the proteins. The organic crystalloids are chiefly important as foods or metabolic products. Staining Reactions of the Cell The cell protoplasm consists largely of nucleoproteins. In the cytoplasm all the primary constituents already men- INTRODUCTORY 31 tioned are present, as well as manj of the secondary constituents, lull the rmcleoproteins predominate, and consisl of nucleic acid well saturated with protein materials, thus permitting t lie reac- tion of the cytoplasm as a whole to be neutral or slightly alkaline, in which condition it naturally elects the acid stains. The nucleus is very largely composed of nucleoprotein, but the nucleic acid portion of the molecule is not so "well saturated with protein as in the cytoplasm, and the nucleus as a whole is acid in reaction and elects the basic stains. Because the unsaturated nucleoprotein stains so readily and intensely, it is called chro- matin. When the nucleus is in the process of mitotic division, the nucleic acid portion of the chromatin (nucleoprotein) becomes still less saturated than when in the resting or vegetative state, hence stains more intensely. The linin, as well as the nucleolus, is composed of well-satu- rated nucleoproteins, and therefore resembles the cytoplasm in staining reactions. The staining reagents most commonly used are the anilin dyes, manufactured from coal tar, and are derivatives of benzene and its homologues. Some of these stains are acid, others basic in reaction, and require the opposite reaction in the tissues in order to stain well. The tissue elements may be classified into: (a) Oxyphillic, acidophillic or eosinophillic, which comprise the cytoreticulum, centrosomes, attraction spheres, nuclear mem- branes, linin, nucleoli and certain cytoplasmic granules. The general normal reaction of these elements is slightly alkaline. The more important of the acid or cytoplasmic dyes are eosin, erythrosin and acid fuchsin. (b) Basophillic, which comprise the substances rich in nucleic acid as chromatin and certain cytoplasmic granules (other than those already mentioned). The more commonly used of the basic dyes are hematoxylin, methylene blue, gentian violet, thionin blue, Bismarck brown and basic fuchsin. (e) Some tissue elements have the power of combining with, or absorbing either acid or basic dyes, and are therefore called amphophillic. 32 GENERAL PATHOLOGY (d) Other elements, again, are stained by the neutral salt dyes, as the eosinate of methylene blue (Romanowski) and the triple stain of Ehrlich. The fine granules of the polymorphonuclear leucocytes are neutrophillic. The Physiology of the Cell All true cells (or those which have nuclei) have the funda- mental properties of nutrition, growth, irritability, motility and reproduction. Nutrition. — The cell is able to receive food substances from with- out and transform them into living protoplasm (andbolism) ; also to break down old and worn protoplasm into waste products (ca- tabolism), and extrude these from the cell. The sum total of these anabolic and catabolic chemical processes is called metabolism. Growth, or increase in size of the cell, is a natural consequence of nutrition, and is due to greater activity on the part of the anabolic than of the catabolic processes. Irritability. — This is a definite response to external stimuli. The character of the response depends upon the nature of the protoplasm ; the muscle cell contracts, the glandular epithelium secretes, and the nerve cell conveys impulses. Motility is the power of executing spontaneous movements and is exhibited in different forms : (a) Protoplasmic movement, which is an intracellular move- ment as shown by the circulation or "streaming" of the pro- toplasm. The minute granules, the nucleus, and other constit- uents move about, though in a restricted manner within the living cell. (b) Ameboid movement is a similar but more specific move- ment on the part of the protoplasm, consisting of a protrusion of certain parts of the cell (pseudopodia) beyond its usual outline. These pseudopodia may retract or may proceed until the whole cell has been drawn after them, changing both the shape and the position of the cell. (c) Ciliary movement is the wave-like motion of minute hair- like extensions of specialized cytoplasm, called cilia. Only the columnar variety of epithelium is ciliated. A cell may have from one to two dozen cilia. INTRODUCTORY '■'>'■'> Iii all cases of cellular motion resulting in a change of shape of the cell, as in ameboid and ciliary motion, and in functionating muscle cells, il is the spongioplasm which contracts; the hy- aloplasm plays only a passive role and is believed to represent nutritive material. Reproduction is the derivation of one or more cells from a parenl cell. Cel] reproduction occurs in one of two ways— by direct cell division and by indirect division. Tn the direct form, amitosis, Hie nucleus divides withoul any demonstrable preliminary changes in its histology. This method of division is common in protozoa and other lower forms of life. In the indirect cell division, mitosis or Tcaryokinesis, the nucleus passes through certain complex changes, and these changes, to- gether with alterations of other constituents of the cell, are usu- ally described as taking place in the following stages or phases: The Prophase, in which changes preparatory to division occur. The chromatin network is formed into one or more threads (skein or spireme), which later divides into segments (chromo- somes), the number of which is fixed and definite for each species of plant or animal cell. The centrosome develops a distinct attraction sphere and di- vides into two "stars" or asters, which separate, going to oppo- site poles of the cell, but still connected by fibrils of linin (achromatic spindle). The chromatin segments arrange them- selves along the equatorial line of the spindle. The nuclear membrane and nucleolus disappear during this phase. The Metaphase, in which actual division of the nucleus occurs. Each chromosome (or segment of chromatin) splits longi- tudinally, forming daughter chromosomes. The Anaphase, in which the changes are in the main the re- verse of those occurring in the prophase. The daughter chromosomes separate, one-half going to one pole along the linin threads of the achromatic spindle, the other half going to the opposite pole, where they form daughter nuclei. The Telophase, the finishing stage, in which the cell body di- vides at right angles to the axis of the spindle into two cells, each now having received an equal portion of the nucleus and one GENERAL PATHOLOGY of the newly formed eentrosomes. A nuclear membrane and a nucleolus appear in each new cell. Nothing is at present known regarding the function of the nucleolus. (Fig. 2.) Fig. 2. — Diagrams of successive phases of mitosis. A. Resting cell, with reticular nucleus and true nucleolus; c, attraction sphere with two eentrosomes. B. Early prophase. Chromatin forming continuous thread — the spireme; nucleolus still present; a, amphiaster; the two eentrosomes connected by fibrils of achromatic spindle. C. Later prophase. Segmentation of spireme to form the chromosomes; achromatic spindle connecting eentrosomes; polar rays; mantle fibers; fading of nuclear membrane. D. End of prophase. Monaster — mitotic figure complete; cp, chromosomes arranged around equator of nucleus; fibrils of achromatic spindle connecting eentrosomes; mantle fibers passing from eentrosomes to chromosomes. (E. B. Wilson, "The Cell.") Origin of the Blastodermic Layers The matured ovum, after union with the spermatozoon has oc- curred {fertilization), enters upon a series of repeated divisions {segmentation) . The first result is a solid spherical mass of cells {morula). This mass soon forms a cavity in its center, which grows until there is a hollow sphere (the blastodermic vesicle) sur- rounded bv a single layer of cells attached to the inner surface IN'TK HiiKV 35 of the vesicle excepl a1 one point of the inner surface where a small mass of cells persists which is called the embryonic area, because it is in this small mass of cells that the future embryo Fig. 2. — Diagrams of successive phases of mitosis. E, Metaphase. Longitudinal cleavage; splitting of chromosomes to form daughter chromosomes, ep; n, cast-off nucleolus. F, Anaphase. Daughter chromosomes passing along fibrils of achromatic spindle toward centrosomes; division of centrosomes; if, interzonal fibers or central spindle. G, Late anaphase. Formation of diaster; beginning division of cell body. H. Telophase. Reappearance of nuclear membrane and nucleolus; two complete daughter cells, each containing a resting nucleus. (E. B. Wilson, "The Cell.") first makes its appearance. As cell division proceeds, two layers of cells are produced; viz., the ectoderm, which corresponds to the original layer of the blastodermic vesicle, and the entoderm, or inner layer. Later a third layer appears between the ectoderm and the entoderm, called the mesoderm. The three layers together are called the blastoderm. The tissues derived from these layers are as follows : Ectoderm. — Epithelium of the skin and all its appendages, as hair, nails enamel of teeth, mammary, sebaceous and sweat glands, includ- ing the muscle of latter. ob GENERAL PATHOLOGY All epithelium not mentioned under mesoderm and entoderm, viz., the epithelium of mouth and nose with their glands and cavi- ties; of membranous labyrinth of car; of anus and of that portion of male urethra anterior to the prostate gland. Entire nervous system, with the retina, crystalline lens, and mus- cle of the iris. Mesoderm. — All connective tissue. All muscle tissue, except as stated under ectoderm. All lymphatic tissue, spleen, bone-marrow and blood cells. All endothelium* (of vessels and serous cavities). The epithelium of the genito-urinary tract, except ureter, Madder, female urethra and prostatic portion of male urethra. Entoderm. — Epithelium of alimentary tract (except mouth and anus) ; of Eustachian tube and tympanum. Epithelium of respiratory tract (except nose) ; also of thymus and thyroid glands. Epithelium of urt tt r, bladdt r, f< male urt thra and prostatic portion of male un thra. 1 The endothelia arc included among the epithelia by some histologists; others again distinguish between the "endothelium"' of blood and lymph vessels, and the ''mesothelium" ot serous cavities, the genito-urinary epithelium of mesodermal origin, and striated and heart muscle. CHAPTER II THE ETIOLOGY OF DISEASES While therapeutics is the art of healing disease, pathology is the science of investigating disease, and this investigation is usually pursued under the following headings : 1. Etiology, or investigation of the causes of disease. 2. Morbid, or pathologic anatomy, the changes of structure. 3. Morbid, or pathologic chemistry, the changes in composi- tion. 4. Morbid, or pathologic physiology, the changes in function. Of these, morbid anatomy has been the most highly developed, and forms the major portion of the text in most works on pa- thology. Morbid anatomy, or morphologic pathology, is divided into : (a) Gross, or macroscopic pathology, dealing with the gross or naked-eye appearances, and (b) Pathologic histology, or microscopic pathology, dealing with minute or microscopic appearances. Etiology of Disease The causes of disease are usually divided into (a) predispos- ing, indirect or mediate causes, and (b) specific, direct, imme- diate, exciting or determining causes. Predisposing causes in- clude all conditions, influences and agencies which increase the individual's susceptibility to disease, while the specific causes are the direct and final factors which culminate in the outbreak of disease and determine its nature. There is no definite divid- ing line between the two divisions; predisposing causes may at times become exciting causes and vice versa, as when the ex- posure to extreme cold may directly cause necrosis or inflamma- tion, while a prolonged chilling may predispose to pneumonia, rheumatism, etc. In the main, however, predisposing causes form a class distinct from the determining causes, and in the great majority of instances, the body as a whole, or the part 37 38 GENERAL PATHOLOGY or parts subsequently affected, are first acted upon by the pre- disposing causes, preparing the tissues for the successful inva- sion or development of the real specific causative factors. Predisposing causes may be such biological conditions as sex. age. or race: or the predisposition may be acquired by previous disease, traumatism, injurious occupations, unsanitary surround- ings, bad habits of life, personal vices, etc., or again, such pre- disposition may be hereditary. Some of the principal predisposing causes may be briefly con- sidered: Age. — Children are especially liable to gastrointestinal disease because of the delicacy of these organs, and the abundance of lymphoid structures ; to osteomyelitis, because of the vascularity of the growing bones: to rickets, a nutritional disease involving principally but not exclusively the bones of the body: to diph- theria, whooping cough, measles, chicken pox. scarlatina, etc. Some of these diseases, particularly measles, are very contagious and confer life-long immunity, hence their prevalence in child- hood and their rare occurrence in later life. In adolescence certain physical and mental disorders and anemic conditions are apt to be met with. The "prime of life," from maturity to middle age. is on the whole probably the period most free from disease, still at this time occur those diseases which depend upon free association with other persons, upon exposure to inclement weather and to occupational hazards. After middle age incipient degeneration of the vital organs and tumors, particularly carcinomata. appear, while old age is subject to more pronounced organic changes and sclerotic conditions of the vessels and the trabecular of organs, predisposing to distinct visceral disease, apoplexy, etc. Sex. — Apart from the diseases peculiar to the different sexual organs of the male and female, men as a rule are more exposed to adverse climatic conditions, to dangerous pursuits, hence suf- fer from diseases liable to be favored by these predisposing fac- tors. Men, as a class, are also inclined to a far greater extent than women to indulge in excesses of all kinds, and are, there- fore, more subject to alcoholism, gout, and venereal disease, and to the great number of mental, nervous, and visceral pathologic changes which follow such diseases. ETIOLOGY OF DISEASES 30 Race. Sonic races are more susceptible to certain diseases, especially infectious diseases, than are others. The negro is relatively immune to yellow fever and malaria, probably because his tissues produce a greater number of antibodies due to sub- infections or the fact that his race has been exposed to such dis- eases for a longer time and to a greater extent than the white race. On t lie other hand, the negro is more susceptible to tuber- culosis. The American Indian and the Eskimo are free from tuberculosis in the native surroundings (lack of exposure?) but succumb readily to this disease when brought into civilized com- munities (due largely to lack of resistance — antibodies). The Japanese are said to be comparatively free from scarlet fever, the Chinese from cholera, while the Hebrew race is said to be more susceptible to diabetes than other races. Idiosyncrasy. — This is a marked susceptibility which certain in- dividuals have to the action of certain drugs, infections, foods, and even odors. The smallest doses of quinine will cause ex- tensive and painful eruptions in some persons; the pollen of cer- tain plants will result in coryza and hay fever, or "pollen dis- ease." Strawberries, raspberries, lobster, and many foods give rise to urticarial eruptions in certain individuals. No satisfac- tory explanation of this individual hypersensitivity has yet been offered. A pronounced excitability of the nervous system may partly explain some cases, while in regard to idiosyncrasies to- ward drugs or chemicals it has been assumed that the cell con- stituents of the individuals affected contain atomic groups which readily combine with the substances. Traumatisms. — Injuries of all kinds act by causing shock and reducing the normal vital resistance. A fracture of the shoulder or other part of the body framework may predispose to pneu- monia; extensive burns lead to degenerations of the internal or- gans, etc. Injurious Occupations. — The inhalation of noxious gases predis- poses to respiratory and anemic disease; dust, particularly coal dust, leads to fibroid pneumonia and tuberculosis. Painters ab- sorb lead and suffer from intestinal derangements in consequence. Occupations requiring mental worry or prolonged and intense concentration have a marked depressing effect upon the general health. •40 GENERAL PATHOLOGY Unsanitary Surroundings. — It must be self-evident that the health of individuals who dwell or work in buildings that are poorly ventilated, or that are located amid unclean or filthy sur- roundings, or in low, poorly drained sections, or where the in- mates are subjected to the dust, smoke or fumes of large indus- tries, will be seriously affected and predisposed to disease. Habits. — Intemperance, whether in eating, drinking, use of to- bacco, use of drugs, sexual indulgence, etc., drains the human economy of its health reserve factors and makes it vulnerable to disease. Overwork and excessive play or recreation, in fact, ex- cess in any line of human activity should also be included in the term "intemperance." A proper variation of work and play, of mental or physical exertion and rest, is the only rule by which the normal health of the average individual may be conserved. Heredity. — Heredity is the transmission of certain characteris- tics or tendencies from parent to offspring. The maternal charac- teristics are present in the ovum, and the paternal in the sper- matozoon, the essential living parts of these parental elements being known as the germ plasm. Heredity therefore refers to the qualities contributed by either parent at the time of impregna- tion, and has nothing to do with conditions which may affect the health or development of the fetus during its life in utero. Thus certain diseases, as smallpox, measles, or syphilis, may be ac- quired by the mother subsequent to impregnation, and may be transmitted to the fetus through the placental circulation. The evidences of these diseases may be evident when the child is born, but they are not hereditary, but congenital, that is, dis- eases "acquired in prenatal life." It is usually held, however, that certain diseases, particularly syphilis, may also be trans- mitted through the germ plasm and, therefore, be hereditary, but as a rule it is merely the tendency to disease ; i.e., the par- ticular impairment of health which favors the subsequent devel- opment of a certain disease, that is inherited, and not the dis- ease itself or its specific cause. As an example, tuberculosis may be given, for it is generally accepted at the present time that a lowered resistance or predisposition to tuberculous infection may be inherited, but not the tubercle bacillus. Diathesis is merely another term for an inherited predisposition to disease ; thus we speak of hemorrhagic, rheumatic or tuberculous diatheses. In ETIOLOGY OF DISEASES 41 consanguineous marriages (marriages of blood relatives) the off- spring may suffer from an accentuation or "accumulation" of certain family weaknesses or diatheses. Tl "will be seen that heredity is usually a predisposing factor, and only in ;i few instances (and these no1 admitted by all au- thorities) the direel cause of disease. Specific or Determining Causes. — These may be physical or chemical agencies, living organisms or autointoxication. Traumatism. — Mechanical injuries, as blows, falls, knife or gun- shot wounds, etc., result in concussion, contusion, abrasion, lac- eration or rupture of the soft tissues, or fracture of the bony tissues. Tn all, except concussion, there occurs a certain amount of hemorrhage, which may be interstitial, as in contusions, or external, or into natural body cavities. Disintegration of the blood and injured tissues results with more or less inflammation. Concussion is the violent jarring of an organ, accompanied by slight, profound, or fatal shock, but unaccompanied by visible changes in the structure of the organ. In concussion of the brain, the vital centers are excessively stimulated by the blow, then depressed, or in fatal cases, paralyzed. Contusion (or bruising) and laceration may be, and often are, associated with concus- sion, but are not essential features of the latter. SJiock is a depression of the vital centers, particularly the car- diac and respiratory centers, resulting in weakened heart action, irregular breathing, lowering of the bodily temperature, pallor, and clamminess of the skin. Shock may be caused by an injury, or by a strong emotion, as great fear, acting upon the nerve centers. Pressure upon a part, if continuous, will result in atrophy. In- termittent pressure will cause atrophy of some of the constituents of the tissues affected, and hyperplasia of others, particularly the connective tissues. Heat. — A moderate excess of heat, locally applied, will cause hyperemia; a higher degree will cause, in addition, necrosis, par- ticularly vesication (liquefaction necrosis). A still higher de- gree of heat will char or burn the tissues, with oxidation of the superficial parts and necrosis of the deeper parts. Burns which cover one-third of the surface of the body are nearly always fatal, due to absorption of toxic products formed in the burned 42 GENERAL PATHOLOGY tissues, and to the fact that a large part of the eliminating sur- face of the skin is destroyed. In severe cases death is due to shock. First degree burns are those that are characterized by swelling and reddening of the skin; second degree burns, by the forma- tion of vesicles (or blisters) and bulla?; third degree burns, by destruction of all the layers of the integument with more or less of the subcutaneous tissue and ulceration. The burns so de- scribed refer only to burns of the skin. Burns may proceed deeply into the tissues (sometimes called fourth degree burns) with coagulation of the cells and other forms of necrosis and oxidation, until in fact the whole body is incinerated (completely oxidized). Sunstroke may be caused by exposure to the heat of the sun. The bulbar heat centers are depressed or paralyzed by the heat, or metabolic poisons are formed by the heat which act upon the centers, resulting in very high temperatures (107° to 112°) with labored breathing, headache, vertigo, nausea, delirium and finally coma. Heat exhaustion results from high temperature with humidity, or less often from exposure to the sun alone. This is probably due to vasomotor paralysis, and the symptoms are those of col- lapse with subnormal temperature ; rapid, weak pulse ; rapid, shallow breathing; and livid color. Cold. — The primary effect of cold to the surface is contraction of the superficial capillaries causing the parts to appear blanched and anemic. Soon the vasoconstrictors are paralyzed, the ves- sels dilate, and the parts become swollen and livid and more or less painful {frostbite). In a severe frostbite the part becomes covered with vesicles, the blood plasma coagulates with disinte- gration of the blood cells and thrombosis of the vessels ; gangrene may or may not follow. Unless gangrene sets in, recovery takes place, but in many cases chilblain, or pernio develops as a secon- dary effect of frostbite. This is a condition in which swelling and pain or tingling sensations return in a previously frostbitten part upon approaching a fire, upon exercising, or exposure to slight cold. Kepeated attacks lead to vesication and ulceration. Excessive cold will coagulate the cells and fluids of a part, with subsequent gangrene. Sudden exposure to very low tern- ETIOLOGY OF DISEASES 43 peratures produces lesions practically identical with those caused by burns. Atmospheric Pressure. — Increased atmospheric pressure causes the tissues and fluids to hold more gases (almost exclusively nitrogen), and subsequently when the return to normal pressure is too sudden, bubbles of gas appear in the tissues and blood ves- sels. At first these bubbles are located, only in the capillaries, which may rupture with interstitial hemorrhage, bleeding from mucous surfaces, as nose, accompanied by symptoms of nausea, palpitation of the heart, prostration, delirium and palsies. The tiny bubbles may coalesce into larger ones and form air emboli, or gas emboli, which are apt to be fatal. At necropsy congestion of the central nervous system and thoracic organs have been found, with hemorrhages into the meninges and vacuolization of the spinal cord. This condition is called caisson disease. Decreased atmospheric pressure causes vascular and nervous disturbances, with apparent increase of the red blood cells and hemoglobin due to the escape of the plasma into the tissues (rel- ative polycythemia). The symptoms may be due to lack of oxygen, together with the mechanical effect of decreased pres- sure upon the tissues. This condition is sometimes called moun- tain disease. Electricity. — Powerful electrical currents usually kill by pa- ralysis of the heart. The local effects may be demonstrable or not, according to the nature of the conductors and the parts affected, as well as the intensity and duration of the current. Frequently there are burns, which may be deep and dry; the brain and meninges are congested, and there may be minute hemorrhages into the gray matter, floor of the fourth ventricle, and other parts, with congestion of the thoracic and abdominal organs. Lightning strokes often cause peculiar branching linear burns upon the skin ; and the clothing, and particularly the foot Avear, may be torn into shreds, and even internal organs have been found to be lacerated. Light. — Light is usually regarded as beneficial to the health of the higher organisms, but it is harmful to unicellular organ- isms, as bacteria; in fact sunlight is bactericidal. Strong sun- light may cause hyperemia or inflammation of the skin (sunburn), 44 GENERAL PATHOLOGY which, if severe, may proceed to vesication and ulceration. In- tense light of any kind, as calcium light, may cause retinitis. X-rays. — X-rays cause degenerative changes in the cells, and finally disintegration. The cells of diseased tissues are more easily destroyed than healthy cells. Chronic dermatitis with a tendency to epitheliomatous change is apt to follow x-ray burns of the skin. Highly specialized cells, as spermatozoa, are readily destroyed by exposure to these rays. Chemical Agents. — Any substance which by its chemical ac- tion destroys (corrodes) tissues, or which, when absorbed and carried to various cells, causes harm, is called a poison. A sub- stance may be a therapeutic agent as well as a poison, depending upon the amount introduced into the tissues. One-fortieth of a grain of arsenic is a stimulant to the nervous system and the hematopoietic organs, and therefore a useful tonic, but one or two grains will cause death. The study of poisons is too extensive a subject to be under- taken, even in a summary manner, in a work of this kind, and the reader is referred to works on toxicology for their further consideration. Living Organisms. — Living organisms are the most important direct causes of disease, and will be considered in Chapter VIII. Autointoxication, or self-poisoning, is a diseased condition caused by the accumulation in the tissues of an abnormal amount of normal waste products, as a result of impaired elimination, or by the formation of abnormal, toxic substances, as a re- sult of impaired metabolism, or impaired gastrointestinal di- gestion. Poisoning due to the mere absorption of products of intestinal putrefaction is not included in this term. CHAPTER III PATHOLOGIC PROCESSES All pathologic processes are either (1) simple — those in which the changes are of one kind only, as in atrophy, or (2) compound — those in which two or more simple processes are taking- place at the same time, as in inflammation. Pathologic pi'oeesses may also be divided into (a) progressive, in which tissues are built up, and (b) retrograde or retrogressive, in which tissues are broken down. RETROGRADE PROCESSES Atrophy Atrophy is a simple retrograde process, resulting in the de- crease in size of a part or an organ. Normal examples are the atrophy of the thymus gland after the first few years of child- hood, of the uterus after parturition, of the overies after the menopause. Atrophy may be divided into simple atrophy, which is a de- crease in the size of the cells, and numerical atrophy, a decrease in the number of the cells. More often these two types are as- sociated or combined, hence sometimes called combined atrophy. Simple atrophy when unaccompanied by any other pathologic proc- ess is a true atrophy, while numerical atrophy, in which the cells are usually first degenerated (hence degenerative atrophy), is usu- ally accompanied by a replacement of the destroyed cells by fatty tissue or a hyperplasia of connective tissue, making it ex- tremely difficult to distinguish between atrophy and degenera- tion with replacement. The term "atrophy" usually refers to local atrophy (affecting one or more parts) while atrophy of all, or nearly all parts of the body (emaciation) is sometimes called general atrophy. Hypopla- sia, infantilism, nanism, ateleiosis, etc., are terms referring to va- rious forms of underdevelopment or stunted growth, and must not 45 46 GENERAL PATHOLOGY be confounded with atrophy. Aplasia or agt nesia moans total lack of development of a part. Etiology. — The causation of normal atrophy is not well under- stood, but pathologic atrophy is due to diminished nutrition of a part, depending upon : 1. Prolonged, continuous pressure ("pressure atrophy," as by tumors, aneurysms, corsets, etc). 2. Disuse, as in fractures, paralysis, habit, etc. 3. Loss of trophic influence, as, in muscular atrophy due to disease of the spinal cord (neuropathic atrophy). 4. Starvation, general or local, as from obstructed blood vessels. 5. Senility, affecting especially the heart, lungs, liver, kidneys, testicles, uterus and bones. Locations. — Any part of the body may become atrophied. ■\ I I. f-fj | r / : I * Fig. 3. — Brown atrophy of the heart muscle. (Stengel and Fox.) Gross Morbid Anatomy. — In true atrophy, the part or organ is diminished in size without change in shape or consistence. In the degenerative type, the shape is usually much altered, the size unaltered or decreased, and the consistence increased, or de- creased according to the nature of the tissue which has re- placed the atrophied cells. In both forms the color is usually increased, becoming darker, from a relative or absolute increase of pigment. Pathologic Histology. — In true atrophy the cells are smaller than normal, and pigment granules can usually be seen. In brown atrophy of the heart, these granules are arranged about the poles of the more or less elongated nucleus (Fig. 3). In numerical atrophy, the parenchymatous cells are smaller, fewer in number, and in places altogether absent, and in their stead PATHOLOGIC PROC1 47 may be seen connective-tissue elements, hyaline, Eatty or mucoid material, and some type of pigmentation. Pathologic Physiology. — Since the parenchyma of organs is chiefly though no1 exclusively affected, function is always im- paired — secretion diminished, muscular activity lessened, etc. Results. — If the process is arrested early, partial or complete restoration may be attained; if not, death of the part will result with iis disappearance and replacement by other tissue. Degenerations (or Metamorphoses) Degenerations are simple retrograde processes in which the cells or the intercellular substances are converted into a ma- terial abnormal in kind or quantity. Fig. 4. — Albuminous degeneration — kidney. (Delafield and Prudden.) There are six types of degeneration: Cloudy swelling, or parenchymatous or albuminous degenera- tion. Fatty degeneration. Mucoid or myxomatous degeneration. Colloid degeneration. Hyaline degeneration. Amyloid degeneration. "Whether amyloid is an infiltration or a degeneration can not be definitely stated — even its chemical composition is not yet definitely determined (see Etiology of Amyloid Degeneration). 48 GENERAL PATHOLOGY Cloudy Swelling-, Parenchymatous or Granular Degeneration Cloudy swelling is a simple retrograde process in which the soluble albuminous elements of the cells are precipitated as in- soluble granules, associated with an increase of fluids in the cells. (Fig. 4.) Etiology. — Cloudy swelling is caused by the action of poisons, as (a) toxins of infectious diseases, particularly scarlet fever, diphtheria, and typhoid fever, (b) extraneous poisons, as ether, chloroform, mercury, etc.; and (c) poisons formed within the body, as in autointoxication, the metabolic disturbances accom- panying high temperature (pyrexia), absorption of necrotic tis- sue or disintegrating materials, etc. Locations. — Chiefly the parenchyma of organs, particularly renal epithelium, mucous membranes, liver cells, voluntary mus- cle and heart. Gross Morbid Anatomy. — The organ is uniformly enlarged, owing to the swollen conditions of the cells ; paler than normal, due to the whiteness of the granules and the anemia caused by the pressure of the swollen cells;. softer, owing to the increased fluid content. On section the surface is moist and the parenchyma protrudes. Pathologic Histology. — The cell is full of fine granules, which partly or wholly obscure the nucleus and the striations of muscle fibers. The cells are increased in size and more or less irregular in outline. The cell vail is sometimes indistinct, causing the cells to have the appearance of having coalesced. Reactions. — The granules may be dissolved in acetic acid, thus causing the reappearance of the nuclei, but they are insoluble in alcohol or ether, thus differentiating them from fat globules or granules. Pathologic Physiology. — Function is impaired due to the pres- ence of the granules and the intracellular fluids. Results. — Granular degeneration is a temporary condition oc- curring in acute disease, and complete recovery is the rule, but if the causes persist, fatty or other degeneration ensues. Fatty Degeneration Fatty degeneration is a simple retrogressive process in which there is disintegration of the cellular protoplasm, with appearance PATHOLOGIC PROCESSES I'l of fat within the cell. Normal examples are the production of t'al globules in the secretion of milk, and the change of red (fetal) ft) yellow (adult) bone marrow. (Fig. 5.) Etiology. Since cloudy swelling may pass into Tally degenera- tion, the prolonged action of toxins and poisons which cause the former will also cause the latter. Patty degeneration also oc- curs in pernicious anemia and in cachexias, due to some form of toxin; and in the involution of tissues, as thymus, corpora lutea, uterus, etc. Locations. — Fatty degeneration occurs in the parenchyma of organs, and at times also in the connective tissues, as in athero- matous vessels. Gross Morbid Anatomy. — The organ is smaller (though in early Fig. 5. — Fatty defeneration — kidney. (Delalield and Prudden.) stages it may be enlarged) and softer than normal. The color is pale yellow, due to the presence of fat, but congestion, pigmen- tation, or jaundice may alter the color. The specific gravity is reduced. The area affected may be uniform or the degeneration appear in streaks, as in the heart and liver, thus producing a mottled appearance. On section the knife becomes greasy. Pathologic Histology. — The cells are in the early stages usually somewhat larger than normal, but later are shrunken, irregular in shape, and more or less degenerated as shown by their di- minished staining qualities. The cells are partly or in later stages completely filled with small, discrete, highly refractile fatty granules, scattered irregularly throughout the cytoplasm. In acute or very advanced cases these fat granules may coalesce into globules, which in exceptional cases may become quite large. 50 GENERAL PATHOLOGY At first the nucleus is not affected, but in late stages of the dis- ease it shows degenerative changes (karyolysis). Cells crowded with fat granules are sometimes called "compound granule cells." Pathologic Chemistry. — In fatty degeneration, the cells are first degenerated by the poisons indicated in describing its etiology, followed in the main by an infiltration of fat from without. In the kidneys, spleen, and muscles, 1 however, the fat is formed principally by the setting free of the intracellular fat from its combination with the protein substances by autolysis, i.e., the fat previously present but invisible is rendered visible. Reactions. — Fat is soluble in alcohol, ether, and chloroform; but is not dissolved by acetic acid. It is stained red by Scharlach E, and orange by Sudan in. Osmic acid stains fat a deep black, due to the olein present in all natural fats. Pathologic Physiology. — Impairment and finally destruction of the secreting or muscular functions (as in heart muscle) result, In the liver and kidney secretion, however, is well maintained even in advanced cases. Results. — Mild cases with uninvolved nuclei may recover, but the condition is generally irremediable, the degeneration pro- ceeding to complete death of the cells (necrobiosis) with depo- sition of fatty acid crystals, cholesterin, etc., or the damaged tis- sue may undergo calcification. Mucoid Degeneration Mucoid degeneration is a simple retrogressive process in which there is a conversion of the cells or intercellular substance into some type of mucin. Normal examples are the secretions of the goblet cell of the mucous membrane, and Wharton's jelly of the umbilical cord. (Fig. 6.) Etiology. — The causes which bring about this form of de- generation are not definitely known. Inflammation is a factor when mucoid degeneration appears in mucous membranes. Locations. — (a) Mucous membrane, affecting the columnar cells, resulting in the formation of a large number of goblet cells, (b) Intercellular substance of subcutaneous, subserous and submucous 'Wells, II. Gideon, Chemical Pathology, Philadelphia, W. B. Saunders Co. PATHOLOGIC PROC] SSES 51 tissues, either as a diffuse process (myxedema), or as a local process in nasal polyps, hydat il'orm moles, etc. (c) In tumors, as ovarian cysts, carcinoma springing from mucous membranes (the so-called "colloid cancers"), myxomata, etc. Gross Morbid Anatomy. — The mucous membranes are covered with a viscid semigelatinous and colorless material, while in the antrum of Highmore, salivary glands, etc., there are cyst-like col- lections of the same material. When affecting the connective tissues, these are soft, elastic and tear easily. In tumors the mucoid material is drier; in ovarian cysts the material may as- sume large proportions. . > Fig. 6. — Mucoid degeneration of fibrous tissue. (Delafield and Prudden.) Minute Morbid Anatomy. — The cells are partly or completely filled with the mucus: the typical "goblet cells" are distended and the nucleus pressed to one side. The material is usually homogeneous, but in connective tissues it may appear as granules or as coarse shreds lying between the cells; the cells present all stages of degeneration from the normal appearance to typical mucoid cells, with irregularly stellate outline. Pathologic Chemistry. — Mucin is a compound protein (gluco- samine normally secreted by the epithelium of mucous mem- branes, and also occurring in the mucoid tissue of the fetus, where it is the precursor of the adult connective tissue. The mucoid degeneration associated with inflammation of mucous membranes (catarrhal inflammation) is in reality only a path- 52 GENERAL PATHOLOGY ologic increase of mucinous secretion of epithelial cells, which is essentially true also of this substance in "colloid cancers" and ovarian cysts; the pathologic connective-tissue mucin is merely a reversion to the fetal type of connective tissue. In ovarian cysts this product differs somewhat in chemical properties from true mucin, hence called pseudomucin. Reactions. — Mucin swells in water, dissolves in alkalies, is in- soluble in acids and alcohol, and is precipitated by acetic acid. It is acid in reaction, hence takes the basic stains. Pseudomucin is not precipitated by acetic acid, is alkaline in reaction, and takes the acid stains. Pathologic Physiology.— Function is moderately impaired in mucous membranes, resulting in catarrhal conditions. In connec- tive tissues, the change is apt to be permanent but usually causes no serious harm. Colloid Degeneration This is a simple retrograde pathologic process in which there is a conversion of the cell into a yellowish brown transparent ma- terial, resembling in physical appearance the colloid material of the thyroid gland. (Fig. 7.) Pathologic Chemistry. — The colloid of the thyroid is an iodin- containing globulin, but the term as used in "colloid degenera- tion" is not chemically definite, but includes such substances as have a colloid appearance (just described). "Colloid cancer" was so named because the mucoid material found within it had a colloid appearance, due to its compression within a confined space, and to its partial loss of water. Apart from that found in the thyroid, colloid resembles the mucins in chemical composi- tion, particularly pseudomucin. Etiology. — The etiology is obscure. Pathologically it is partly a secretion and partly a degeneration of the epithelial cell. Locations. — It occurs in goiters and other tumors of the thyroid gland, in the hypophysis cerebri, kidneys, adrenals, prostate gland, and seminal vesicles, and many other locations. Gross Morbid Anatomy. — The organs affected may be larger, and either harder or softer than normal. The colloid substance occurs in cystic collections, having a yellowish brown transparent PATHOLOGIC PROCESSES 53 appearance, varying in size from minute bodies to large masses, having the consistence of calf's fool jelly. A serious transuda- tion may dissolve the colloid. Leaving cavities Idled with choco- late-colored fluid. Pathologic Histology. — The material firsl appears in the epi- thelial cells as droplets; the latter become completely trans- formed into colloid, and as new layers of cells are formed and successively degenerated, the acini, tubules or cystic cavities formed to receive the material, become distended to various de- grees. The substance is usually homogeneous in appearance, but may show concentric lines corresponding to the layers of cells which have undergone the change. F'g- 7. — Colloid degeneration of the thyroid gland showing masses of colloid matter in the gland acini. (Karl and Schmorl.) Reactions. — Colloid does not swell in water; is not precipitated by acetic acid, but is precipitated by tannic acid. Like pseudo- mucin, it elects the acid dyes, but the more nearly it approaches the mucins in composition, the more variable are its staining properties. Pathologic Physiology. — Function is impaired, probably on ac- count of the pressure to which 1 lie vital elements are subjected by the material. Results. — Absorption with regeneration of epithelial cells is possible in some cases. When the process has caused destruction 54 GENERAL PATHOLOGY of considerable amounts of parenchymatous cells, colloid de- generation is usually followed by hyaline mucoid, necrotic or calcareous change. Hyaline Degeneration Hyaline degeneration is a simple retrograde morbid process with the appearance in the cells and intercellular substance of a homogeneous, glistening, opaque, albuminous material, called hyaline (glass-like). (Fig. 8.) Pathologic Chemistry. — This material is closely related to col- loid and amyloid substances, being distinguished mainly by its Fig. 8. — Hyaline degeneration of an ovarian capillary. Oc. 2; ob. 9. (McFarland.) physical properties and its distribution. Hyaline is not a chemical entity, but includes a number of different chemical substances, i.e., various forms of degeneration or necrosis. Etiology. — The causal factors are not well understood. Ar- teriosclerosis, and all forms of arteritis favor its production ; also the toxins of infections (chiefly the acute infections, as scarlet fever) and septic processes, lead poisoning, etc., but chronic in- fectious disease, as tuberculosis, syphilis, etc., may also be fol- lowed by this change. Locations. — It may be found in any part of the body, but there are three principal types: (a) Connective-tissue hyaline, found PATHOLOGIC PROCESSES 55 iii dense tissues, as old scars, sclerotic vessel walls, capsules and trabeculae of organs, especially of the spleen, liver, heart, brain, cord, etc. Von Recklinghausen's hyaline is thai which involves the cap- sules and trabeculae of lymph nodes, especially when the seat of tuberculosis. (b) Cellular hyaline, occurring as round bodies within cells, such as epithelium of mucous membranes and the kidneys. Zen- ker's hyaline occurs in voluntary muscle cells, as the rectus ab- dominis, diaphragm and adductors of the thigh in typhoid fever, though some believe this to be amyloid degeneration, others, a form of coagulation necrosis. (c) Necrotic hyaline, found in old blood clots (hyaline thrombi), in fibrinous and inflammatory exudates (exudative hy- aline), and in necrotic tumors, tubercles, gummata, etc. Russell's "fuelisin bodies" are small round hyaline bodies, con- centrically striated, found within and between cells of epithelial tumors, and sometimes in normal tissues. Their true nature is not known, but they resemble hyaline material in appearance and in affinity for acid fuchsin stains. Gross Morbid Anatomy. — Hyaline is not usually sufficiently abundant to be seen by the naked eye, but when so, it appears similar to hyaline cartilage, is smooth, and cuts with the same re- sistance. In mucous and serous membranes, small collections may appear as opaque irregular plates. Pathologic Histology. — (a) In the blood vessels hyaline is seen in and beneath the endothelium as a homogeneous material, also between the vascular coats, or around the vessels (such perivas- cular hyaline is especially well seen in cylindromata). The ves- sel wall is thickened, the lumen narrowed, and possibly ob- literated, (b) In interstitial tissues, hyaline material is found between the muscle fibers, hepatic cells, renal tubules in the reticulum of lymph glands, in the retina, in cicatrices, and in neoplasms, (c) Within cells, hyaline material occurs as homo- geneous bodies in muscle cells, giant cells, epithelium, and to a lesser extent in leucocytes and wandering cells. Reactions. — Hyaline is resistant to reagents, being unaffected by acids, alkalies, and alcohol. The staining reactions are varia- ble, owing to its variable composition, but usually hyaline ma- 56 GENERAL PATHOLOGY ferial has a decided affinity for acid fuehsin. and other acid stains ; but the older the hyaline, the paler it stains. Thionin stains it red and other tissues bine. Pathologic Physiology. — Hyaline degeneration does not impair function as a rule: but if it is extensive, it may affect the paren- chyma by compression or by anemia through narrowed blood ves- sels. Results. — It may be absorbed, or converted into fatty degenera- tion, or undergo caseation or calcification. Amyloid Degeneration (Waxy, Bacony, or Lardaceous Degeneration) Amyloid degeneration is a simple retrograde process with the appearance in the intercellular substance of connective tissues of a waxy albuminous material, called amyloid. (Fig. 9.) Fig 9. — Amyloid infiltration of capillary walls in kidney glomerulus. (Stengel and Vox.) Pathologic Chemistry. — This substance was at first thought to be a form of cellulose because it gave the blue color with iodine when followed by sulphuric acid, and was hence called "amy- loid" or starchlike, but is now believed to be a protein combined with chondroitin-sulphuric acid: though Hansenn failed to find any of the latter in amyloid of the spleen, thus making the cheni- istrv of amyloid material doubtful. PATHOLOGIC PROCESS] S -u The material may be carried by the 1>I 1 in a "preamyloid" soluble form to the tissues, where it is modified and deposited, be- coming ilic insoluble resistive amyloid substance, though it is possible thai in some localities ii may be formed in situ; hence ii is variously called an "infiltration" or a "degeneration." It will be noted, then, that the chemical nature of the four "all uiminous degenerations;" viz., mucoid, colloid, hyaline, and amyloid, is hoi definitely known, and probably varies much in different cases. Etiology. — Toxins of certain chronic infectious processes, espe- cially those formed in prolonged suppurating conditions (particu- larly tuberculous and syphilitic) of bones, though suppurative and ulcerative conditions of various kinds, as gastrointestinal, actinomycotic, etc.. may also cause amyloid degeneration. Aseptic suppuration, as by injection of turpentine, may also cause it. The injection of toxins alone, as in preparation of diphthe- ritic antitoxin, and the toxins of nonsuppurative syphilitic condi- tions likewise cause it. It sometimes occurs without apparent cause. Locations. — The condition may be general (amyloidosis) or lo- cal. The organs most frequently affected are the kidney, liver, and spleen; next in frequency, the larger blood vessels, intestinal mucosa, and lymph nodes, and less frequently the stomach and colon, suprarenals, pancreas, heart, etc. ; rarely the lungs or cen- tral nervous system. Gross Anatomy. — An amyloid organ is enlarged uniformly (oc- casionally an amyloid liver becomes enormous) dense, pale, in- elastic or doughy, sometimes pitting on pressure. The specific gravity is increased. The amyloid material has a glistening, waxy, translucent ap- pearance. In cut sections, the surface is smooth, dry and glossy, the cut edges remain sharp, and the parenchyma neither con- tracts nor protrudes. It is customary in examining gross speci- mens at autopsy to apply iodine (Lugol's). The waxy material is not always uniformly distributed; in the spleen it may be confined to the Malpighian bodies, which stand out in round, transparent bodies, looking like grains of boiled sago (sago spleen); when the process is diffuse, the spleen 58 GENERAL PATHOLOGY looks bacony (bacony spleen). In the kidney, it appears first in the glomeruli. Pathologic Histology. — The material is always found in the connective 1 issue; is usually found in the capillaries, in the media and basement membrane of intima in case of larger vessels; the lumen of the blood vessels is usually narrowed or obliterated. The amyloid material is deposited between the cells, which are pushed aside and atrophied, and disappear as the process ad- vances. The amount of amyloid substance varies from slight deposits to such large quantities as to cause disappearance of the original elements from large areas of the diseased part. Under the microscope, the amyloid in a section of liver is found in the intermediate zone of the lobule (i.e., between the central and perilobular zones) as a pale homogeneous material following the course of the capillaries, and taking the charac- teristic stain: from this zone it gradually spreads until the whole lobule is affected. In the kidney, the capillary tufts are first affected, later the vessels and interstitial tissues; rarely the tubules are said to contain it, though in most cases this material is hyaline or other exudative material and not true amyloid. In the spleen, the Malpighian bodies alone may be affected, or the reticular framework may be generally involved. Reactions. — Amyloid is insoluble in water, acids, alkalies, and very resistant to bacterial decomposition. It stains a dee]) mahogany brown with iodine, other tissues, yellow; if afterward treated with dilute sulphuric acid, it usu- ally turns brown or blue, or may merely turn a deeper brown. This iodine reaction fails in specimens that have been kept some time in preserving fluids, or that have become strongly alkaline: in fact, the blue reaction is usually given well only by splenic amyloid, or by the "amyloid bodies." Gentian violet, or methyl violet (and to a less degree also other basic aniline dyes) stain the amyloid material a pink color, or pale red often with a violet tinge; the other tissues stain the natural violet color. Pathologic Physiology. — Xo impairment of function occurs if Hie material is small in amount: if large, pressure causes atrophy and diminished function, or thrombosis in the blood vessels. PATHOLOGIC PROC] 3S 59 Results. — The process is irremediable; and [f progressive, leads to death. It may also pass into fatly degeneration, caseation, or calcification. Slighl amounts may be absorbed, learned by ex- perimentally extirpating a part of a diseased (amyloid) area of an organ, and some time afterward again examining at necropsy. The "amyloid bodies," or corpora amylacea, found in the pros- tate, lungs, kidney, brain, and posterior cord, also sometimes in inflammatory areas, in infarcts, granulomata, and neoplasms, are small concentrically striated bodies, resembling starch granules, which nearly always react with the iodine-sulphuric aeid. giving a blue color, though sometimes they fail to react typically. Many believe these bodies to be hyaline, others colloid in nature. Path- ologically they are not significant, occurring also in health. Infiltrations Infiltrations are simple retrograde processes in which there is deposited within the cells and intercellular tissues substances that are abnormal in kind or quantity. Fatty Infiltration Fatty infiltration is an abnormal deposition of fat within the cells of a part. The process does not differ essentially from the normal physiologic deposit of fat, and is considered pathologic only when in excess or when deposited where it does not normally appear. (Fig. 10.) Etiology.- — 1. Ingestion of more fat-forming foods — fats and carbohydrates — -than the body needs. 2. Sulfoxidation probably accounts for nearly all, if not all, the remaining cases, as in tuberculosis, carcinoma, inactivity, senility, alcohol, diabetes, etc. Types. — 1. General fatty infiltration, as obesity, adiposity or polysarcia. 2. Local fatty infiltration, as in heart, etc. Locations. — 1. Connective tissues; (a) General deposits, as in subcutaneous, submucous and subserous tissues. Obesity, belongs here. Tissues that are never involved are the eyelids, ears, ala?, nasi, lips ami external e Nucleus not displaced, pushed to one side — "signet ring." Condition not necessarily serious. Always serious. Pigmentary Infiltration Pigmentary infiltration is an abnormal deposit of pigment within or between the cells of any tissue. Etiology. — I. Extraneous pigments (those of external origin) are derived from: 1. Inhalation of smoke and dust particles of all kinds, causing pneumonokoniosis or "lung dust disease." 2. Ingestion of dust and substances like soluble salts of silver, especially the nitrate, also lead salts, etc. 3. Implantation and absorption by skin, as in tattooing, and possibly lead, copper, etc. II. Pigments of internal origin are due to: 1. Disintegration of hemoglobin (hemolysis) either directly in the tissues, or in the blood vessels when the blood is hemolyzed by venins, toxins, poisons, anemias, cachexias, etc., (hematog- enous pigmentation) ; or indirectly, when the blood pigment is converted into bile pigment in the liver, but instead of escaping as normally through the hepatic ducts with the bile, should these ducts become obstructed by catarrhal or other conditions, the bile pigments are forced into the lymph vessels (and to a less extent into the blood vessels) and carried to the tissues through- out the body (hepatogenous pigmentation). 62 GENERAL PATHOLOGY 2. Malarial pigmentation. This is probably formed by the ac- tion of the Plasmodium malaria? upon the red blood cells, liberat- ing and modifying the hemoglobin or hematin. 3. Metabolic pigmentation. Certain cells elaborate the pig- ment out of protein substances possibly by action of intracellular oxidases upon the aromatic groups of the protein molecule (von Furth's theory). Such pigment appears normally in skin, hair, choroid and retinal coats of the eye, in pregnancy (chloasma uterinum) and pathologically in certain tumors, in the shin, etc. The term melanin is applied to all these pigments though they vary much in composition, some being iron or sulphur free, while some contain small amounts of iron, and some contain sulphur in variable amounts up to 10 per cent in melanosarcomata. Lipochromes, or pigments of fatty origin, are usually classed as metabolic pigments, but their nature and formation are not well understood ; they occur normally in fats, in the corpora lutea (lutein) and pathologically in lipomata, xanthomata, (pale yellow), in chloromata (green), in certain nerve cells in old age, and possibly in brown atrophy of muscle cells (but this has also been classed as hematogenous in origin.) 4. Parasitic pigmentation. Some bacteria and moulds form various pigments. Locations. — Mueh of the inhaled pigment probably never reaches the alveoli of the lungs, but is caught by the bronchial ciliated epithelium and in part coughed up, though part is car- ried into the submucous tissue, where some remains permanently and the remainder is conveyed by the lymphatics to the nearest glands, as peribronchial and even mediastinal glands and sub- pleural spaces. In rare cases the pigment reaches the general circulation and is deposited in the kidney, liver, spleen, and alimentary mucosa. Ingested pigments are likewise deposited in the alimentary mucosa and adjacent glands, or as in silver discoloration are dif- fusely distributed between the cells of the internal organs and 1 issues, and in the subepithelial layer of the skin, where de- posited in the form of silver albuminate, it is finally reduced, resulting in a bluish pigment. PATHOLOGIC PROi 63 In chronic lead poisoning, the blue line on the gums is due to th«> formation of lead sulphide. In tattooing, the pigments are Pound in the deep layers of the skin, and in the adjacent lymphatic glands. Hematogenous pigmentation may he (a) general or (b) local. (a) In the general form, blood is hemolyzed, liberating hem- oglobin into the blood stream (hemoglobinemia) j as much of this a^ can be disposed of by the liver is converted into bile, while the remainder is excreted by the kidneys (hemoglobinuria) wholly or in pari ; in the latter case some hemoglobin is broken up and deposited in various tissues. This is best seen in the liver (espe- cially in periphery of lobules), spleen and kidneys. (b) In the local form, as in thrombosis, and interstitial hemor- rhages (including bruises), blood escapes into the tissues, is in part eliminated and in part vailed off and and coagulated; the hemoglobin diffuses out and is broken up into the various deriva- tives of blood pigments in situ. The different shades of color from red or brown to black depend upon successive degrees of re- ductions of the pigments. Local pigmentation is seen in infarcts, hematomata, thrombi, extravasations, etc. A dark or black pigmentation, resembling melanin ("pseudo- melanin") is often seen in the abdominal region of dead bodies, due to sulphide of iron (H 2 S from gastrointestinal decomposition acting on the iron derived from the blood). It may become more or less general in distribution, and also sometimes forms during life in and around gangrenous areas, and other localities where free or loosely bound iron and H 2 S come together. The greenish discoloration in the abdominal region of dead bodies is due to sulphur-hemoglobin, due to H 2 S plus undecom- posed hemoglobin. Hepatogenous pigmentation (jaundice) is found either in the tissues in solution or in crystal form (needles or rhombic plates) especially in liver, skin, mucous membrane, serous membrane and glandular and fatty tissues generally, less often in other tissues — the brain substance alone escaping. Malarial pigment is found in various tissues, especially in spleen, liver, kidney, bone marrow and brain. Metabolic pigments are found locally in certain tumors, as 64 GENERAL PATHOLOGY melanotic sarcomata and carcinomata, pigmented moles, chloas- mic spots, etc., and generally in the skin in Addison's disease, revere anemias and cachexias, abdominal tuberculosis, abdominal tumors, and senility. Lipochromes occur as stated under etiology, and parasitic pig- ments are found in the various tissues invaded by the organisms. Gross Anatomy. — Discoloration is seen as follows: In Lungs : (1) Dark or black in anthracosis (coal dust, smoke, etc.) as in coal miners. (2) Grayish in chalicosis (stone dust) as in stonecutters. (3) Brownish red in siderosis (iron dust) as in iron workers. (4) Grayish in calcicosis (lime dust) as in marble cutters. (5) Grayish in silicosis (silica dust) as in glass cutters. (6") Yellowish in aluminosis (clay) as in potters. (7) Rusty brown in tabacosis (tobacco dust), etc. In skin ; also gastrointestinal walls, kidney, liver, etc. Bluish color in argyria due to AgNO and other soluble salts and silver. Rarely other extraneous pigments cause discolorations, as in lungs. Hematogenous pigments if in sufficient amount will color the tissues: (1) Reddish brown when due to hemosiderin and hematoidin. (2) Dark or black when due to iron sulphide. (3) Dark or black when due to malarial pigment. Hepatogenous pigments : (1) Yellowish red, when due to bilirubin. (2) Yellowish green when due to biliverdin (oxidized bilirubin). Metabolic pigments appear (pathologically); (1) Dark brown or black in tumors, etc., due to melanin. (2) Yellowish brown in skin. (3) Yellow, brown or green in tumors, etc., due to lipochromes. Parasitic pigments are of various colors as blue in B. pyocyaneus; yellow in Actinomyces bovis; black in Mucor niger (on lingual papilla?) ; brown in Microsporon furfur (tinea versicolor) ; etc. Pathologic Histology. — By transmitted light, extraneous pig- ments appear black, and usually coarsely granular and extra- cellular, though leucocytes are apt to contain them (phago- cytosis). Hemosiderin appears as intracellular (less often extracellular) fine irregular granules of yellowish or reddish brown color in various tissues, but is best seen in liver, spleen and lungs, fol- lowing congestion. A certain amount of oxygen seems to be necessary in its formation, therefore it is seen at the periphery of old necrotic areas, as blood clots, infarcts, etc. PATTTOTiOCIC PROCESSES 65 Fig. 11. — Anthracosis of the lung. (Delafield and Prudden.) 66 GENERAL PATHOLOGY Hematoidin appears in fine acicnlar crystals or rhombic plates, or spherical granules, usually a bright yellowish red, always be- tween cells and oftenest in the center of old blood clots or in- farcts. Oxygen must be absent when it is formed. Iron sulphide appears as black granules. Bilirubin, bilifuscin and biliverdin usually appear as fine granules, occasionally as crystals, yellowish to brown in color, intracellular, pigmenting the nucleus as well as the cytoplasm and are best seen in liver. Malarial pigment is a black, finely granulated pigment, found in the perivascular lymph spaces in organs and tissues, especially of the spleen, liver, kidney, and brain, also in the cells of these organs at times and in phagocytes. Melanin is seen as coarse granular, brownish black pigment in various tissues, as in melanosarcomata, usually within the cells though sometimes free in lymphatic spaces ; in marked cases it may appear in the blood (melanemia) and be excreted in the urine (melanuria) either as melanin, or as melanogen (colorless) which darkens (oxidizes) on standing. Lipochromes are seen within the cells of tumors, etc., and stain with the ordinary fat stains. Reactions. — Hemoglobin is composed of globin (protein) 96 per cent and hematin 4 per cent. The latter contains the coloring matter of the blood. The two principal derivatives of hematin are hemosiderin (iron-containing) normally used for reconstructing hemoglobin, and hematoidin (iron free) isomeric with bilirubin, and nor- mally eliminated. Hemosiderin is colored blue (Prussian blue) when sections are treated with potassium ferrocyanide, 2 per cent aq. sol. followed by HC1 0.5 per cent in glj-cerin, or 1 per cent in alcohol (Perl's test). Hematoidin will not respond to Perl's test — since it con- tains no iron; hemoglobin will not, because its iron is too firmly united with the protein. Bile pigments give the Gmelin's reaction — a play of colors; viz., green, blue, violet, red and yellow, when adding a drop of commercial nitric acid. They also turn green with weak tincture of iodin. Hematoidin also responds to Gmelin's test. PATHOLOGIC PROCESSES 67 Lipochromes are colored by Sudan in and Scharlach R, and usually by osmic acid. Extraneous pigments are usually insoluble; those soluble in acids evolve C0 2 . Carbon is distinguished from melanin and other dark pigments by its insolubility in strong H 2 S0 4 . Pathologic Physiology.— Large amounts of pigment may cause proliferation of connective tissues with atrophy of the paren- chyma, and consequent loss of function. Results. — Pneumonokoniosis is often followed by tuberculosis. Fibrosis follows nearly all forms of extraneous pigmentation. Internal pigments are apt to become absorbed in time, though in some cases they become encapsulated. Albinism is a deficiency or absence of normal amount of melanotic pigment. Leukoderma is an irregular distribution of pigment in the skin, some parts paler, others more pigmented. Canities is grayness or whiteness of hair, due to loss of color, probably resulting from decrease or loss of intracellular oxida- tion of the chromogen. Calcareous Infiltration Calcareous infiltration is the abnormal deposit of earthy salts in the tissues, chiefly phosphates and carbonates of calcium, though magnesium salts are also found. (Fig. 12.) Etiology. — Necrosed or diseased tissue seems necessary (with the possible exception of the calcareous metastases). The min- eral matter in solution is brought by the blood and lymph to the part, and by some local chemical process is deposited in in- soluble form. At present there is a tendency to consider that from the local disintegrated tissues, protein substances arise which unite with the calcium and magnesium, and subsequently are replaced by phosphoric and carbonic acids to form the corresponding salts; or that the fatty acids, liable to appear in degenerated areas, may form calcium and magnesium soaps and may likewise be re- placed by the stronger acids. Calcareous metastasis : In some rare cases of resorption of bone, as in extensive caries, osteomalacea, osteosarcoma, etc., there may be widespread deposition of salts in cartilage, lungs, gastric mucosa, arterial and capillary walls, etc. The tissue here 68 GKXERAL I'ATIIOI.OOY is not known to have been previously diseased, though some claim that the deposit, being intercellular, is "in inert or dead tissue." Senile calcification of blood vessels, etc., has been classed as metastatic since bone is absorbed in old age. but this depends probably upon the hyaline changes occurring in senile sclerosis. Locations. — Sclerotic vessel walls, especially, aorta, coronary, cerebral, radial, etc. Fig. 12. — Calcareous in filtration of the wall of a small artery from the wall of a gumma of the liver. Zeiss, Oc. 2; ob. D. D. (McFarland.) Endocardium (especially of valves); pericardium, myocardium, etc. Pituitary body: meninges; ventricular plexus; ganglion cells, etc. Necrotic foci, as tubercular, parasitic, etc. Sclerotic foci, as sears, infarcts, or thrombi. Joints. Tumors, especially the avascular, as fibroma (particularly uterine), and tumors involving bone and cartilage; also cysts. goiters, psammomata, etc. Long retained dead fetuses (lithopedia). PATHOLOGIC PROCESSES 69 Concretions within the organs or their duds, as tonsils, pros- tate, etc. Gross Morbid Anatomy. -When the deposit is abundant, the parts are hard and brittle, of white, gray, or yellow color and opaque appearance. The lesions are gritty to the touch and section knife. Old tuberculous calcified areas are apt to be sur- rounded by pigmented fibrous tissues, especially in lungs and bronchia] glands. Pathologic Histology. — Fine intercellular granules, less often intracellular (as in the ganglion cells) are seen, appearing black by transmitted, and white and glistening by reflected, light. By coalescence, larger masses form, usually with concentric layers. In blood vessels, serous membrane, etc., calcareous plates are seen. When intracellular, the cells show degeneration. Reactions. — Acids will dissolve the granules, and in case of carbonates with evolution of gas (C0 2 ), observable under the mi- croscope by running 5 per cent IIC1 solution under cover-slip. To differentiate between lime and other salts soluble in HC1, add concentrated BuSO^, which forms needles of CaSO^ (gyp- sum). Lime salts stain blue with hemotoxylin, and black with AgN0 3 . Pathologic Physiology. — Function is impaired or destroyed by pressure, or inflammatory conditions are caused by irritation. In calcified blood vessels, nutrition to various tissues is re- stricted. Results. — Very small deposits may be absorbed, but usually there is proliferation of connective tissue, with capsule forma- tion. Sometimes degeneration of adjacent tissues is caused by the calcareous masses. Ossification. — Ossification which is the deposition of lime salts in a uniform regular order, as in normal bone formation, by the activity of certain cells (osteoblasts) occurs pathologically in tumors connected with cartilage, bone, and periosteum, and in ossifying inflammation of muscles (myositis ossificans). Concretions or Concrements "While calcareous infiltration is a deposit within tissues, con- cretions are deposits of lime and other substances within the ducts and cavities of the body. "0 GENERAL PATHOLOGY In the formation of concretions there is always a small mass of mucus, desquamated epithelium, secretory mailer, parasites or foreign bodies; in other words, usually some pathologic prod- uct upon which, as a nucleus, the various salts or substances forming the hulk of the concretion are deposited, "much as cane sugar crystallizes on a string to form rock candy, but with the important exception that the concretions are mixed with mucin or other organic matter which remains as a frame work when the salts are dissolved out." Gallstones (biliary calculi) are made up of variable amounts of cholesterin, the chief constituent of the great majority of these stones, and of bile pigments and calcium. Renal calculi kidney stones) are composed of uric acid, oxalate of lime, or phosphates; less frequently of other substances. Vesical cal- culi (of the urinary bladder) are composed of phosphates, uric- acid, and oxalates of lime ; rarely of other substances. Calcium salts form the chief mineral constituent of rhinoliths. broncholiths, phleboliths (which are calcification of organized thrombi; often found in the prostate or uterus), salivary, ton- sillar, lacrimal, cutaneous, appendicular, pancreatic and preputial concretions and prostatic calculi. In the intestines, concretions or enteroliths, usually consist of ammonio-magnesium phosphates, though the finer "intestinal sand" consists of calcium. Occa- sionally concretions of fat and soaps may follow the ingestion of large doses of olive oil, and be mistaken for gallstones. Hydropic, Dropsical, or Serous Infiltration Hydropic infiltration is an excess of fluid within the cells in the form of globules. It must be distinguished from edema, dropsy, or anasarca, which is due to an outpouring of serum from the blood vessels into the tissues to an abnormal decree, while in hydropic infiltration certain cells imbibe more fluid than nor- mal, though the lymph surrounding them may not lie abnormal in quantity. (Fig. 13.) Etiology. — The etiology is not definitely known, apart from a disturbed osmotic pressure, which may be due to "dissociation of the colloids, whereby crystalloids are liberated into the cyto- plasm" causing endosmosis of lymph. Toxins are probably a causal factor, at least in some cases (smallpox). PATHOLOGIC PROCESSES 71 Gross Morbid Anatomy. II' abundant, the pari is enlarged, soft, and boggy. Pathologic Histology. — Vacuoles of varying sizes, containing serous fluid, arc seen in the cells, which are enlarged and in some cases ruptured. Tn edema the cells also may contain fluid, i.e., edema may be accompanied by hydropic infiltration. Locations. — Any type of cells may be affected, but most com- monly the epithelial cells, as those of mucous membranes, glan- dular viscera, epithelial tumors, etc. Results. — This condition is not serious, unless very extensive. Fig. 13. — Dropsical infiltration of the epithelial cells of a carcinoma of the breast: a, ordinary epithelial cells; b, b, dropsical cells; c, dropsical nuclei; d, enlarged nucleoli, i Ziegler.) Glycogenic or Glycogenous Infiltration Glycogenic infiltration is an infiltration of glycogen in cells normally free from it. or an excessive deposit in cells which normally contain it. Etiology. — The cause of pathologic deposits is not known. Locations. — In diabetes (in which disease it is most frequently found) glycogen occurs in the renal epithelium, heart muscle, liver, and leucocytes. In tumors, it occurs within the tumor cells, especially those of malignant connective tissue tumors. In septic and inflammatory conditions, the local cells and leucocytes are affected. Glycogen granules may also be found free in the blood stream. Gross Morbid Anatomy. — Sometimes an organ is slightly en- larged; often there is no change. fZ GENERAL PATHOLOGY Pathologic Histology- -Small globules or granules are seen usu- ally within the cells, but sometimes also between the cells, or even free in the blood or in fluid exudates. The intracellular granules are usually near the nuclei, which are usually well pre- ed, even in advanced cas Reactions.— Soluble in water, the granules are dissolved and leave empty 3 when sections are treated with water; the margins of these - ;es for some unknown reason tend to take the basic stain-. To preserve the glycogen in the tissues, the latter must be fixed in alcohol in which glycogen is insoluble and rapidly — because the granules quickly change into glue after death of the tissue. Glycogen stains mahogany brown as does amyloid) or wine color with iodine dissolved in glycerin, or in the form of the tincture diluted with four parts of absolute alcohol. No blue color is produced on adding II _>' I . The brown color disappear- on heating, or on addition of alkalies, but reappears respectively on cooling or acidifying. Ptyalin rapidly converts glycogen into dextrose, and may be section, showing microscopically whether the granules are glycogen. Pathologic Physiology. — Normally glycogen is formed within the cells by intracellular enzymes, which dehydrate and poly- merize the sugar brought by the blood. The liver and the mus- - are the chief normal storehouses of glycogen, which when needed by the tiss - - again converted into dextrose by a re- verse enzymotic process. Pathologically, glycogen is diminished or absent from the normal situations, and appears in excess in other locations. The result is always serious, since the accompanying or causal conditions, as diabetes, malignant tumor. re usually fatal. Necrosis Necrosis means death of tissue. There are three grades: 1. Necrobiosis, or death of individual cells, occurring path- ologically in the various degenerations, and normally in the break- ing down of secreting cells, as in the formation of sebum, and in other cells, conspicuously the outer cells of the epidermis. PATHOLOGIC PROC1 SS] - 7:! 2. Necrosis proper, or death of a portion of ;i tissue in the midst of, or attached to, Living tissue. 3. Somatic death — death of the entire organism. Necrosis by which term the second form is usually referred* to — lias the following general etiology: 1. External agencies, as heat, cold, electricity, x-ray, trauma, poisons, microorganisms. 2. Interna] agencies, as circulatory and nutritional disturb- ances, trophic and vasomotor influences, toxins. These various causes do not always produce the same type of necrosis, but may cause one form in some cases, and another in other cases. Any part of the body may he affected. When in- volving soft tissues, about to be detached, the area is called a sphacelus, or slough; when involving a hone, a sequestrum. Changes may be seen in the intercellular substances and cells; the latter become shrunken or swollen, fragmented or dissolved (cytolysis) and take the stain very poorly. The nuclei may show fragmentation of the chromatin (karyorrhexis) with extrusion of the fragments into the cytoplasm where they finally disappear; or may retain their form but stain less and less distinctly until they dissolve (karyolysis) ; or may shrink (pyknosis) staining more deeply, before they dissolve and disappear. Fate of Necrotic Tissue: 1. It may be absorbed, with regeneration of normal tissue, or with scar formation. 2. It may be retained, and become encapsulated. 3. It may be removed en masse spontaneously or artificially. The following types are usually recognized: Coagulation necrosis. Liquefaction, or colliquative, necrosis. Caseous necrosis, or caseation. Fat necrosis. Gangrene. Coagulation Necrosis Coagulation necrosis is death of tissue in which the protein suffers a change similar to, or identical with, coagulation (Fig. 14). Coagulation is the conversion of the soluble colloids into a:i insoluble form. 74 GENERAL PATHOLOGY Etiology. — Any of the general causes already mentioned, but especially physical agents, as heat, cold, and trauma. Loss of nutrition, as in infarcts. Chemicals, as caustics. Toxins, espe- cially of pyogenic cocci, B. tuberculosis, and B. diphtherias. Physical and chemical agents cause coagulation by direct ac- tion. In exudates the action is analogous to, or identical with, blood coagulation, which consists of the conversion of fibrinogen (present in blood, lymph and exudates) into fibrin by action of the thrombin (fibrin ferment). The thrombin is thought to be produced when "prothrombin" (possibly a nucleo-protein ex- isting in leucocytes, blood platelets and tissue cells, and liberated when these are injured) is activated by the calcium salts of the blood or lymph. S i Fig. 14. — Coagulation necrosis of the hepatic cells in a case of puerperal eclampsia. (Karl and Schmorl.) In anemic areas the tissue cells possibly coagulate from the action of coagulins contained within the cells, though this has never been actually demonstrated. "When lymph infiltrates such areas, fibrin is formed. Locations. — Seen in tissues rich in protein, especially. 1. In bloodless parts, as anemic infarcts, and tubercles in the early stages of tuberculosis. 2. In inflammatory exudates, including "false membranes" upon mucous surfaces, fibrinous exudates upon serous surfaces, around abscesses and ulcers. 3. In blood clots — extravascular or intravascular (thrombi), in interstitial hemorrhages and hemorrhagic infarcts. PATHOLOGIC PROCESSES 7.~> 4. Tn striated muscles, in eases of typhoid and other fevers. Gross Pathology. — The parts are usually dry, firm, pair, glazed and more or less swollen. Solid tissues present the appearance of boiled flesh. Later the color becomes grayish and the pari inclines to soften. False membranes, which are a coagulation necrosis of certain inflammatory exudates, have a gelatinous or mucoid consistence, and arc not readily detached from the un- derlying tissue. Blood clots are red and semifluid, and break with a gelatinous fracture when fresh ("currant jelly" clots) ; are yellow and gelatinous when leucocytes predominate ("chicken-fat" clots); and "white" clots when the cells have largely disappeared and fibrin alone remains. Pathologic Histology. — The cells lose their staining power early, become indistinct, and later disintegrate completely. Mus- cle cells lose their striae, and in cardiac muscle the intercellular cement substance often dissolves out, and the fibers separate and may present vaeuolation and fragmentation. The nuclei stain faintly and later disappear. The blood vessels at the margins of the necrosed area are thrombosed. In blood clots, there is usually more or less fibrin, which in recent clots consists of a dense reticulum of fine fibril- be with "nodal points" at their points of intersection. In older clots and in exudates the nodal points are not seen, the fibrils are less distinct, or the fibrin may appear as granules. In anemic infarcts or other anemic areas, the fibrin is very small in amount or may be wholly absent, and in any case may require special staining (as Weigert's) to demonstrate. Physiologic function is usually considerably disturbed. Results. — Small areas may be liquefied and absorbed. Larger areas may undergo caseation and calcification, or may liquefy and suppurate and be replaced by normal tissue or by scar tis- sue; they may also liquefy and become encysted. Liquefaction Necrosis Liquefaction necrosis is death of a tissue with transformation into fluid. It may be primary, as in the central nervous system; or secondary, as when following coagulation necrosis, cheesy necrosis, inflammation, gangrene, and tumors. (6 GENERAL 1'ATIIOLOGY Etiology. — 1. Lysins, or liquefying enzymes are the causal fac- tors. Aseptic softening- following proteolysis by enzymes either from the dead cells ('autolysis) or from leucocytes (heterolysis). In septic softening, the bacteria elaborate the lysins, as in sup- puration, gangrene, etc. In the central nervous system, thrombosis of a terminal artery infarcts) which elsewhere would cause coagulation necrosis, here causes liquefaction necrosis — cause being unknown, probably lack of coagulins. . 2. Fluids may infiltrate the Tissues and dissolve them. Locations. — Liquefaction necrosis occurs in any tissue. It is common in acute inflammation, abscesses, vesicle or cyst forma- tion, and in anemic and hemorrhagic infarcts of brain. Gross Pathology. — The tissue is soft, at first semifluid, pale or yellow from fatty material, reddish brown or greenish from blood pigments or bile. Later there is fluid containing broken down cells and debris. Microscopically. — The cells undergo disintegration, fat, choles- terin, etc.. being liberated, resulting in a fluid debris, containing granules, and a few leucocytes which are sometimes engorged with fat globules. Results. — The contents may coagulate, become encysted, be absorbed or discharged, and the space if small, occupied by nor- mal tissue, or if larger, by connective tissue (cicatrization). Cheesy Necrosis, or Caseation Cheesy necrosis, or caseation is death of a part with the forma- tion of a cheese-like material. (Fig. 15.) Etiology. — Toxins, especially of B. tuberculosis. It may fol- low coagulation, or as some state it, be a form of coagulation necrosis of the proteins with appearance of a certain amount of fat. Locations. — Old tuberculous lesions, gummata, blood clots, in- farcts, and areas of coagulated necrosis. The typical cheesy necrosis is that occurring in tuberculosis; whether that which occurs in other situations is true caseation is still a disputed point. Gross Pathology. — The area is pale yellow with the appearance cheese, but more granular. A dry form occurs which is rounded, PATHOLOGIC PROCESS] S 77 circumscribed, and often encapsulated, and never Larger than a hazelnut. The moist form is softer, paler, and li^s sharply circumscribed. Microscopically.- Pine granules of proteiu material, with fatty debris, arc seen, the latter in advanced cases showing- fatty acid and cholesterin crystals, and sometimes leucin and tyrosin. The cells can uol be recognized, at least in fully developed cases, except sonic of the leucocytes. Results. — Areas may persist a long time without undergoing change or absorption (possibly due to destruction of autolysis by SKI"**. Fig. IS. — Large tubercle of the lung, showing cheesy necrosis. (Stengel and Fox.) toxins); the leucocytes do not enter the area (lack of cheniotac- tic substances). Finally calcification occurs, or cysts form which may persist, or be absorbed with cicatrization. Fat Necrosis Fat necrosis is a form of necrosis occurring in fatty tissues and apparently due to the action of pancreatic juice. Etiology. — It is believed that trypsin injures the cells, and the lipase (steapsin) splits the fat into fatty acids and glycerin, the latter being absorbed (and may appear in the urine) while the acids later unite with calcium to form insoluble soaps. 78 GENERAL PATHOLOGY Any condition permitting escape of pancreatic juice from its normal channels, as obstruction of the duct, acute pancreatitis, tumors, etc., may act as a cause. Locations. — This necrosis is seen in abdominal walls, the fat in and around the pancreas, etc. Gross Pathology. — The areas are white or yellowish, circum- scribed, varying from the size of a pinhead to a pea, may be soft ^ p ■:5s) a r ■*''. ' ':& & Q t , «* Q © i T 1 ' / \ f v ',* - i * 1 < * t o 6- V <■" 0. \ f BQ .- •'■* ,i© • ® Fig. 16. — Focal necrosis in the liver in pneumonia. (Delafield and Prudden.) or gritty, and may or may not be surrounded by an inflammatory border. Microscopically.— Usually but little of the original structure remains. The necrotic debris consists chiefly of calcium soaps, crystals of fatty acids, etc. Results. — While the necrotic areas themselves are not danger- ous to life, the causal conditions are usually fatal. When re- covery does take place, the necrotic foci disappear quickly. Focal Necrosis Small areas of necrosis (microscopic in size or sometimes visi- ble to naked eye) are often found in the liver, less often in the i ■ a'i i ii ii ,< i. , i« • p[;o('i:ssi:s 70 kidney, spleen and elsewhere, in eases of typhoid fever, less often diphtheria, septicemia and other infections, and presumably due to toxins. ( Fig. 16.) Gangrene Gangrene has been defined as (1) death of a considerable mass of tissue, which may become dried (dry gangrene, or mummifica- tion) or may putrefy (moist gangrene) due to saprophytic inva- sion, or (2) and probably more correctly, as putrefaction of ne- crotic areas. Primary gangrene is that due directly to bacterial invasion, as in malignant edema, and hospital gangrene. Secondary gangrene is necrosis subsequently invaded by bac- teria. Etiology. — The various causes as given under necrosis apply here. Putrefactive bacteria are said to be present in all cases, but as the fluid evaporates from the part, as in superficial tissues, bacterial action becomes less and less conspicuous, and finally, in complete mummification, ceases. Dry gangrene is of tenest caused by arterial obstruction ; freez- ing may block the vessels with thrombi; ergotism and Raynaud's disease may contract the vessels and shut off the blood supply; senile gangrene is due to arteriosclerosis with enfeebled heart action. Dry gangrene may also follow moist gangrene when putrefaction is slow and evaporation marked. (Fig. 17.) Moist gangrene is usually due to venous obstruction, but may follow any circulatory obstruction or destructive agency: (a) Strangulation of a part — bowel, appendix, torsion of spleen, kid- ney, tumor, etc. (b) Internal emboli as in pulmonary arteries and veins, or mesenteric arteries, (c) In the lungs, it may fol- low pneumonia, abscess, bronchiectasis, tumors, and diabetes. (d) In extremities, it may follow trauma, diabetes, physical agencies, etc. (e) In mucous membranes, it may follow the ac- tion of toxins, as in noma of the mouth or genitals, (f) In cystitis, it may follow trophic disturbances, (g) In decubitus, it is due to trophic and circulatory disturbances combined. Locations. — Any part may be affected, but particularly the distal ends of upper and lower limbs, bowels, lungs, etc. 80 GENERAL PATHOLOGY Gross Pathology. — Gangrene is a dark greenish or black (some- times "white" or anemic, especially in early stages) area, tem- perature is below normal, the area is usually circumscribed, and more or less odorous. The part is separated from the living tis- Fig. 17. — Senile dry gangrene of the lower extremity, showing line of demarcation. (Hektoen.) sue by a red inflammatory narrow zone — -"the line of demarca- tion. ' ' The dry form has the following distinctive features: The part is harder and the surface rough, shrunken, noncrepitant, of slight odor, and nearly always circumscribed. The line of demarcation advances slowly. The moist form has the following distinctive features: Is softer than normal, somewhat swollen, skin covered with vesicles PATHOLOGIC PROCESSES 81 or blebs, and discolored fluids ooze from sections or injured parts. There is crepitation, due to gases of decomposition. The line of demarcation advances more rapidly than in the dry form. Occasionally I here is no line of demarcation, as in diabetes. Oc- casionally there arc metastatic forms of gangrene. Pathologic Histology. — The cells have become converted into granular debris, consisting of protein matter, fatly granules, crystals of fatty acids, cholesterin, leucin, tyrosin, phosphates, carbonates, blood pigments, etc. The connective tissue and elas- tic fibers persist longer than the cells, but finally become lique- fied. Bacteria are also present. Results. — The process may go on until by absorption of toxic products death ensues (especially true of the moist form, due to primary invasion of bacteria, or to disease as diabetes). In other cases the mass is cast off as a slough or sphacelus at the line of demarcation, or encysted if within the body, followed by resorption and calcification or cicatrization of the gangrenous materials. CHAPTER IV THE CIRCULATORY CHANGES The circulatory changes are usually studied under the follow- ing headings: fa) Ischemia, or Local Anemia; (b) Hyperemia; (c) Hemorrhage; (d) Thrombosis; (e) Embolism; (f) Infarcts; and (g) Edema. Ischemia, or Local Anemia Ischemia, or local anemia, is a decrease of blood in, or total absence from, some part of the body. Etiology. — According to cause we have — 1. Co'/i//ov// anemia, due to blood having passed in excess to some other part, as cerebral anemia from shock or fainting, the blood passing to the dilated abdominal vessels. 2. Obstructive anemia, or ischemia, due to obstruction of the blood supply to any part, as anemic infarct, pressure of tumors, tight bandage, ligatures, cicatrices, obliterating endarteritis, etc. 3. Neurotic anemia, due to (a) stimulation of the vasoconstric- 1 ni-s (neurotonic anemia) as in the first stage of Raynaud's dis- ease, ergotism, etc., or to (b) paralysis of the vasodilators (neu- roparalytic anemia) as in pallor from strong emotions, fright, anger, etc. 4. Anemias due to causes acting directly on the vessels and in other ways not fully understood (hence the "idiopathic ane- mias" of some authors), as heat, cold, toxins, etc. Gross Morbid Anatomy. — The part is pale, lower in tempera- ture, smaller in size, less in weight, and more or less bloodless on section. Minute Anatomy. — Blood cells are abnormally decreased or ab- sent from the vessels. In long standing cases, atrophy, degenera- tive and necrotic changes may be noted. Pathologic Physiology. — Function is unaffected or may be di- minished. Occasionally the part is painful or tremulous. S2 CIRCULATORY CHANGES 83 Results.- -Mild degrees recover, especially if treated. In cases due to blocking of the vessel, anastomotic circulation may fully restore the part. In severe and prolonged cases, atrophy, de- generative and necrotic changes result. Hyperemia Hyperemia is excess of 1)1 ood in a part. It is active when excess of blood is brought to a part by the arterial system; pas- sive, when the normal removal of blood is interfered with by the venous system. Active Hyperemia Etiology. — According to cause Ave have — 1. Collateral hyperemia, due to anemia in another part, as around anemic areas, or by bandaging a limb preparatory to amputation, etc. 2. Increased heart action may cause hyperemia, though proba- bly only supplementary to other causes or local conditions. 3. Neurotic hyperemia, due to (a) stimulation of vasodilators (neurotonic hyperemia) as in certain forms of neuritis, as herpes zoster, or the rash of teething infants, etc., also in erythro- melalgia (red, painful, pulsating areas of hands and feet) blushing, etc., or due to (b) paralysis of vasoconstrictors (neuroparalytic hyperemia) as in hyperemia of a side of the face from pressure of a tumor upon the cervical sympathetic; certain forms of migraine may also belong here. 4. Cases due H^,, agencies whose action is imperfectly under- stood, as heat, reaction from temporary pressure, certain drugs, toxins, increased functional demand, etc. Gross Anatomy. — The part is red — color disappearing on pres- sure, temperature of superficial parts somewhat raised, size and weight increased (due in part to hypertrophy). The part is bloody on section. Minute Anatomy. — The vessels are abnormally filled with blood, occasionally there is a capillary hemorrhage into the tissues. Pathologic Physiology. — Function is unaffected or increased when hyperemia is moderate and uncomplicated. In tensely fdled encapsulated organs the function may be impaired from compression of the parenchyma. 84 GENERAL PATHOLOGY Results. — Mild cases recover. Mild prolonged cases may cause hypertrophy. In severe and prolonged cases capillary hemor- rhage may occur, or the vessels may remain weak and liable to repeated dilatation from slight causes or be followed by in- flammation. Passive Hyperemia Etiology. — 1 General causes are enfeebled heart action from obstructive heart disease or from any cause ; also insufficient muscular exercise, disease of lungs interfering with outflow of blood from right side of heart, etc. 2. Local causes, as pressure on veins by tumors, aneurysm, & ■ '", • ■ ' , Id Fig. 18. — Chronic passive congestion of the liver. (Delafield and Prudden.) etc., or interference of passage of blood through veins as parietal thrombi, syphilitic or other phlebitis, etc. Gross Anatomy. — The part or organ affected is dark or bluish (cyanotic), the color disappearing on pressure. The brain and cord, however, are not cyanotic when congested. Size and weight are increased, temperature of superficial parts reduced. (Fig. 18.) Minute Anatomy. — All vessels are distended with blood. Edema (excessive lymph within tissues) is often noted. In prolonged cases, other forms of degenerations may be seen. Pathologic Physiology. — Function is impaired. The part or organ is at first painful, later anesthetic (probably pressure on nerve endings). CIRCULATOR'S CH \\<;i s 85 Results. Mild cases may recover, but tin' process is more ap1 to be chronic than in the active hyperemia. Gradually developed and prolonged cases lead to atrophy, degeneration, edema, pig- mentation or cyanotic induration (fibrosis). Severe and rapidly developed cases may lead to coagulation necrosis and gangrene. Hypostatic Congestion Hypostatic congestion is passive congestion or hyperemia oc- curring in dependent parts, tine to enfeebled heart action. It occurs especially in debilitating diseases, in low fevers, and also commonly just prior to death from any cause, and is seen usually in the skin and subcutaneous tissues of back and buttocks, and in the lungs. Hemorrhage Hemorrhage is the escape of blood from blood vessels. Type I. According to source of blood: (1) Arterial hemorrhage. (2) Venous. (3) Capillary. (4; Mixed, or parenchymatous. Type II. According to mode of production: (1) Hemorrhage by rhexis or laceration. (2) Hemorrhage by diabrosis or ulceration, caustic action. (3) Hemorrhage by diapedesis or oozing of blood from capil- laries or venules through the intercellular cement spaces ("stomata") and due to increased blood pressure or altered vessel walls. Type III. According to destination: (1) External Hemorrhages — upon exterior of body or into cavi- ties communicating therewith, as Epistaxis — hemorrhage from nose Hemoptysis " " lungs. Hematomesis " " stomach. Hematuria " " urinary tract. Enterorrhagia " " intestines. Metrorrhagia " " uterus between menses. Menorrhagia " " uterus during menses. Hematidrosis " " sweat glands. (2) Internal Hemorrhages into (a) Closed cavities, as Hemothorax — hemorrhage into pleural cavity. Hemoperitoneum ' ' into peritoneal cavity. Hemoperieardium ' ' into into pericardial sac. Hematocele " into tunica vaginalis testis or other small cavity. 86 GENERAL PATHOLOGY (b) Interstitial or Concealed Hemorrhages, as Ecchymosis — circumscribed hemorrhage beneath skin or mucous membrane. Suffusion of Blood or Suggillation — diffuse hemorrhage in same locations. Petechia? — minute or circumscribed hemorrhage (often punctiform). Hematoma — a tumor-like collection of blood. Hemorrhagic Infarct — a wedge shaped area of blood. Etiology. — (1) Traumatism. (2) Erosion by surrounding dis- ease, as ulcer, tuberculous cavity, etc., or by corrosion of caus- tics. (3) Increased blood pressure, as in great excitement, mus- cular effort, increased atmospheric pressure (caisson disease), hypertropliied heart associated with arteriosclerosis, etc. (4) Alteration of vessel walls, resulting from degenerative changes, as in aneurysm, apoplexy, cachexia?, pressure atrophy, poisons, toxins of bacteria, plants or snakes. (5) Nervous influences: disease or section of the cord, apoplexy, suppression of men- struation, etc., sometimes cause hemorrhage from other parts, as stomach, nose, etc. Gross Anatomy. — The blood may be bright red, dark or black, according to length of time retained in tissues or cavity. In in- terstitial hemorrhage the part is swollen. Microscopically, the tissue is infiltrated with blood cells or blood pigment, and where coagulation has occurred, fibrin may be seen. Hemorrhage is checked by: (1) Formation of clot plugging the bleeding vessel. In certain conditions, especially hemophilia (see below) the blood shows little or no tendency to clot. (2) Reduction of blood pressure. (3) Contraction of vessel at site of hemorrhage with retraction and curling up of the middle coat in cases in which arteries are cut transversely. The contraction is usually followed in a few hours by relaxation, which may cause secondary hemorrhage. (4) Pressure of extravasated blood upon capillaries in interstitial hemorrhages. Results. — Depending upon age, health, etc., about y 5 to *4 of total amount of blood in body may be lost without fatal re- sults. One large hemorrhage is more apt to result seriously than a larger amount of blood lost in small and oft repeated hemor- rhage. The total amount of blood (usually given as % 3 ) is CIRCULATORY CHANGES 87 probably only '| i; to ' L . u of the body weight, or aboul 8 pounds for average adult. Blood escaping into a large smooth cavity (as pleural or peri- toneal) docs not clot readily and may be wholly or in large part absorbed by lymphatics and returned to the circulation. Hemophilia Hemophilia is a condition characterized by spontaneous or readily induced homorrhages, and especially by delay or absence in clot formation at the site of hemorrhage. It is usually hereditary though acquired cases are also re- ported. Males arc much more frequently affected than females (about 12 to 1), but the diathesis is almost exclusively transmit- ted through the female sex. Pathology. — Various alterations in the blood have been ob- served, as a deficiency in calcium salts, in blood platelets and in prothrombin but these changes are not constant. The shed blood in many cases coagulates as rapidly and as firmly as in normal conditions. The occurrence of local hemophilia (where vessels in certain regions alone show this tendency) argues against gen- eral blood changes. It is probable that the prothrombin neces- sary for fibrin formation at site of hemorrhage is largely fur- nished by the endothelial cells of the vessel walls, and the theory has been advanced (Sahli) that these cells are deficient in this particular enzj'me in cases of hemophilia. Results. — Hemophiliacs or ''bleeders" are apt to succumb to fatal hemorrhage during the early years of life — the later the diathesis manifests itself, the more favorable the prognosis. Secondary anemia is usually observed. Thrombosis Thrombosis is coagulation of blood in heart or blood vessels during life. The coagulum is called a thrombus. Occasionally thrombi of fibrin and leucocytes appear in the lymph vessels. Coagula formed postmortem, or those formed outside of the vessels are called clots, (this distinction is, however, not main- tained by all writers). Types of thrombi: 88 GENERAL PATHOLOGY I. According' to extenl and time of formation: (1) Primary thrombi are those first formed and confined to the original site. (2) Propagated thrombi — those portions subsequently formed and reaching to the nearest branch of the vessel or further (some call these "secondary"). (3) Secondary thrombi — those formed upon an embolus detached from a primary thrombus, or upon a pre- existing thrombus. II. According to location: (1) Cardiac; arterial; venous, in- cluding portal; capillary; and lymphatic. (2) Proximal — those on the cardiac side of a causal obstruction; and distal — those on the other side of the obstruction. III. According to shape: Parietal; annular; valvular; ob- literative; saddle or riding (at bifurcation of vessels); polypoid or pedunculated, seen usually in left auricle; ball thrombi — de- tached pedunculated forms. IV. According to composition: (1) Red or currant jelly thrombi — rapidly formed, as in complete stasis, ligation, and death (post- mortem clots), and containing all the cellular elements of the blood. (2) Yellow or chicken-fat tlirombi — slowly formed, as in prostrating diseases, or in slowly approaching death, the red cells gravitating to the lower parts, leaving the white cells on top. The chicken-fat clot is formed after death in anemic, espe- cially leucemic diseases. (3) White thrombi — consist of fibrin with a varying number of leucocytes and of platelets; are formed in flowing blood, and occur in heart and large vessels, as peduncu- lated or parietal forms. (4) Stratified thrombi — consist of alter- nating lamince of white and red cells, due to alternating slowing and accelerating of the blood current, and seen in dilated vessels and aneurysms. (5) Marantic tlirombi are dark colored, composed almost wholly of red cells, seen in dependent vessels, in brain sinuses, etc., and in the lower parts of chicken-fat thrombi ; they are due to enfeebled circulation and exhaustive diseases, maras- mus, etc. Many of these thrombi have been found to be in- fective. (6) Agglutinative or hyaline tlirombi appear to be homogeneous and colorless; usually seen in plaque thrombi, which are composed of blood platelets fused together, and occurring usu- ally in the heart and large vessels: also in conglutinative thrombi, consisting of almost colorless red blood corpuscles fused together and seen in diseases attended with hemolysis; as anemias, infec- CIRCULATOR'S ('II We 89 tions, poisons, etc. These occur usually in small visceral veins. (7) Organized thrombi — those which have been replaced wholly or in part by new connective tissue. (8) Calcified thrombi — found usually in veins, as phleholiths, and rarely in arteries as arte- rioliths, and in hearl as cardioliths. (9) Canalized thrombi -those through which an opening has been formed by simple softening (liquefaction i rosis) or rarely by dilatation of a longitudinally disposed newly-formed blood vessel in an organized thrombus. (10) Infectivi thrombi — may be infective from the start, as in septic emboli, or may be subsequently infected. Etiology. — (1) Altered cardiac or vessel vails. Any agency which roughens the intima or endocardium, as injury in ligation or laceration, pressure of tumors, etc., or disease as atheroma, local inflammatory or degenerative conditions, or action of para- sites, tissue cells, etc. (2) Altered rate of blood current. Slow- ing favors agglutination of leucocytes and platelets to cardiac and vessel vails and to one another. Thrombosis is apt to occur in sinuses of the heart, and brain; in dilated vessels, aneurysms, etc. (3) Emboli. (4) Altered blood. Experimentally the in- jection of tissue extracts (thymus, suprarenals, etc.) containing fibrin ferment: of hemolytic agents, as nitrobenzol, ether, phenol, phytotoxins, zootoxins, and bacterial toxins will cause thrombosis. Increase of calcium salts, hyperinosis as in pregnancy, etc., favor thrombosis. Gross Anatomy. — Fresh thrombi are jellydike, moist and break with a gelatinous fracture. Old thrombi are firm, due to fibrosis or calcification. The color depends upon the type. The postmortem clot is distinguished from a thrombus by be- ing loose, showing no evidence of attachment to heart or vessel; is moist and shows no distinct stratification, though in slowly forming clots, the upper layer may be paler than the lower. Microscopically.— -Freshly formed fibrin presents a dense net- work of very fine fibrils, with "nodal points" or granular mat- ter at the points of intersection. The blood cells are usually present in normal proportion. In older thrombi, red and white cells or fibrin predominate, as stated under the various types. In organized thrombi, young connective-tissue cells and fibers, and newly formed capillaries are seen, the elements of the thrombi 90 GENERAL PATHOLOGY disappearing- by absorption. "When degenerative processes take place the evidence of such is observed. Results. — If the circulation is completely stopped, necrosis of the part follows, and even gangrene when putrefactive organ- isms invade. Frequently, however, collateral circulation saves the part from injury in which event the thrombus may undergo resolution, or it may soften so rapidly that detached portions become emboli. Again thrombi may become fragmented, or whole thrombi de- tached, thus resulting in serious embolism. Hyaline degeneration with calcification may occur. Organiza- tion will often displace the thrombus, converting the vessel into a solid fibrous cord, or into an irregular channel with fibrous trabecular, the latter becoming covered with endothelium. Embolism Embolism is the transportation and lodgement of any substance within the circulation, capable of obstructing the flow of blood. Such substance (solid, liquid or gas) is called an embolus. Types of Emboli : I. According to location: 1. Cardiac (rare)- — a large venous thrombus, detached and doubling upon itself may occlude the pulmonary orifice in the heart, or a ball thrombus may plug the valves. 2. Arterial — the most common emboli are found usually in small arteries or arterioles. The pulmonary branches are the most frequently affected, the embolus coming from a thrombus in the right side of heart, or venous system. Next to the pul- monary arteries, the following are affected in order of frequency: arteries of kidney, spleen, cerebrum (especially the middle cere- bral) and less often, or at least less often detected, in lower ex- tremities, upper extremities, liver, stomach, retina, and more rarely elsewhere. The emboli come from left cardiac and aortic thrombi or atheromatous ulcers, and rarely from the right side of the heart or venous circulation (paradoxical emboli). 3. Capillary — usually composed of tissue cells, bacterial cells, oil globules, gases, pigments (malarial) etc. Various metastases are thus explained. CIRCULATORY CH Wilis 01 4. Venous. Since veins become larger in the direction of the blood current, embolism occurs in the systemic veins only when the venous bloo<3 currenl becomes slowed and momentarily and repeatedly reversed, or when ;i foreign body by its own weighl gravitates againsl the blood stream. This is called retrogressive embolism. The portal vein narrows in the direction of the blood stream like an artery, hence emboli from the spleen, pancreas, gastrointestinal tract are frequently caugh.1 in the liver. They are often infective. 5. Lymphatic — retrograde embolism occurs as in veins and ex- plains certain crises of metastasis to more distal points as can- cer of humerus from axillary "lands. G. Paradoxical or crossed embolism occurs when emboli orig- inating in systemic veins or right auricle find their way to the arterial system. They pass through either a patulous fora- men ovale or when small through the pulmonary capillaries (which are larger and more dilatable than the systemic capil- laries). II. According to composition, emboli consist of: 1. Fragments of thrombi — most frequent of emboli — and rarely whole thrombi; as from pelvic veins. 2. Fragments of cardiac A'alves and vegetations. 3. Calcareous and atheromatous matter from atheromatous ul- cers. 4. Tumor cells and fragments (neoplasmic emboli) which have penetrated the vessel. 5. Tissue cells, as from liver, placenta, chorion villi. Lym- phocytes and leucocytes infiltrate liver, etc., in myeloid leueemia. 6. Parasites. Animal (as filaria, echinococcus, etc.), and bac- terial emboli. By "septic emboli" is usually meant those in- fected with, or consisting chiefly of, pyogenic bacteria. Pyemia is thus caused. 7. Extraneous matter, as oil globules from laceration of fatty tissue, including fractures or operations on long bones; pieces of bone in comminuted fractures; bubbles of air, as may happen when veins are ruptured or cut as in operations, especially about the neck. All such emboli entering vessels through injuries are called traumatic. GENERAL PATHOLOGY Gaseous emboli may also occur from the activity of aerogenic bacteria, or in caisson disease, where from increased atmospheric- pressure gases (chiefly N) may accumulate, and expand with the formation of bubbles on reduction of pressure. Results of Embolism. — I >cclusion of valvular orifices, pulmo- nary artery or one of its main branches, one of the coronary ar- teries, or a large cerebral artery, usually causes sudden death. Iii smaller pulmonary branches, recovery may occur after a period of great dyspnea. When many small branches or capil- laries are plugged, death may ensue: fat or air embolism may thus be fatal. It is also thought that air in sufficient quantity can cause death by forming foam which interferes with the heart's action. In cases of small emboli, when single or few in number, col- lateral circulation usually relieves the part from degenerative change. If. however, the embolus lodges in a terminal vessel. an infarct results. Thrombi are apt to form upon emboli. If an embolus should not have completely occluded a vessel, the thrombus will stop the floAv. Embolism often results in metastasis of malignant tumors, as sarcoma, and of infections, as "embolic abscesses'" — pyemic, ame- bic, etc. Metastasis means the transportation of living material from a focus of disease, capable of reproducing the disease at the points of deposit. Infarcts Infarcts are more or less rone-shaped necrotic areas, caused by obstruction of the terminal or "end vessel" of a part (the latter being an artery having no collateral branches beyond the point where it breaks into capillaries . Occasionally the occlusion of a number of adjoining arterioles or capillaries causes infarcts of very irregular outline. The essential necrotic change in infarcts is coagulation nec- rosis, except in the brain where liquefaction necrosis develops from the start. Two forms of infarcts: (A) anemic or white, which are de- void of blood, and found most frequently in kidney, spleen, heart. CIRCULATOR'S CH ^NGES 93 brain, stomach and intestine; and (B) hemorrhagic or red, which .,,,. infiltrated with blood, and round mosl frequently in Lungs, less often in spleen, kidney, and other Locations. Etiology.-- Embolus or thrombus in a terminal artery. This. however, is not necessarily followed by infarction, as may be seen in lungs and liver, where there is free circulation. Nor need the occlusions always be in a terminal artery— infarcts may occur m intestines with free anastomosis. Again, hemorrhagic infarc- tion is said to occur by occlusion of a terminal vein. If the blood supply be too slowly occluded, collateral circulation will prevent infarction. The manner and sequence in which anemic and red infarcts develop have occasioned much discussion. Some claim that the anemic infarct is the first result of embolism, the red infarct, a secondary condition. Adami believes that the essential factor in formation of an anemic infarct is the rapid death and coagula- tion of the hemorrhage; should the death of part be slowly de- veloped, hemorrhage is permitted to occur (red infarct). Why anemic and red infarcts may be found at different times in the same organ depends chiefly on the condition of the cells at the time, for experimental ligation of the renal artery is followed by necrobiosis in one and one-half hours, but if some poison (diph- theritic toxin- he previously injected, it follows in three-quarters of an hour. Anemic infarcts develop usually in dense tissue, as kidney and hemorrhagic infarcts in loose tissue, as lung; this has thus been explained: the capillaries around the necrotic area become congested (zone of hyperemia) and exude serum which infiltrates the "cells in the immediate vicinity, causing compression of the capillaries and prevent the progression of blood into the necrotic area. In loose tissue the capillaries rupture, infiltrating the area with blood. The exceptional cases are explained by path- ologic variations in looseness or density of the tissues, as in fatty degeneration or in fibrosis respectively. in essential factor in infarct formation is smallness of the area involved: large areas suddenly deprived of blood be- come gangrenous. A possible explanation may lie in the fact, as Weigert claimed, that pervasion of an area with blood serum 04 GENERAL PATHOLOGY is necessary for coagulation necrosis — large areas can not thus be bathed before gangrene has set in. Gross Morbid Anatomy. — An anemic infarct is a cone-shaped or irregular whitish or yellowish area, softer than normal, with apex toward occluding vessel and base toward periphery, its outer surface depressed below the general surface of the organ. The red zone of hyperemia can usually be seen. Fig. 19. — Old anemic infarct of spleen. C Stengel and Fox.) The hemorrhagic infarct has the same shape and location as the anemic, but is red or dark in color, firmer than normal, and its surface elevated. Subsequent changes will alter the consist- ency in both forms. Microscopically. — In the anemic form, bloodless areas with co- agulation necrosis, fibrin or fibrinoid material, and necrotic cells are seen. Hemosiderin is sometimes seen and rarely hematoidin in the central parts. In the hemorrhagic form, blood cells with pigment and fibrin, also necrotic tissue cells are seen. CIRCULATOR'S CHANGES 95 The occluding embolus or thrombus may sometimes lie seen grossly as well as microscopically in sections which pass through these occluding bodies. Results. — -(1) The area may become encapsulated, and Ihe con- tents undergo fatty change, calcification, caseation or liquefac- tion. It may be gradually absorbed and replaced by ingrowth of fibrous tissue, which subsequently contracts, forming a scar or cicatrix. Infection may take place when infarcts are so located as to be readily reached by microorganisms, as in lungs. Those caused by infective emboli are of course followed or associated with infectious processes. (Fig. 19.) Edema, Dropsy or Anasarca These terms signify an excess of fluid in the tissues or body cavities. The term edema properly applies to interstitial infil- tration of fluid in any part; anasarca, to widespread subcuta- neous infiltrations: wheals, to small circumscribed cutaneous in- filtrations: drops)/, to fluids in cavities; transudation, to fluid poured out in noninflammatory conditions ; and exudation, to fluid poured out in inflammatory processes. Etiology. — 1. Increased capillary blood pressure due to pas- sive congestion, pressure upon veins, etc. 2. Increased permeability of capillaries, due to: (a) Alteration of blood, containing toxic substance as in in- fectious diseases, Bright 's disease, anemias, and cachexias. (b) Local disease of walls, as in inflammation. (c) Nervous influence, as in paralysis or disease of brain or cord, in neuralgia, and various nervous irritations. This may act by vasomotor depression, by trophic disturbance of intima, and in other ways not understood. 3. Disturbed osmotic conditions. The tissue fluids may be hypertonic (contain more NaCl than the blood) causing tran- sudation in the effort to establish isotonicity. Increased NaCl content of the affected tissues has been demonstrated in cardiac and renal dropsies. 4. Extensive obstruction of lymphatic vessels will prevent the normal removal of lymph, as in chylous ascites, in elephantiasis. 96 GENERAL PATHOLOGY etc. In moderate obstruction, the venous capillaries can remove all the lymph. 5. Decreased pressure in tissue, as when the space left by atrophy or destruction of tissue in brain or cord is filled with fluid ("edema ex vacuo"). In individual cases it is impossible to determine how many of these causal factors may ho associated, or in some cases even to name the chief factors. We have the following types of edema: Cardiac — from weak heart action (passive congestion) seen in dependent parts, as ankles, wrists, hands, bases of lung, etc. Renal — from nephritis (seen in some forms, as acute nephri- tis), also in loose tissue (about eyelids). In other cases, it re- sembles cardiac edema. Cachectic — seen in loose tissue about eyelids, backs of hands, etc., may rarely be widespread. This is seen in malignant diseases. Mechanical — due to venous or rarely lymphatic obstruction. Toxic — often widespread and due to alterations of the blood as a result of toxins. Angioneurotic — as in some forms of urticaria, due to vaso- motor disturbances. Lymphatic — often widespread; the fluid sometimes is milky in appearance, due to presence of fat, mucoid substance, etc. Pulmonary edema — so called when the air cells are filled with fluid. Chemosis — subconjunctival edema. Dropsy in cavities is known as: Hydrothorax, Hydropericardium, Hydroperitoneum or Ascites, Hydrocele (in tunica vaginalis), External Hydrocephalus (in cerebral meningeal sac), Internal Hydrocephalus (in cerebral ventricles), External Hyclrorrhachis (in spinal meningeal sac), Internal Hyclrorrhachis or Syringomyelia (in central spinal ca- nal), Hydrops Articuli (dropsy of joints), etc. Gross Anatomy. — The part is swollen, tense and shiny on the surface, pale, pits on pressure, has a doughy consistence, and subnormal temperature (deficient circulation). On incision watery fluid escapes, which is usually clear, thin, pale or yel- lowish (sometimes red, greenish or milky) ; contains but little CIRCULATOR! CHANGES 97 fibrinogen and albuminous matter; specific gravity — 1.00s to L.014. [nflammatory fluid contains more albuminous matter and usually coagulates readily; specific gravity 1.018 to 1.020. The tissue infiltrated is firmer than normal. Microscopically. I) r< 1 1 »sica I fluid may sometimes be seen in tissue, appearing homogeneous and electing the acid stain. In- flammatory edema is usually granular and contains ;i certain amount of cellular elements. The tissue cells are separated and may be hydropic of otherwise degenerated. Result. — Acute cases recover if the cause can be removed. though if very extensive (as in pulmonary edema) or in unfa- vorable location (as in edema of gdottis), death may ensue. Where the condition is permanent or the cause can not be re- moved various forms of degenerations and fibrosis result. CHAPTER V INFLAMMATION Inflammation is a compound pathologic process represent- ing the reaction of tissues toward an irritant. Etiology. — Any mechanical, physical, chemical, infectious or nervous irritation, sufficient to cause local injury, but insuffi- cient to cause immediate extensive necrosis. Perhaps in all cases, the injured (degenerated or necrosed) tissue becomes the direct irritant, though some substances as toxins, etc., may also cause emigration of leucocytes by their chemotactic influence. Nervous irritation probably acts primarily through the vaso- motor nerves. The causes may be divided into external and internal — the latter being products of abnormal metabolism. Again we have simple, or noninfective, and septic, or infective, causes — the es- sential difference being that the simple are not reproductive, while the infective are constantly being reproduced and usually increased until the reparative processes overcome the destruc- tive, or death ensues. Inflammation is either acute — in which the vascular phenomena predominate; or chronic — in which the proliferative changes pre- dominate. Gross Pathology of Acute Inflammation. — Heat, redness, pain, and swelling (calor, rubor, dolor, tumor — of Celsus) are the chief general characteristics. (The distinctive features of the various types must be separately described.) Microscopically, the following histologic changes have been noted : The arteries and arterioles temporarily contract, but soon begin to dilate, and in "an hour or so" full dilatation of all the vessels is seen, with increased blood flow (hyperemia). Gradually the blood stream becomes slower, the corpuscles leave the central axial stream (in the larger vessels) and the leucocytes adhere to the vessel walls (marginatum) . The endothelium be- 98 INFLAMMATION !)!) (•(nut's swollen niid probably more adhesive, and the vessel more permeable. The (irst elemenl which escapes from the vessels is Hie fluid of the blood (a transudation) ; Later the fluid is found to be rich in albuminous substances which aid in proliferative processes, and this modified blood plasma villi the blood cells which per- meate the area is called the inflammatory exudate. The leuco- cytes emigrate before the red blood cells pass through the vessel walls and in larger numbers, due to the positive chemotaxis which attracts them to the irritant. Red blood cells always pass out of the vessels into the affected area (diapedesis) but this is conspic- uous only in severe grades of inflammation. The leucocytes are chiefly of the polymorphonuclear (phago- cytic) variety, but in some cases especially in inflammation due to animal parasites, eosinophils are also found. In later stages lymphocytes abound, derived from lymph channels and from proliferation of local lymphoid-tissue cells. Plasma cells, which arc probably altered lymphocytes, with distinct and eccentrically placed nuclei, may be found in any type of inflammation. Proliferation of the fixed connective-tissue cells and the endo- thelium of lymph spaces and capillaries occurs sooner or later, thus forming "round cells" with large pale nuclei. At this stage many of the leucocytes have disappeared, but those that remain together with the lymphocytes and proliferated cells just mentioned constitute the so-called "round-cell infiltration." Some of the newly formed connective-tissue cells become "wan- dering cells" which are more or less phagocytic, while the re- mainder elongate and form fibrous tissue (fibroblasts). Degenerative changes are always present in varying degrees, con- sisting of cloudy swelling, mucoid or fatty degeneration, coagula- tion necrosis, liquefaction or other necrosis. A typical, acute inflammation is therefore characterized by Hyperemia of the affected area, Exudation of serum from the vessels, Emigration of leucocytes, Diapedesis of red blood cells, Proliferative changes in the fixed tissues, Degenerative changes. (Figs. 20, 21, and 22.) There are ten types of inflammation: 100 GENERAL PATHOL* I. Edematous or Serous. — In this type there is an excessive fluid exudation, with little tendency to fibrin formation, and relatively few cells, due to intense irritation. - steam or cor- rosives: or to mild subacute or chronic irritation, as in serous effusions. II. Fibrinous. — The exudate is especially rich in fibrin factors, the fibrin appearing as fibrillar, granular or homogeneous de- Fig. 20. — Acute inflammation. (Mallory.) m ■* % "^ f f -OCA Fig. 21. — Inflammation of the : show- ing overfilling of the blood vessels, with emigra- tion of let: liapedesis of red corpuscles. (Ziegler.) - • < Mallory. > posits. This type is seen most typically on serous surfaces, but it also occurs in tissi III. Diphtheritic or Croupous. — This is ntially the same as the fibrinous, but with more pronounced coagulation necrosis of the cellular elements, thus forming a tough membranous pellicle — the false membrane. This type is met with most typically on [NFLAMMATION I'll mucous surfaces, due to bacteria (as the diphtheritic bacilli, strep- tococci, etc.)j steam, chemicals, etc. I Pig. '23.) IV. Suppurative. — Characterized by excess of leucocytes and liquefaction of the exudate and fixed tissues. Clinically prob- ably always due to pyogenic organisms (usually pyococci, less often pneumococci, colon and typhoid bacilli, and other organ- isms) bul injections of sterilized cultures, toxins, croton oil, tur- pentine, calomel, iodoform, etc., can also cause pus formation. The irritant being strongly ehemotactic accounts for the ex- ive local leucocytosis. Enzymes liberated from the leuco- ranous inflammation of the uvula: a. a, masses of micrococci; b, b, necrotic cells; c, c, round-cell infiltration; d, d, fibrin network. (Ziegler.) cytes and probably other cells, and perhaps also in part by the bacteria, prevent fibrin formation, or liquefy what does form, together with the exudate and tissue, thus forming- pus. Pus, is a yellowish, thick, usually alkaline (specific gravity 1.020 to 1.040) fluid, containing pus cells in suspension. Pus cells consist chiefly of polymorphonuclear leucocytes, also a small number of proliferated connective-tissue and endothelial cells, all more or less degenerated (typically cloudy, swollen, clearing on adding acetic acid) or necrotic (shown by karyoly- sis, etc.) Pus may contain as many as 1.000,000 cells per c.mm.; 1 oz. (30 c.c.) would thus contain nearly as many leucocytes as does the total amount of blood, illustrating the enormous cell reproductive power of the body tissues. K'2 GENERAL PATHOLOGY The fluid (liquor puris) contains proteins normal to blood, as well as derived proteins, albumoses, peptones, etc., also shreds of muscles, fibrous or elastic tissue variously degenerated, blood pigment, sometimes bacterial pigment, fatly acid crystals, cho- lesterin, etc. Bacteria may be present, free in the fluid or with- in the cells; frequently, however, the bacteria are destroyed by products of their own manufacture, or by action of the cells and exuded fluids. Such pus. as well as thai caused to form by noninfective agents, is called "sterile pus." Suppuration may occur: Within tissues, as a circumscribed collection of pus (abscess) or as a diffuse infiltration (purulent infiltration or phlegmonous inflammation). On free surfaces, with considerable loss of tissue (ulcer). On serous surfaces or in serous cavities as an empyema. On mucous surfaces, as purulent catarrh, pyosalpinx, etc. Abscess Formation. — When a suppurative inflammatory area first liquefies in the center (which it does usually in forty-fin lit hours) an abscess is formed, i. e., a cavity filled with pus sur- rounded with a wall of inflammatory tissue, rich in leucocytes. The abscess grows by liquefaction progressing from within out- ward, the inflammatory wall growing with equal pace. After sufficient time (four to ten days) granulation tissue (see Repair) forms. A fully developed abscess wall therefore consists of an inner zone composed largely of leucocytes, exudate and intercellular matter about to liquefy; next a zone of inflammatory exudate with its granulations projecting into the preceding, and of con- gested capillaries (the source of leucocytes) hence called "pyo- genic zone," (formerly "pyogenic membrane"). The outer part of this zone, being the youngesl part of the wall, usually shows more fibroblasts and mitotic figures than the middle por- tion. Results. — The abscess travels in the direction of least resist- ance (called "pointing") which is usually tOAvard the surface of an organ or part, because the pressure is less on that side and because there is greater vascularity on its inner side, hence more leucocytes and resistance. [NFL v.m \i \ti<>\ 103 Rupture or incision of an abscess relieves tension and causes the fluid exudate in the abscess wall to flow toward and into the cavity, flushing out the tissue spaces of bacteria and toxic prod- ucts, and favoring protective (phagocytic, bacteriolytic and probably antitoxic) and reparative processes. In small abscesses or pustules, complete restitution may oc- cur; in Larger ones, cicatrization follows healing (see Repair). Sometimes encapsulation, with inspissation or calcification, oc- curs. Death may ensue from intoxication when abscesses are very Large or multiple, or when vital organs are involved, or when rupture occurs into large vessels, peritoneum, etc. In acute bacterial action, stasis is apt to occur in the vessels of affected areas (thrombosis and thrombophlebitis) thus prevent- ing hemorrhage even when eroded; but bacteria are also liable to grow into and through these plugged vessels and constitute one of the ways in which metastasis occurs. Special forms of abscesses : A Furuncle (boil) is a subcutaneous abscess, beginning in a sweat gland, sebaceous gland, or hair follicle. A Carbuncle is a similar but more extensive abscess, beginning in several glands or follicles simultaneously. Its favorite seat is in the back. A Pustule is a term properly applied to a suppurat'.ig vesicle, though often applied to any minute superficial absce ,s. Pyemia is a condition in which multiple abscesses e - ist through- out the body, due to emboli of pyogenic bacteria. An acute abscess is often called a "hot abscess," in contrast to the so-called "cold abscess," a term practically limited to lique- faction of tuberculous bone disease, as in lumbar vertebra?. Phlegmonous Inflammation. — This is a spre ding inflamma- tion with a tendency to suppuration. In these < ises "wall build- ing" characteristic of abscess is inadequate; tl i bacteria are not confined, the process spreads more or less ra idly, and metasta- sis is apt to occur through lymph and bloc . vessels. It is al- ways serious and sometimes attended with xteusive loss of su- perficial tissue. 104 GENERAL PATHOLOGY An Ulcer is an area of superficial suppuration with erosion of the skin or mucous membrane. The floor of the ulcer is similar histologically to an abscess wall. Ulcers may be divided into: Phagedenic — rapidly spreading and destructive. Serpiginous — snake-like and irregular, healing on one side and progressing on another. Fungous — in which excessive granulation tissue forms. Indolent — in which granulation tissue is slow in forming. Gangrenous — in which putrefaction is an added feature. Follicular — small in extent as in crypts or follicles of glands. Fig. 24. — Tuberculous ulceration of the intestine. fStengel and Fox.) Specific — due to tuberculous, syphilitic or other infection. (Fig. 24. Peptic — due primarily to the digestive action of enzymes. V. Catarrhal Inflammation is inflammation of a mucous mem- brane, characterized by degeneration of epithelium (mucoid, fatty or necrotic) which is discharged with the abundant serous exudate upon the surface. The submucous tissue is infiltrated with a more or less serous exudate. (See Fig. 25.) AVhen there are abundant leucocytes we have a purulent or mucopurulent catarrh. In chronic forms, productive processes lead to overgrowth of connective tissue, giving an appearance of hypertrophy of the mucosa. Later 'on. contraction of the fibrous tissue causes atro- phy. IM'I.AMM ATIOX 105 Follicular Inflammation are terms applied to swollen lymph follicles, or in mucous glands (from obstructed duets; the resull of inflammation. VI. Parenchymatous Inflammation are terms used when the degenerative changes occurring in the parenchyma Tor function- - Fig. 2: -Acute bronchial catarrh, showing the escape of leucocytes from the submucous tissue between the epithelial lining cells. (Thoma.) r Fig. 26. — Chronic interstitial nephritis: great increase of connective tissue around the glomeruli, renal tubules, and blood-vessels; from a case of arteriocapillary fibrosis. I Stengel and Fox.) 106 GENERAL PATHOLOGY ating cells) of an organ are more conspicuous than the inflamma- tory changes in the interstitial tissues. VII. Interstitial Inflammation. — Strictly speaking, inflamma- tion proper occurs only in interstitial tissue, but the term is ap- plied to more or less chronic inflammation of an organ, attended by decided overgrowth of fibrous tissue. (Fig. 26.) VIII. Hemorrhagic Inflammation occurs when the diapedesis of red blood corpuscles is excessive, due to intense irritation. IX. Necrotic or Gangrenous Inflammation occurs when irrita- tion is intense or the body resistance is low, as cancrum oris. X. Productive Inflammation — when proliferative changes pre- dominate over the degenerative and other changes. Two types of productive inflammation may be considered: (1) When the framework of organs or tissues is especially proliferated, we have interstitial inflammation (see Type VII). (2) When loss of tissue is being replaced we have the phenom- ena occurring in repair of wounds, healing of abscess or ulcer, organization, etc. (A) Repair of Wounds.- — (a) Healing by Immediate Union : When the margins of a very slight, clean wound are closely apposed, there is a minimum of capillary hemorrhage, the coagulation of which cements the margins of the wound together, holding them firmly so that repair work may proceed, which consists of a minimum of exudation, emigra- tion of leucocytes and cellular proliferation; the dead cells are removed by phagocytosis, liquefaction and absorption; the tissue cells and epithelial cells undergo division until the space is bridged over; the capillaries throw out bud-like processes from both sides which unite across the gap ; there are no new vessels formed, and no scar tissue produced. (b) Healing by First Intention: In larger aseptic wounds, the margins of which are more or less separated, and the gap filled with coagulated blood, the healing processes are the same as in (a), but there is greater inflammatory reaction and more cellular proliferation. New blood vessels are formed and fibrous tissue formation with cicatrization (scar formation) occurs. (c) Healing by Second Intention: This occurs when the gap between the margins is not filled with blood or exudate, and the margins are not approximated, or when the filled gap becomes infected and pus separates the margins, or when, as in an ulcer, tNFLAM \l V.TION 107 there is loss of surface tissue. Here new capillaries form to sup- ply nutrimenl for the extensively proliferating processes; then endothelial cells become swollen and scud ou1 solid protoplasmic processes, which unite with similar processes from the same or neighboring capillaries, thus forming loops which become cen- trally perforated to carry the Mood; these loops as they project into the area of injury, covered with proliferated tissue cells, look like granules, hence the tissue is called "granulation tissue." This forms until all the lost tissue has been replaced. Contrac- tion of the fibrous tissue results in a scar of greater or lesser extent. (Figs. 27 and 28.) (d) When two granulating surfaces meet, as is well shown in a, no'tfyivAi Fig. 27. — L,oops of blood-vessels in granu- lation tissue. (Thiersch.) Fig. 28. — Formation of new blood-vessels as seen in the tail of a tadpole. (Arnold.) opposite walls of an abscess, or large gaping wound, the process is sometimes called "healing by third intention." (B) Adhesions between serous surfaces, organization of thrombi or other dead areas, healing through fragments of bone, ivory or sponge (''healing upon a scaffold") are all processes similar essentially to healing by first intention. The foreign body may be softened and absorbed, or encapsuled (surrounded by dense fibrous tissue). When repair processes are relatively extensive or prolonged, giant cells — "the giant cells of repair" are found. They origi- 10S GENERAL PATHOLOGY nate either by division of nuclei without division of cytoplasm, or by confluence of cells. Many of them are phagocytic. Repair of a slight wound in avascular tissues, as the cornea, may occur directly by proliferation of the lost cells, without the essential phenomena of inflammation. Regeneration Regeneration is the formation of new tissue to replace that which has been lost. Physiologic regeneration occurs constantly either to counter- balance the loss from wear and tear, or to form new cells (in ex- cess of those destroyed) in the process of growth. Pathologic regeneration is often atypical and usually exces- sive. The etiology is not known. The cells have an inherent Fig. 29. — Fibroblasts forming fibrous tissue. (Ziegler.) tendency to multiply, with some restraining influence. In dis- ease there may be stimulation of reproduction by toxic products or other agencies, and a reduction of restraint by removal of pres- sure, etc. Pathologic Anatomy. — The cells swell, and multiply by mito- sis, or rarely by amitosis. The latter is supposed to be "a ret- rograde process in every instance." The cells subsequently form their characteristic intercellular substance. The less specialized a tissue may be and the younger the or- ganism, the more capable it is of regeneration, e.g., the connec- tive tissue of an organ will always outstrip the parenchyma, if the latter regenerates at all. Pathologic Regeneration. — In connective tissue, the cells swell and multiply by mitosis. The new cells are round or oval with paler nuclei than normal, and occur in great numbers ; hence the tissue is said to have reverted to the embryonal type. The cells INFLAMMATION 1 09 form intercellular substance or fibrils (i.e., they arc "fibro- blasts") and later elongate and become relatively less numer- ous, as well as decreased in size The polymorphonuclear leu- cocytes which infiltrate inflammatory areas, do not become con- verted into connective-tissue cells, and whether other types of leu- cocytes and endothelial cells do, is undetermined, though the budding processes of endothelial cells in the formation of new blood vessels seem to indicate the possibility of such conversion. I Fig. 20.) Epithelial cells are regenerated by mitosis, and usually in ex- i .«<■ ■ «k> 4.1'fi &•>* *£ V t ' ' -. - - ■>' - ',' ^ Fig. 30. — Regeneration of epithelium. (Delafield and Prudden.) cess of those lost — the surplus being later degenerated and ab- sorbed. (Fig. 30.) Striated muscle cells regenerate to some extent, but rarely completely so. The destroyed area is first replaced by connec- tive tissue, into which the new muscle fibers grow. Smooth muscle fibers are probably never regenerated. Nerve fibers regenerate, but highly specialized cells as the multipolar cells of the cord do not. Fatty tissue begins with the formation of fat-free cellular tis- sue — later the cells become infiltrated with fat. Elastic tissue is capable of regeneration. 110 GENERAL PATHOLOGY Cartilage may be regenerated, beginning from the perichon- drium, the proliferated cells of which (chondroblasts) are at first indistinguishable from fibroblasts. Fibrillar tissue first forms, which is later removed or becomes transparenl and hyaline, thus forming cartilage. To a certain extent, the original cartilage cells near the line of injury also proliferate. "Very commonly, however, regeneration of fractures of cartilage is mainly fi- brous. ' ' Bone is also regenerated from the periosteum, the proliferated cells being indistinguishable from fibroblasts ; fibrous tissue forms, which later is infiltrated with lime salts (the cells now being called osteoblasts). Essentially the same process takes place from the marrow. The infiltrated tissue forms the callus or splint which holds the margins of fractured bones together, until the true osseous tissue is formed. Glandular tissue is but imperfectly regenerated, or not at all. Metaplasia is the direct conversion of one form of tissue into another, as when connective tissue becomes cartilage, bone or mucoid tissue ; or when epithelium changes from the columnar form to the squamous, as in covering of a healing ulcer in the trachea. Metaplasia is true only of tissues of the same type, e.g., epithelium can never become connective. Heteroplasia means production of a tissue within a part to which it is foreign, as when cartilage or bone forms in the pa- rotid gland, ovary or testicle. It is really metaplasia, since it is the connective tissue of the part which is converted into bone, etc. CHAPTER VI PROGRESSIVE TISSUE CHANGES Hypertrophy Hypertrophy is a simple progressive process, resulting in ab- normal increase of a part or organ. There are two types : (a) Simple hypertrophy is an increase in the size of the cells. (b) Numerical hypertrophy or hyperplasia is an increase in number of the cells. Both types are usually found associated (combined hyper- trophy). True hypertrophy is increase in size of all the tissues of which a part is composed, and the relationship of the parts is not ma- terially altered, as in hypertrophy of heart, uterus, etc. False hypertrophy or hyperplasia occurs, when one or other of the constituent tissues is alone increased, or in excess of the other parts. Examples are cirrhotic liver, fatty or amyloid in- filtration, the enlargement of muscles in pseudohypertrophic paralysis, etc. The term "hyperplasia" is loosely used as has been indicated, but is most commonly applied to increased production of con- nective tissue in a part or organ. Giant growth when general is not hypertrophy in a true sense, but rather an abnormality of development. Hypertrophy is a pathologic change occurring in a previously normal tissue. Etiology. — 1. Repeated or intermittent pressure. 2. Increased functional demand. It is called "work hyper- trophy" when due to increased exercise, and "compensatory hypertrophy" when an organ is called upon to do more work because of degeneration or destruction of a companion organ (as in kidney) or of other parts (as heart when vessels are dis- eased), etc. 3. Nervous influence, as in hemihypertrophy (when one-half of face or body is hypertrophied). Ill 112 GENERAL PATHOLOGY 4. Excessive eating and drinking'. The heart is said to en- large from this cause. 5. Obscure causes, as disturbance of certain internal secre- tions, e.g., acromegaly is associated with alteration in the pitui- tary body. In so-called physiologic hypertrophy, as of mammary glands in pregnancy, there is no existing increased work which causes the hy- pertrophy, but rather the anticipation of such work, and un- doubtedly depends upon nerve influence. Gross Pathology. — In true hypertrophy, the part is uniformly enlarged and consistence usually increased. In hyperplasia, the increase in size and consistence is apt to be irregular. Microscopically, the cells are increased in size or number or both. In hyperplasia, there is usually decrease of parenchyma, with increase of other tissue elements. Pathologic Physiology. — In true hypertrophy function is in- creased — as secretion, muscular power, etc. In hyperplasia, function is usually decreased. Results. — Hypertrophy always reaches a limit sooner or later, at which degeneration and atrophy usually set in. In some cases, as in enlarged thyroid, serious general disturbance results. CHAPTER V 1 1 TUMORS In the broad sense of the term, a tumor means any form of swelling of limited extent from a dislocated joint, pregnant uterus or hematoma to tumors proper and cysts. In the more restricted sense, however, as commonly used in pathology, a tumor may be thus defined: A tumor, or neoplasm, is an independent new growth, without known cause, true function, typical structure or definite limitation of growth. It is independent of external stimu- lation or functional demand in its development, and has an ade- quate vascular and nerve supply of its own. It does not increase function, as does hypertrophy, and the occasional secretions are apparently purposeless. It grows so long as the body can supply sufficient nourishment, and may grow rapidly even when the body is wasting. Tumors grow by numerical hypertrophy of cells normal to the body at some time or other in its development; no foreign ele- ments are introduced, i.e., tumors are not "heteroplasms." The structure of tumors is atypical, for while they retain certain characteristics of the parent tissues from which they spring, the arrangement and proportion of cells and stroma are atypical. Theories of Origin and Causation The Irritation Theory (Virchow). — This accounts for about 20 per cent of tumors, as smokers' cancer of the lips, scrotal cancer of chimney-sweeps, sarcoma of injured bone, papillomata of anal and genital regions, etc. On the contrary, parts especially subject to repeated injuries, as the hands, feet, nipples, are rarely affected. The Inclusion or Embryoblastic Theory (Cohnheim). — During fetal development, embryonic cells are included in tissues where they remain quiescent as cell "rests" or "remnants," until some irritation starts proliferation. This theory explains dermoid cysts, certain carcinomata at points of epithelial transition, as of 113 114 GENERAL PATHOLOGY lips, cervix uteri, ehondroid tumors in bone and sarcomata from pigmented moles, etc. However, many locations of complex developmental processes, as in the heart and nervous system, are seldom the seats of tumor growth. The Parasitic Theory (Paget). — This was suggested by the fact that many tumors give rise to metastasis, recur when removed or may be transplanted ; also by reports that cancers have oc- curred in epidemics, or are contagious and hereditary, but chiefly by the fact that protozoon-like bodies resembling coccidia, par- ticularly in Paget 's disease of the nipple, have been found in certain tumor cells. Many of these bodies, however, are probably products of cell activity or cell degeneration, while transplanta- tion resembles skin grafting too closely to justify credence that parasites are a factor in tumor transplantation. The Habit of Growth Theory (Adami) .—Cells have two func- tions — the performance of work and reproduction. During cell reproduction no work is performed, and vice versa. Irritation Avhether parasitic or otherwise may so modify the cell activities that reproduction becomes excessive and function diminishes or disappears. The Nervous Theory. — Thyroid tumors (goiters) seem to de- pend upon nervous excitement. Papillomata, as warts, are known to disappear by mental suggestion. "Omophobia" is a fear of tumors. The theories of Ribbert (disturbance of tissue tension), of Thiersch (of tissue equilibrium), of Billroth (diathetic — an ir- ritant in the circulation — which has never been demonstrated) and many others seem to be purely speculative. Predisposing Causes.— Age : Tumors occur more frequently after middle age. Of tumors occurring in early life the connec- tive tissue type is the most frequent; in early life the most fre- quent seats are the eye, kidney, bones and testicles. In adults and the aged, the stomach, uterus, liver and mammae are most frequently affected. Sex: Tumors in general occur twice as often in females as in males, although in regard to location, tumors of the stomach, tongue and lips are more frequent in males. TUMORS 115 Beredity, occupation, race and climate are often said to be pre- disposing causes, bu1 this has never been determined. The shape of tumors depends upon (a) the pressure of sur- rounding structures; (b) its consistence — the softer the tumor the more irregular; and (c) the part from which it grows; when growing upon a surface, it will form a tuberous growth (round top with broad base), polypoid (pendent with narrow pedicle), papillomatous (elongated with long narrow neck), (fungous) .large head and short thick neck), cauliflower (irregular projec- tions), dendritic (a highly branched cauliflower type), etc., and (d) the manner of growth — centrally or peripherally. "When growing by proliferation at the center of the tumor, a uniform, round swelling or node forms, which often becomes encapsulated, the surrounding tissues being pressed aside. In peripheral growths, the surrounding tissues are infiltrated, the shape be- comes irregular, capsules are infrequent and metastasis frequent. Tumor growth is always accompanied by formation of new blood vessels which are usually thin and imperfectly formed. Metastasis takes place when tumors are highly vascular and cellular, and in those which are not encapsulated; it occurs via the blood vessels when these are in intimate contact with the tumor cells, as in sarcoma, or via lymphatic channels when these are in intimate contact with the cells as in carcinoma. Metastasis is also said to occur by direct extension over certain surfaces, as serous surfaces. Metastatic tumors are malignant, and malig- nancy means, in pathologic language, (a) invasion of tissues by infiltration, (b) ability to cause metastasis, (c) tendency to recur when removed, and (d) the injurious effects, other than mere pres- sure suffered by the patient, such as general anemia, or some form of intoxication. Such a condition is called cachexia. Sar- comata and carcinomata are the types of malignant tumors. Benign tumors are such as do not invade tissues, do not me- tastasize or recur when removed, but usually become encap- sulated and do harm only by their pressure upon other tissues or organs, or by gradually sapping the strength of the patient. A primary tumor is one originating at the site in which it is found. A secondary tumor is one originating by metastasis of cells (cell emboli) from a primary tumor. Primary tumors may 11 G GENERAL PATHOLOGY be multiple, but usually are single; secondary tumors are almost invariably multiple. Degenerative changes occur in tumors as they do in the tis- sues from which they spring. Classification of Tumors. — Many different classifications have been suggested. In Virchow's Histogenetic classification, his law that "every tumor grows from previously existing cells of the same type" is made the basis of classification: (1) Histioid tumors — those growing from one kind of tissue only, as fibroma. (2) Organoid tumors — those growing from parenchymatous and connective tissues, as cancer. (3) Teratoid tumors (or syste- moid) — those made up of combinations simulating a system, as dermoid cysts. Cohnheim's embryoblastic classification divides tumors accord- ing to their epiblastic, hypoblastic or mesoblastic origin, but no note is here taken of the fact that many tumors similar in histology and function are derived from all the layers of the blastoderm, and vice versa. Adami's modification endeavors to remedy this defect, and is considered by Beattie and Dickson as the "most complete and scientific classification compatible with present knowledge." First the tissues, embryologically considered are divided into (a) lepidic ("rind") or lining membrane group, without lymph or blood vessels or stroma between the cells; and (b) hylic ("pulp") or body framework group. The tumors are divided in lepidomata, including the papillomata, adenomata, carcinomata and endothe- liomata, and hylomata, including neuromata, gliomata, sarcomata, myomata, fibromata and other connective-tissue tumors. The commonest and perhaps the most practical classification is that which is based upon the type of tissue involved : 1. Connective tissue ; fibroma, myxoma, chondroma, osteoma, lipoma. Embryonic or malignant type — sarcoma. 2. Muscle tissue; leiomyoma and rhabdomyoma. 3. Nerve tissue; glioma and neuroma. 4. Vascular tissue ; angioma — hemangioma and lymphangioma. 5. Epithelial tissue; papilloma and adenoma. Embryonic or malignant type — carcinoma. 6. Teratomata or complex new growths. TUMORS 117 Fibromata Fibromata are tumors composed of wavy bundles of connec I ive tissue. Etiology. Some of these tumors result from injury or contin- ued irritation; the causation of others is obscure. The favorite seats are the subcutaneous and submucous tis- sues, periosteum, sheaths of tendons and nerves, uterus, ovaries, kidney, heart, dura mater, etc. There are two types of these tumors — the hard and the soft. Gross Pathology.— Hard fibromata vary in size from a ■ minute point to a fist; they are sometimes lobulated and frequently mul- tiple; are pale, firm, cutting like leather. On section, surfaces Fig. 31. — Hard fibroma. (Warren.) show irregular bands or whorls of fibers, often resembling the grain in wood. They are usually encapsulated. A subvariety is the "painful subcutaneous tubercle," being about the size of a coffee bean, very firm and circumscribed. Fibromata of the ^ uteru s are a combination of fibroma and myoma, often called fibromyoma, or simply "fibroid." These may become very large, weighing fifty pounds or more; are usu- ally multiple and very hard. Keloids are hard subcutaneous fibromata, of irregular star- like outline, not encapsulated, but tend to spread: they often look like the scars of burns, and usually arise from scars in those who manifest a congenital predisposition. Keloids occur oftenest in negroes. 118 GENERAL PATHOLOGY Microscopically are seen dense, matted, fibrous bands with rel- atively few cells; blood vessels are few and have thick fibrous walls, but no muscular or elastic coat. When cut transversely the bundles have a granular appearance. (Fig. 31.) The soft fibromata are usually found in subcutaneous tissues and the submucous tissue of the pharynx and digestive tract. In gross appearance they are usually larger than hard fibromata, soft and pink on section. Frequently they are poly- poid in form. Microscopically a loose fibrillar network is seen, with stellate and spindle cells irregularly distributed and some- times in islands. The vessels have distinct walls. (Fig. 32.) Fig. 32. — Soft fibroma of the subcutaneous tissue. (Stengel and Fox.) Molluscum fibrosum (neurofibromatosis) is a soft fibromatoid growth occurring along the course of subcutaneous and submucous nerves. They range in size from a pinhead to an orange and are usually multiple. Degenerations. — These are the same as those which occur in normal fibrous tissues — hyaline, mucoid, fatty, calcareous and liquefaction. Results. — A fibroma is usually very slow in growth and benign. If very large it may cause pain or pressure symptoms, or even death from hemorrhage, exhaustion or absorption of degeneration products. Fibromata do not recur when removed, except keloids and certain polypoid new growths, though keloids may disappear spontaneously or upon continued pressure. TUMORS 119 Myxomata Myxomata are tumors composed of mucoid tissue Mucoid tis- sue is the precursor of connective tissue in fetal life. Etiology. — Chronic irritation may cause some forms, but the etiology is obscure. Myxomata usually occur in adult life. bu1 may be congenital. The favorite seats are the subcutaneous tissues, especially of the mammary gland; also submucous tissue, especially nasal; in- termuscular septa, nerve sheaths, brain and spinal cord. In gross appearance these tumors are pale gray or reddish white tuberous or polypoid growths, soft and gelatinous on section, exuding a mucous material on pressure. The growth Fig. 33. — Section of a myxosarcoma, a, myxomatous tissue; b, strands of cells; c, fibrous tissue. (Ziegler.) is usually well circumscribed and encapsulated, varying in size from a cherry to a walnut, though sometimes larger. Occasionally the growth is diffuse and noncapsulated. Microscopically, irregular stellate cells with long anastomosing processes are seen lying within a transparent or slightly granular material; the vascular supply is usually poor, though the vessels are large and thin walled. (Fig. 33.) Results. — The growth is slow and benign, but is often associated with sarcoma (myxosarcoma) or with cancer (carcinoma niyxo- 120 GENERAL PATHOLOGY matodes) which is malignant. Hemorrhage may convert this form of tumor into a blood cyst. Chondromata Chondromata are tumors composed of cartilage. Etiology. — Irritation and trauma account for some cases. In others remnants of cartilaginous tissue deposited in abnormal places, as in the parotid gland, or left unconverted in the de- velopment of bone form the starting point for these tumors, while congenital predisposition and heredity also play a part. They are often associated with rickets, and are rare after puberty. Two chief types: (l)Ecchondromata (ecchondroses) are out- Fig. 34. — Chondroma of the thumb. (Warren.) growths from the perichondrium, occurring oftenest at the epi- physeal attachments of long bones, especially the phalanges of the hands, also at the interpubic and occipitosphenoidal junctions. They occur also as outgrowths from articular cartilages or syno- vial membranes in rheumatoid arthritis. (2) Chondromata, or enchondromata, originate in noncartilaginous tissues, usually boiie, but also glandular organs as the parotid gland, testicle, ovary, and in muscles and tendons near their bony attachments. Gross Morbid Anatomy. — Chondromata are hard, resistant to the section knife, and vary in size from small nodes to large tumors. The ecchondromata are apt to.be very irregular out- growths, often multiple, and firmly or loosely attached to the tissues from which they spring, and occasionally even detached. TUMORS ]21 Ti H . enchondromata are rounded growths, often lobulated when large, the Lobules separated by connective tissue which carries the blood vessels. (Fig. 34.) Microscopically, the tissue resembles hyaline cartilage, Less often white fibrous or elastic cartilage. The cells are Less regu- larly arranged than in aormal cartilage. Association with myxoma or sarcoma is frequent. Calcification or ossification also frequently occur. Results.— These tumors are usually benign except when com- bined with sarcoma, but occasionally metastasis occurs even in pure chondromata, the secondary growths being found usually in the lungs. Degeneration with cyst formation is frequent. Chordomata Chordomata are tumors arising from the remains of the noto- chord or chorda dorsalis. They are found principally about the intervertebral disks and base of skull, and are seldom more than one-half inch in diameter. These tumors resemble cartilage gen- erally, but with ''balloon-like" cells having small distinct nuclei, and apt to be vacuolated. Osteomata Osteomata are tumors composed of osseous tissue. Etiology. — Osteomata occur at any time of life ; irritation and trauma account for some cases, and heredity seems to play a part, especially in the multiple osteomata of early life. There are two chief types: (1) Hyperostoses, which are in- flammatory outgrowths, including exostoses (wart-like out- growths) and osteophytes (flat, extensive and loosely attached outgrowths). These outgrowths spring from preexisting bone and are usually traumatic in origin. (2) Osteomata proper, which may spring from hone (homoplastic) or from nonosseous tissue (heteroplastic), such as the testicle, ovary, and meninges. Gross Pathology. — As in chondromata, a sharp distinction can not always be drawn between the inflammatory outgrowths and the true tumors, although the tumors are usually more rounded, more tumor-like in outline, and when large are apt to be lobu- lated. According to their density osteomata are (a) hard or compact, resembling the outer layer of long bones, and (b) soft, 122 GENERAL PATHOLOGY cancellous or spongy, resembling- the inner cancellous bony tis- sue with a shell of compact bone on the exterior. (Fig. 35.) A sub variety — eburnated (ivory-like) osteomata — consists of very hard and usually multiple growths, occurring on the inner table of the skull bones (here often syphilitic in origin), in the antrum of Highmore and elsewhere. Microscopically, these tumors resemble bony tissue, but the Haversian canals and blood vessels are usually quite irregular and smaller than in normal bone. Associations with chondromata, myxomata, fibromata, and sar- comata are frequent, and degenerative changes, as softening and necrosis, occur. Fig. 35. — Osteoma of the lower jaw. (Warren.) Odontomata Odontomata are tumors growing from the pulp of teeth, and are not strictly osteomata. Lipomata Lipomata are tumors composed of fatty tissue. Etiology — The etiology is not known. Usually they appear in adult or middle life, but sometimes in childhood and occasionally congenitally. Lipomatosis is a condition in which there is local diffuse fatty growth in certain parts. Obesity is the general increase of fatty deposits throughout the body. TUMORS 12'j The usual seats are the subcutaneous tissues of the back, shoul- ders, buttocks and limbs, also submucous and subserous tissues and the mammary glands. Gross Pathology. — A lipoma is a circumscribed, encapsulated tumor, usually lobulated with connective-tissue septa. On the exterior, the new growths are somewhat hemispherical, rarely polypoid, and movable. They vary in size, and may beeome (mormons. In the interior of the body they are usually polypoid, and oeeasionally found detaehed. Microscopically, lipomata resemble fatty tissues in general, al- though the cells are larger, and large thin-walled vessels are seen. Results. — These tumors are benign, although recurrence may take place after removal. Calcification and less often softening occur. The fat of lipomata is not used by the system in starva- tion. Sarcomata Sarcomata are tumors composed of connective tissue of the em- bryonic type, having very little intercellular substance and a large number of cells. Etiology. — These tumors occur in youth and early adult life, and are sometimes congenital. Some cases follow traumatism. They are more frequent in males. Locations. — Sarcomata are found in the subcutaneous, perios- teal, tendinous, and muscular tissues; in bone, cartilage, lymph glands, submucous and subserous tissue; in the kidneys, liver, spleen, thyroid, testes, etc. Gross Pathology. — Sarcomata are more or less rounded, usually without demarcation between them and the surrounding tissues, although when fully developed, or when growth is slow, a cap- sule or apparent capsule may form. Superficial tumors are apt to be flat or irregular elevations; typically a sarcoma is flesh- like in appearance when sectioned, pink in color, though many are pale or gray. Dilatation of blood vessels may cause a hemor- rhagic appearance, and actual hemorrhages into the tumor are frequent. Sarcomata infiltrate adjacent tissue and are not readily movable. They may be hard or soft according to the relative amounts of cells and intercellular substance. A whitish liquid exudes on section. 124 GENERAL PATHOLOGY Pathologic Histology. — The cells are round, cylindrical, spin- dle-shaped, or polymorphous, and contain large vesicular or gran- ular nuclei. Mitotic figures may he seen in rapidly growing tumors — less commonly amitotic division occurs. Nuclear de- generation is frequent. The cells are irregularly arranged, though occasionally in more or less parallel columns. The intercellular substance is scant, homogeneous with few or no distinct fibers, and found in immediate relation with the cells, thus differing from carcinoma. The blood vessels usually consist of a single endothelial coat, though in some cases they are more fully developed and form the skeleton of the tumor ; they penetrate the tumor tissue and come in direct contact with the cells (again differing from car- cinoma) — in fact, parts of the tumor may grow into the vessels permitting the blood to circulate in clefts ;nnong the tumor cells; hence sarcomata metastasize through the blood vessels as a rule, while carcinomata which have more distinctly formed blood ves- sels metastasize through the lymphatics. Association with other tumors, especially of the connective type is frequent. Results. — Sarcomata are malignant as a rule. The round-celled and melanotic are the most malignant — the giant-cell and fibro- sarcomata are the least malignant. In general the smaller the tumor cells, the more malignant the tumor. Degenerations, .as myxomatous, liquefaction, blood cysts, etc., occur frequently. Anemia, leucocytosis and fever often attend the disease. Sarcomata are classified as follows: 1. Round-celled sarcomata — both large-celled and small-celled, including lymphosarcomata. most of the alveolar sarcomata, an- giosarcomata and sarcomatous cylindromata. 2. Spindle-celled sarcomata — large-celled and small-celled, in- cluding a few alveolar sarcomata. 3. Melanotic sarcomata. 4. Giant-celled sarcomata. Round-celled Sarcomata Round-celled sarcomata are usually found in loose connective tissues in viscera, as kidney, ovary, brain, lymphatic nodes, otc. TUMORS 125 Grossly they are white, gray or pink, soft, usually rounded and well-defined but not encapsulated; they bleed easily, are often quite soft and cheesy in the center, the small-celled being softer than the large-celled tumors. Histologically, the cells when small resemble lymphoid cells. There is no fundamental difference between the small-celled and large-celled varieties; in the latter the cells are larger with rel- atively more cytoplasm, the nuclei stain less deeply, the inter- cellular substance is more fibrillar, and the blood vessels are fewer but better supported than in the small-celled variety. The lymphosarcoma is a small round-celled sarcoma occurring in lymph nodes, lymph adenoid tissue, and sometimes in other organs, as the thyroid, thymus and salivary glands. It resembles a lymph node in appearance and structure, the chief distinguish- Fig. 36. — Small round-celled sarcoma: in the center is seen a blood vessel with its wall of endothelium. (Stengel and Fox.) ing feature being its tendency to spread beyond the capsule or normal limitations of the nodes or organs, and in case of the lymph nodes, causing the separate nodes to fuse together, ob- literating the normal appearances, as germ centers, cortex, and medulla. The alveolar sarcoma is grossly similar to other forms of sar- coma and occurs mainly in lymph nodes and serous membranes, moles of the skin, warts, etc. Histologically there are trabecu- le of spindle-shaped cells and intercellular substance, dividing the tumor into alveoli containing round sarcoma cells. Blood vessels traverse the trabecule and rarely if ever enter the cell groups. These tumors are difficult to differentiate from car- cinomata, though in the latter the blood vessels are said to be usually better developed. 126 GENERAL PATHOLOGY Angiosarcomata spring from the adventitia of blood vessels. They occur in 1 lie salivary glands, serous membranes, and in the skin, and consist of round-celled masses surrounding the blood vessels. These tumors are more or less benign, but often become melanotic and malignant. "Cylindroma" originally meant any tumor "showing gelat- inous masses or trabecule traversing; its substance," but dif- \ I'ig. 37. — Large rout ( DrlalirM and I'iik ten.) Fig. 38. — Alveolar sarcoma. (Warren.) ferent histologic structures are described under this name. Sar- comatous cylindromata may be defined as sarcomata in which hyaline and myxomatous degeneration have occurred in more or less insular collections; also as angiosarcomata with similar de- generation of the sarcomatous cells surrounding the vessels, re- sulting in either case, in branching cylinders of gelatinous ma- terial throughout the tumor. (Figs. 36, 37, and 38.) TUMORS 127 Spindle-celled Sarcomata Spindle-celled sarcomata occur in dense tissues, as periosteum, tendons, fasciae, less often in loose I issues. Grossly, they are harder than the round-celled tumors, and more grayish and flesh- tinted. The cells are spindle-shaped with tapering ends and sometimes branching extremities, and apt to be arranged in par- allel rows. In the small-celled variety, the intercellular sub- stance is less fibrillar and the blood vessels more imperfect than in the large-celled form. (Fig. 39.) When the intercellular fibrils become very evident, it is called Fig. 39. — Spindle-cell sarcoma of the mammary gland. Oc. 3; ob. 9. (McFarland). fibrosarcoma. The so-called "recurring fibroids" are fibrosar- comata. Melanotic Sarcoma, or Melanomata Melanotic sarcomata, or melanomata, spring from some pig- mented tract, as the uveal tract of the eye, pigmented mole, etc. The cells contain metabolic pigment (melanin) varying greatly in amount, and distributed uniformly or in patches. The nuclei are poor in chromatin and show a distinct network. These tu- mors are very malignant, metastasize to any tissue, but chiefly 128 GENERAL PATHOLOGY through the lymphatics to the lymph nodes. Sometimes the cells are epithelioid and arranged in alveoli. Giant-celled Sarcomata Giant-celled sarcomata are composed of spindle or round cells with a variable number of giant cells. They spring from the medulla of long bones, are circumscribed, and usually encap- sulated; may be firm or soft, reddish-brown on section and some- what fibrous. They occur oftenest in the young, at the lower end of the femur, upper tibia, lower radius and lower jaw (one form of epulis). (Figs. 40, 41, 42 and 43.) Two rare forms of connective tissue tumors are: Fig. 40. — Large spindle-celled sarcoma. (Delafield and Prudden.) 1. Xanthoma, which is a lipoma with large fat cells and a certain amount of round-celled infiltration, and of a peculiar yellowish color; is found usually about the eyelids, and occa- sionally in diabetes, more generally distributed. 2. Chloroma, which is a variety of lymphosarcoma or round- celled sarcoma, occurring in the periosteum of the bones of the head, especially the orbit, and having a peculiar greenish color; it is malignant, giving rise to secondary tumors in lymphadenoid tissue and especially the bone marrow. TUMORS 12«J V Fig. 41.— Melanosa Stengel and Fox.) Fig. 42. — Giant cell sarcoma of the thigh, a, giant cells; b, spindle cells. (McFarland.) 130 GENERAL PATHOLOGY Rhabdomyomata Bhabdomyomata are tumors containing striped muscle tissue. They are rare and usually congenital. In the genitourinary sys- tem, they are probably due to the inclusion of lumbar muscle fibers. Their favorite seats are the kidneys, testicle and other parts of the genitourinary tract, also heart muscle, lumbar and gluteal muscles. The tumors are round or irregular in shape and more or less encapsulated, and if superficial, pedunculated. Microscopically the muscle fibers are imperfectly developed and Fig. 43. — Metastatic melanosarcoma of lung, showing pigmented and nonpigmented nod- ules (from a specimen in the possession of Dr. Allen J. Smith.) associated with a varying amount of connective tissue. When the latter becomes embryonal in type, a rhabdosarcoma develops, which is much more frequent than the pure rhabdomyoma. Leiomyomata Leiomyomata are tumors containing smooth muscle fibers. They spring from preexisting smooth muscle, usually of an organ or the media of blood vessels. In the uterus it may arise from congenital ly misplaced portions of the Wolffian body or ducts of Mueller. TUMORS 131 The favorite locations are the uterus, gastrointestinal tract, ovaries, less often blood vessels, sk in, nipples, etc. Gross Pathology. -The I iimors are firm, rounded, nodular masses, closely resembling fibromata, but usually darker in color, and varying in size up to many pounds. The large tumors are usually a combination of myoma and fibroma — a fibromyoma, such as the uterine "fibroid" which may grow to an enormous size Leiomyomata are encapsulated, and on section have a ) V Fig. 44. — Submucous fibroid in the uterus. The tumor forms a large mass in the in- terior of the organ whose wall is much attenuated at the fundus. The cervix is nearly- normal in size, though somewhat altered in shape. The ovaries and tubes which are still attached are normal. (McFarland.,) striated appearance, the striae being concentrically arranged or in a wave-like manner. They are usually grayish or flesh-colored, but may be red, due to dilated blood vessels. Uterine fibromata are usually multiple, and either submucous, interstitial (intramural), or subserous in origin. The intramural tumors do not, as a rule, project from either surface of the uterus. Uterine fibromata occur oftenest during the third or fourth dec- 132 GENERAL PATHOLOGY ades of life, and continue to increase in size up to the time of the menopause, thereafter usually decreasing. (Fig. 44.) Leiomyomata of the skin occur in young adults, or even in children. They are multiple and often painful. Histologically, bundles of muscle cells are seen, running in dif- ferent directions and having cylindrical nuclei. Sometimes elas- tic tissue elements are present, and nearly always connective tissue cells. Blood vessels are scant, though often with well de- veloped middle coats. Calcification is common, especially in uterine fibromata ("womb stones") preceded by hyaline or fatty change. Results. — Growth is slow and the tumors are benign, although sarcomatous change may add a malignant character. ilk I **% £*■:•« *- Fig. 45. — Glioma of the brain. (Delafield and Prudden.) Glioma Glioma is a tumor composed of neuroglia. The favorite seats are the brain and cord, optic tract, nerve and retina, and parts of the olfactory tract. Glioma of the retina occurs usually between the second and fourth year of life. (Fig. 45.) Gross Pathology. — Gliomata are usually single, rounded masses, gradually merging into surrounding tissue. Somewhat harder than brain, their color is but slightly changed, though some- times dark red. They vary in size from a pea to a lemon. Glioma of retina may extend to eyeball or along optic nerve. Pathologic Histology. — Great numbers of cells are seen with round or oval nuclei and with scant cytoplasm (glia cells). They are usually larger than the normal neuroglia cells. Fine wavy fibrils (neuroglia) lie parallel to the axes of the cells to which TUMORS 133 they are attached at the sides, the cuds of the fibrils being free. In the I'd inn. the cells are similar to its granular layer. Results.- Benign, 1ml may be dangerous from pressure or loca- 1 ion. Glioma of eye may recur after removal. Glioma Ganglionare, or Ganglionic Glioma, or Neuroma This is a mixed tumor composed of neuroglia, nerve fibers, and ganglionic cells. It usually occurs in multiple nodular growl lis throughout the brain and cord, or in the sympathetic ganglia, varying in size from that of a millet seed to that of an apple. Gliomatosis is a diffuse proliferation of glia throughout the central nervous system. Neuroma occurs in two forms — true and false. True neuroma is a very rare tumor composed of nerve fibers. False neuroma (the common form) is a fibrous tumor spring- ing from the perineurium and endoneurium of nerves. The etiology is not known, though traumatism accounts for amputation neuromata. They are usually found upon the periph- eral nerves, but may occur in any part. Sometimes the nerves are involved near their roots, or at their endings within organs. Gross Pathology. — False neuromata are usually found as mul- tiple thickenings along the course of nerves. They may occu in the form of a network (plexiform neuromata). After ampu- tation small, rounded growths occur at the ends of some of the nerves, are firm and not sharply circumscribed. Pathologic Histology. — False neuromata are composed of re- ticulated connective tissue, pushing aside or surrounding the true nerve fibers — the latter being often degenerated from pres- sure. True neuromata are composed of medullated fibers (myelinic neuromata) or of nonmedullated (amyelinic neuromata). Ampu- tation neuromata are usually a mixture of myelinic and false neuromata. Results. — These tumors usually cause pain. They are benign, though often rapid in growth. Angiomata Angiomata are tumors composed of, or following the type of, blood or lymph vessels. Used alone, "angioma" refers to the hemangioma. 134 GENERAL PATHOLOGY Hemangiomata, or angiomata, are tumor-like formations con- sisting- principally of dilated and elongated blood vessels, some of which may be independent new growths. A certain amount of connective tissue is always formed which holds the vessels to- gether. Usually the angioma is connected with the general circu- lation through a few, sometimes but one, arterioles or veins. Three forms are described : (a) Angioma simplex, or Nevus, which consists of dilated capil- ^JB r ■ - V ■■■ ' 7 i Fig. 46. — Cavernous angioma of liver. The illustration shows tumor tissue only: o, blood channels filled with corpuscles; b, fibrous framework supporting delicate walls of blood sinuses. (McFarland.) laries, arterioles and venules woven into a plexus. It is usually congenital (birthmarks). It may be red in color (arterial) or dark (venous) ; pigmented (pigmented mole) or covered with fine hairs. It may be found on the skin, lips, tongue, conjunctivae and rarely the meninges. (b) Cavernous angioma, or eavcrnoma, which consists of widely dilated blood cavities separated by connective tissue partitions and lined by epithelium. It is dark in color, larger than the simple TUMORS l?);") form, and may pulsate. II is round most Frequently in the liver, where it may be multiple, skin, breast, hones and internal organs. (Fig. 46.) (c) Plexiform angioma, which consists of a dilatation and elon- gation of a group of arteries of moderate size, and found upon the head, face, perineum, legs, forearm and elsewhere. It is in reality a "congeries of cirsoid aneurysms" forming a tumor-like enlarge- ment. Lymphangioma is a tumor-like formation, consisting of dilated lymph vessels, rarely of newly formed lymph channels. Three forms are described: (a) Lymphangioma simplex, or lymphangiectasis, is a simple dila- tation of a group of lymph vessels forming tumor-like masses. A congenital forms occurs usually upon the face and neck, and often confined to the papillary layer of the skin. The acquired form is due to lymphatic obstruction (as elephantiasis, due to filarias) tending to dilatation of the lymph vessels and overgrowth of con- nective tissue. (b) Cavernous lymphangioma, which corresponds to the caver - noma of the blood vessels. It may affect the tongue (macroglos- sia) or lip (macrocheilia) or the mesentery. These conditions are congenital. (c) Cystic lymphangiectasis, which occurs commonly about the neck, as cystic hygroma, consisting of multiple clear cysts lined with endothelium and having fibrous walls. Among special forms of lymphangioma ta may be mentioned the common pigmented mole, which is a slightly elevated growth, soft and flabby, occurring on the skin in early youth. It is a cutaneous outgrowth consisting of a stroma of fibrous tissue and containing pigmented cells. When consisting of telangiectatic vessels, it is called a pigmented nevus. Papillomata Papillomata are tumors growing from the papillary processes, Avhich they resemble in structure. Etiology. — Irritation is the cause of many, if not all, of these tumors. They are found in the skin of the back, neck, and hands, the mucous membranes, particularly of the bladder, nose, larynx and gastrointestinal tract, and glandular ducts, as the 13G GENERAL PATHOLOGY female breasts. They also occur within cavities of cystic adeno- mata (papuliferous cysts). Gross Pathology. — Various forms are described: (1) Hard fibromata, verruca or warts, occur singly or in groups upon the skin. They may be smooth or cauliflower-like in outline, varying in size from a pinhead to a walnut. (2) Venereal warts or con- dylomata acuminata. These occur about the genitals and anus, rarely elsewhere, are softer, more vascular, and more polypoid than the ordinary warts, and caused by gonorrheal discharges. The condyloma latum, or mucous patch, is also a warty outgrowth upon mucous membranes and moist dermal surfaces, occurring during secondary syphilis. (3) Soft papillomata are usually seen on mucous surfaces as soft cauliflower-like growths, red, or gray in color, or sometimes as villous outgrowths. (4) Intracystic papil- lomata are villous outgrowths springing from the walls of cysts, especially mammary, thyroid and ovarian cysts. The growths may fill and greatly distend the cysts and occasionally rupture them. Pathologic Histology. — The normal relation of cells to the membrana propria persists in all papillomata. There is a cen- tral stroma which contains the vessels and is covered with epithelium — stratified squamous in case of skin growths, tend- ing to horny change and sometimes horny concentric whorls or pearls. The structure in the mucous membrane is the same where the epithelium is of the squamous type, as in parts of the larynx, but there is little tendency to horny change. In the gastrointestinal tract and bladder, the growths are soft and vil- lous or dendritic, and Ihe epithelium is scant and of the type peculiar to the location. The relative amounts of connective tis- sue stroma and covering epithelium vary; when the latter pre- dominates, it may suggest an epithelioma, though papillomata always tend to grow outward rather than into deeper structures. Many of the soft papillomata are quite vascular and bleed easily. (Figs. 47 and 48.) Results. — Papillomata are benign, but large tumors may im- pair health by repeated hemorrhages, as in the gastrointestinal tract, or by interfering with function, as in bladder or larynx. TUMORS 137 Fig. 47. — Papillomata of the vocal cords (from a specimen in the Museum of the Phila- delphia Hospital). Fig. 48. -Papilloma of the scalp. The branching fibrous stroma is covered by an abnor- mally thickened, irregular epithelium. (Boyce.) 138 GENERAL TATHOLOGY Adenomata Adenomata are tumors resembling in structure an epithelial gland and developing from glandular epithelium. Etiology. — They are caused by irritation, as in gastrointestinal adenomata, by tissue inclusions, as in renal adenomata. In other cases the causes are obscure. Their favorite seats are the mucous membrane, especially of the pylorus, duodenum and rectum; the skin — sebaceous and Fig. 49. — Adenoma of the mamillary gland, with cystic enlargement of acini and abundant interglandular hyperplasia of connective tissue. (Stengel and l"ox.) sweat glands; certain organs, as the mammary glands (the most frequent seat), liver, kidney, adrenals, thyroid, ovary and uterus. Gross Pathology. — Adenomata occur as more or less diffuse, sessile growths, sometimes pedunculated or papillomatous in form; or within organs as nodular tumors, firm, usually single and encapsulated, capable of being shelled out, though at times adherent. On section the cut surfaces usually bulge and resemble, more or less, the parent gland, being grayish pink in the mammae, and red in the thyroid gland. tumors 139 Pathologic Histology.- Acini with single layers of columnar epithelium (sometimes several layers) are seen enclosed by con- nective-tissue reticula, which contain the blood vessels. The ex- cretory duds are absent or poorly developed. When the tissue corresponds closely to the normal arrange- ment, the tumor is a simph adenoma; when the stroma pre- dominates, fibroadenoma; when acini greatly predominate, acinose, racemost or alveolar adenoma; when duels are conspicuous, tubu- lar, or canalicular adi noma. Results. — Pure adenomata are benign, but may sometimes cause metastasis, especially the hepatic and thyroid tumors. General health may suffer from hemorrhages, interference with vital func- tions, or from ulcerations. Gastric and uterine adenomata are apt to become carcinomatous. (Fig. 49.) Carcinomata Carcinomata are tumors embryonal or atypical in character, which always arise from epithelial cells. Etiology. — Irritation accounts for some cases. They occur usu- ally after middle life, being rarely found in early life or child- hood. They are more frequent in women, and in the Caucasian race. Tumors springing out of connective tissues, as bone, can only be explained by the inclusion theory. The favorite seats are the uterus, skin, esophagus, pylorus, rec- tum, mamma?, ovaries, less often the liver, kidney, thyroid gland, prostate and testicle. Carcinomata, however, may spring from any epithelial tissue. Secondary tumors usually do not affect the parts in which the primary growths are frequent, and occur usually in the lymph glands, liver, spleen, lungs, serous membranes, and bones. General Structure. — The cells are very diverse in outline — round, oval, squamous, fusiform, cylindrical, cuboidal or cau- date, and have large, clear nuclei. Compression develops poly- hedral forms. The stroma consists of fibrous tissue, which forms irregular spaces, or alveoli, which communicate with one another, within which lie the cancer cells in branching or anastomosing columns, due probably to the fact that cancer cells proliferate along the lymph channels. The stroma may be infiltrated with leucocytes 140 GENERAL PATHOLOGY and plasma cells and even mast cells. In slowly growing tumors the stroma is fibrous; in rapidly growing tumors it approaches the embryonal or mucoid type. The stroma contains the blood ves- sels, which have distinct walls and do not penetrate the alveoli. The lymphatics are continuous with the alveoli, thus affording a ready means of metastasis. In general, skin cancers resemble enlarged papillae penetrat- ing into the tissues, and gland-celled cancers resemble acini of glands, filled with many layers of cells, but in all cases, there is noted the tendency of the cells to penetrate the basement or limiting membrane and infiltrate the tissues. Secondary carcinomata are usually multiple, more circum- scribed and less infiltrating, and as a rule softer than the primary tumors. The histologic differentiation between carcinoma and sarcoma can not always be made from the morphology of the cells, for they are polymorphic in both forms of tumor, and it finally rests upon : (a) Grouping of the cells — in alveoli in cancer; irregularly in sarcoma. (b) Intercellular fibers — none in cancer; always a few in sar- coma. (c) Position of blood vessels — in trabecula? in cancer; among the individual cells in sarcoma. In alveolar sarcoma, however, these distinctions are not so evident, but here the intercellular fibrillar may be seen to be con- tinuous with the perialveolar fibrous tissue, and the blood ves- sels are thin-walled and not so well supported as in cancer. Degenerative Changes. — These are frequent, especially fatty de- generation. The cells may be cloudy, swollen, dropsical or vacuo- lated. Nuclear degeneration may occur, giving the appearance of parasites. True colloid degeneration may occur but is very rare, the term "colloid cancer" usually refers to myxomatous change of the stroma. Liquefaction may form cysts. Calcifica- tion occurs, especially in ovarian cancers. Inflammatory changes are common. On free surfaces, ulcera- tion results from traumatism, irritation or infection. Erysipelas, tuberculosis and syphilis may be associated. Hemorrhages are frequent both into the stroma and from the ulcerating surfaces — TUMORS 141 the latter are apt to be extensive in cancer of the stomach and uterus. Malignancy. — Cancers are malignant; the medullary gland- celled being most, the squamous-celled the least malignant. Me- tastasis occurs through the lymphatics, but occasionally through the blood vessels (veins) especially through the portal vein to the liver in cases of intestinal carcinomata. Hemorrhages, hem- olysis, and probably some form of toxemia cause the anemia and cachexia so characteristic of these tumors. Carcinomata are divided into: 1. Epithelioma ta, or squamous-celled carcinomata. 2. Gland-celled carcinomata: (a) Adenocarcinomata, or cylindric-celled carcinomata. (b) Hard, scirrhous, fibrous, or chronic carcinomata. (c) Soft, medullary, encephaloid or acute carcinomata. (d) Carcinoma simplex, or simple cancer. Epithelioma Epithelioma is found in the skin and squamous mucous mem- branes, especially the lip, nose, tongue, esophagus, pharynx and cervix uteri. It is apt to develop where different types of epi- thelium join. Gross Pathology. — Irregular, hard, wart-like, immovable ele- vations are seen, which tend to ulcerate, exuding a sanious fluid. On section they are firm and comparatively bloodless. Pathologic Histology. — Irregular, branching columns of squa- mous cells are seen, though pressure may alter their shape, ex- tending from the papillae down into the deeper tissues. In normal skin the cells spring from the rete malpighii, and become flat- tened and horny as they proceed outward, but in the tumor instead of growing outward toward a free surface, they are packed in more or less rounded masses, the older cells being forced to the center and becoming cornifled, thus forming the concentric whorls or "epithelial pearls" so characteristic of epitheliomata. Often these pearls are large enough to be visible to the naked eye. (Pearls are also occasionally seen in papillo- mata, ulcerative processes and in granulation tissues around in- growing nails.) The stroma is usually well marked, consisting of fibrous tissue. 142 GENERAL PATHOLOGY Growth is usually slow and sometimes latent for years; while malignant, epitheliomata are less so than glandular earcinomata, and metastasis may not occur for years, but in rare instances has occurred in the first year. I Fig. 50.) Rodent ulcer is an epithelioma occurring upon the upper parr of the cheek. Its cells are polygonal or even spindle-shaped in- stead of squamous, and are arranged in anastomosing columns. Pearls are not found. These and other growths of like structure have been called c^ Fig. 50.— Squamous epithelioma, a. epithelial masses; b. epithelial pearls; c, connective tissue; d, capillary blood vessels. (McFarland.) basal cell earcinomata, because the cells retain their resemblance to those of the basal layer of the rete malpighii from which they are derived, whereas in the more slowly growing skin cancers the cells become flat and squamous in appearance. The molluscum contagiosum is a small, soft epithelioma, found ofteriesl ou the face, arm-, chesl and external genitals, and usu- ally multiple. It consists of radial, hyperplastic columns of the TUMORS 143 rete malpighii, with degenerated cells in the center, which usu- ally show granular bodies, believed by some to be parasites. Adenocarcinomata Adenocarcinoma, or "malignant adenoma," is a carcinoma resembling the glandular tissue from which it springs. Tliis tumor arises primarily from the mucous membranes, especially of the stomach, rectum, uterus, oviducts, gall bladder and bile ducts. It is secondary in the liver, lymph glands, lungs, kidneys, and bones. These tumors arc more apt to occur in the young than the epitheliomata. Gross Pathology. — Adenocarcinomata are usually soft and on section appear gelatinous; there is a tendency to infiltrate and tn grow outwardly into polypoid masses. (Fig. 51.) Pathologic Histology. — Irregular tubular alveoli are seen, lined with columnar cells in one or more layers, the outer layers being the more typically columnar. The alveoli are separated by fibrous or mucoid stroma. In later stages the alveoli are filled with various-shaped epithelial cells and the tubular character may be lust. In typical eases the alveoli are not solidly filled with cells (at least all the alveoli are not so filled) thus distinguishing these tumors from the scirrhous and medullary forms. Malignancy. — Adenocarcinomata usually grow rapidly, and metastasis occurs early. Scirrhous Carcinoma Scirrhous carcinoma is a hard, fibrous tumor found most fre- quently in the breast (female), uterus, pylorus, esophagus, rec- tum, and kidney. Gross Pathology. — Scirrhous cancer is a hard, round or irregu- lar tumor adherent to the overlying skin and adjacent tissues, ex- cept in very early stages. By contraction of the fibrous stroma, in the breasts, it causes retraction of the nipple, and irregulari- ties of the surface. Section shows a grayish white, glistening surface, the central part of which may retract. Yellow areas of fatty tissue are often seen in the center of the tumor. It is not encapsulated, the periphery being the more vascular part of the growth. Sometimes contraction is more rapid than prolifera- tion, causing the atrophic scirrhous cancer. (Fig. 52.) 144 GENERAL PATHOLOGY Fig. 51. — Adenocarcinoma of the body of the uterus, o, may be likened to a main stem from which arise numerous secondary stems, which in turn give off delicate ter- minals, consisting of epithelial cells. The glands may lie divided into groups a, b, c, d, and c, by the stems of stroma /, g, and It. The stems are covered by several layers of cylin- dric epithelium, while projecting into the gland cavities are long slender ingrowths of epithelium, devoid of stroma, as seen in i. Very delicate ingrowths consisting merely of two layers of epithelium are seen at k and k. At / the epithelium is several layers in thickness, and at m many layers with leucocytes. The arborescent character of the growth and peculiar gland grouping are characteristic of adenocarcinoma. (Cullen.) TUMORS 145 Pathologic Histology. Conspicuous bands of fibrous tissue form alveoli, enclosing nests of epithelial cells. The blood ves- sels are thick and fibrous. The alveoli in the center of the tumor are smaller than toward the periphery, and the cells are atrophied or variously degenerated. Secondary involvement of the lymphatic glands occurs "within the first year. Medullary Carcinoma Medullary carcinoma is a soft, rapidly growing, brain-like tumor, found most frequently in the mammae and testes. Secon- - ■*■■*** -..' ' -■ : r- Fig. 52. — Scirrhous carcinoma of breast. Alveoli of epithelial cells small; stroma abun- dant. (Mallory.) dary tumors of this type may follow the scirrhous form. Medul- lary cancer occurs somewhat earlier in life than scirrhous, but is much less common than the latter. Gross Pathology. — This tumor is soft and sometimes fluctuat- ing, nodular in outline, and tending- to ulcerate and bleed (fungus hematodes). The skin adheres early and retracts, but there is no retraction of the nipple when the breast is involved. The tumor is fairly well circumscribed owing to its rapid growth. (Fig. 53.) 14G GENERAL PATHOLOGY Pathologic Histology. — The fibrous stroma is more or less em- bryonic, vascular and scant. The alveoli are Large and filled with epithelial cells proliferating rapidly, sometimes showing mitosis. These tumors are usually rapidly fatal. Carcinoma simplex is a form intermediate between the scir- rhous and the medullary forms in the relative proportion of stroma, cells, and vascularity. Melanocarcinoma is very rare, but occurs in the skin; is soft and malignant. Adamantinoma is rare occurring on the surfaces or within i&t- Fig. 53. — Medullary carcinoma of breast. (Stengel and Fox.) the substance of the jaw bone. It appears to be derived from the enamel of developing teeth, and consists of a fibrillar stroma surrounding irregular masses of epithelial cells. It is usually benign, but may infiltrate and cause atrophy of the jaw, and some- times become sarcomatous. Endotheliomata Endotheliomata are tumors derived from endothelium of blood and lymphatic vessels, also the nicsothelium of serous membranes, and hence are called hemangioendotheliomata, lymphangioendo- theliomata, peritheliomata (from the perivascular lymph spaces) and mesotht liomata. TiM(»i;s 117 In addition to the general locations mentioned, they occur in the meninges, periosteum, bone marrow and other parts. While norma] endothelial cells are elongated and thin, "forming a mo- saic over the surfaces which they line," in the new growths the cells become cuboidal, cylindrical, and irregular in shape. They may occur in tubular masses, or in several layers with an open lumen here ami there, or in solid alveolar masses resembling carcinoma. Pig. 54. A psammoma is usually an endothelioma, occurring in the meninges ami other parts of the brain, consisting of closely ■r Fig. 54. — Endothelioma of the dura mater. a. connective-tissue stroma; b, small- ceiled focus; c, proliferated endothelium from lymph vessels; d, endothelial strand with lumen; c, area of fatty degeneration; /, endothelial cells passing into the connective tis- sue on the right. (ZieglerJ packed concentric masses of cells or whorls. They contain gran- ules of calcareous matter i "brain sand"). Any type of tumor how- ever in these locations containing calcareous granules is called a psammoma. The stroma of endotheliomata may become hyaline, myxoma- tous, fibrous or cartilaginous, or may atrophy, leaving the en- dothelium and blood vessels as the main features. Such tumors in which hyaline or mucoid material occurs in cylindrical masses are often called cylindromata. Endotheliomata are usually benign. 148 GENERAL PATHOLOGY Teratomata Teratomata are tumors of complex or mixed 1 issues, occurring in abnormal Locations, and due to developmental misplacements of tissues. They are said to be endogenous, when superficial tissues have been "included" within internal parts, and ectogenous, when a part of one fetus has been included within another fetus, thus forming the point -of origin of subsequent tumor formation. In this form there are all variations and amounts of inclusions up to double monsters. Dermoid Cysts Dermoid cysts are teratoid tumors, characterized by the pres- ence of skin or one or more of its appendages, as hair, nails, teeth, etc. They may be congenital or begin to form late in life. Seats. — Dermoid cysts are most frequent in the ovary, but also occur in the testicle and oilier organs. They are apt to develop at the junction of fetal clefts and fissures, as the orbital and mandibular fissures, branchial clefts, etc. Gross Pathology. — The growths are solid, but later become cystic by retention of sebaceous mailer, sweat, etc., which gives them a putty-like consistence. They are round, smooth tumors, varying in size up to that of a child's head. Microscopically, tissues of the three blastodermic layers are present. Skin appears in patches over the inner surface of the cyst, with a great preponderance of sehaceous glands. Parts not covered by skin arc usually covered by mucous membrane and glands. Besides the skin appendages, spicules of bone, mus-- eh', nerve and brain tissue may be seen. The tumor is usually benign, but may become carcinomatous. Hypernephroma Hypernephroma, or Grawitz's tumor, springs from a portion of the suprarenal cortex include, I within the kidney. The tumor is a yellow new growth appearang under the renal capsule in the upper portion of this organ. It is usually small, but may be- come large. Histologically there are found epithelial cells ar- ranged in tubules as in the cortex of the suprarenal capsules. TUMORS I I!) No medullary cells are present, hence no secretion of epinephrine has been found. (Fig. 55.) Cholesteatoma is a tumor exhibiting whitish glistening bodies of concentric layers of epithelioid cells. These bodies often con- tain crystals of cholesterin. The tumor occurs in the brain and meninges and is often multiple. Hairs, hair follicles, and horny changes have been found in these tumors, which places them among the teratomata. Chorionepithelioma, or syncytioma malignum, is a rapidly growing tumor, springing from the placental area during- preg- Fig. 55. — Finer structure of the adenomatous form of hypernephroma. and Fox ) (After Stengel nancy or the puerperium. The tissue resembles placental tissue. The uterine wall is rapidly invaded and metastasis occurs to lungs and rarely elsewhere. The tumor has no blood vessels but grows within the placental spaces. (Fig. 56.) Cysts Cysts are abnormal collections of fluid or semifluid materials within a closed, sac-like cavity. They are usually classified and named as follows: 1. Retention Cysts. — These are due to occlusion of the excre- tory ducts of a gland, causing distention with accumulating se- 150 GENERAL PATHOLOGY cretions, e.g., wens, or sebaceous gland cysts; ranulce, from the salivary or mucous glands in the floor of the mouth; also renal, ovarian, parovarian, mammary and pancreatic cysts'. An entire organ may become cystic, as the kidney in hydronephrosis (from an occluded ureter). (Fig. 57.) 2. Softening' or Necrotic Cysts. — These are due to degeneration and liquefaction necrosis of normal or pathologic tissues, and condensation of the surrounding tissue into a limiting area or .Vjp- '*>>-• — "»■ ■ "».—. " "C *■,'■*■ , - • - .^ *- -'":'& f' » c© ®*' ..* *'*■»•--».* ■ 'i '*v»C~ » -•• -* '^ ■■,f :'*■''■■'' ■"■':" ■ ■'■'■ \t£> Fig. 56. — Chorionepithelioma or syncytioma malignum. (By tlie courtesy of Dr. Barton Cooke Hirst from a painting made for him from a slide belonging to Dr. Herbert Fox.) wall. They occur frequently in tumors, infarcts, etc., and may follow hemorrhages (hemorrhagic cysts). 3. Parasitic Cysts. — Necrotic softening occurs, irritation causes the formation of a capsule, and the liquid contents contain epi- thelial debris and parasites. Such are the hydatid cysts, due to the tenia echinococcus, occurring usually in the liver, less often else- where ; also cysts of the trichina spiralis, usually of small size, just visible to the naked eye, and occurring within the muscle tissues. 4. Glandular Cysts, or Cystomata. — These are adenomata, which tend to cyst formation. They occur usually in the ovary TUMOKS i r, i and testicle, but may be found in any glandular tissue. They may be single or multiple, and each may consist of one or many cavities (multilocular cysts). They vary in size up to that of a child's head or Larger. On section a more or less serous, some- times hemorrhagic fluid, or a gelatinous material (usually re- ferred to as "colloid") may be seen. The inner surface may Fig. 57. — Cyst of the parovarium: there is no distortion of the ovary; the Fallopian tube has been much elongated. be smooth, or present papillomatous outgrowths (papuliferous cysts or cystomata). Microscopically, the cysts are lined with typical, or variously modified, columnar epithelium, supported upon a framework of connective tissue. The latter may greatly predominate, causing the cysts to be very small, or the acini few; again the opposite may be true. Cysts are benign, though some have a tendency to become car- cinomatous. CHAPTER VIII THE PATHOLOGY OF INFECTIOUS DISEASES An Infectious Disease is one that is caused by living micro- organisms. A Contagious Disease is an infectious disease that is readily transmitted from one individual to another by direct contact, by fomites, etc. Any organism that lives upon or within the living tissues of plant or animal is called a parasite. An organism which lives upon dead and decomposing organic matter is called a saprophyte. Those parasites or saprophytes which can live and flourish in either condition are known as facultative or optional parasites or sa- prophytes. All pathogenic microorganisms are parasitic; some are habitual parasites, as certain pyococci, the B. coli communis, etc., while other, as the B. tetani, are but temporarily parasitic. All pathogenic parasites, which can be grown upon artificial culture media, are facultative saprophytes. The organisms pathogenic for man may be classified as fol- lows : Bacteria, or Schizonrycetes (fission fungi). Yeasts, or Blastomycetes (budding fungi). Molds, or Hyphomycetes (thread fungi). Protozoa, or unicellular animal microorganisms. Metazoa, or multicellular animal organisms. It is customary to refer to a disease caused by bacteria or protozoa as an infection; to one caused by yeasts as a blastomy- cosis; to one caused by molds as a mycosis; and to one due to metazoa as an infestation. Bacteria are unicellular, vegetable 1 microorganisms, which re- 1 The question whether bacteria belong to the vegetable or animal kingdom is still an open one. They are considered plants by most biologists because many bacteria can be made to grow upon inorganic food, and because in growth and reproduction they resemble plants more closely than animals, bacteria, however, are such primitive forms and so slightly differentiated, resembling plants in rigidity of form, in tendency to filamentous growth and ability of some of them to grow on inorganic food, and on the other hand resembling animals in motility, lack of chlorophyl and apparent neces- sity of some for organic food, that they are generally regarded as occupying a place intermediate between the plant and the animal. In 1878 Haeckel proposed that bac- teria be placed in a separate kingdom to be known as Protista, but this suggestion was never generally accepted. 152 PATHOLOGY OF INFECTIOUS DISEASES 153 produce by fission. Elongated bacteria (bacilli and spirilla) di- vide transversely, thus differentiating them from protozoa which divide longitudinally. Bacteria are divided into (a) Lower Bacteria (Haplobacteria) — each individual organism of which is composed of a single cell, capable of performing all the vital essential functions and (b) Higher Bacteria (Triehobacteria, or Trichomycetes) — composed of filamentous forms (thread-like arrangement of cells) with real or apparent branchings. The end-cells only appear to reproduce, hence there is here the beginning of a division of physiologic function. Bacteria cause disease mainly by the production of specific toxins; i.e., poisonous substances secreted by the bacteria, and peculiar (hence "specific") to the particular organism which se- cretes them. Toxins resemble enzymes in all essential properties, and are usually divided into (a) true, soluble or extracellular toxins, — toxins which in culture media escape from the bacterial cell (extracellular) and diffuse through the medium (soluble), and (b) intracellular, endotoxins, such as the toxins of pyococci, the typhoid bacillus and most of the pathogenic bacteria — toxins which remain within the bacterial cells (intracellular) and are liberated in disease when the bacterial cells disintegrate. In addition to the specific toxins, bacteria may also form various other metabolic products, such as hemolysins, coagulating, pro- teolytic and other ferments, as well as various nonspecific and specific substances. When bacteria with their toxic products gain entrance into the blood and tissues, they stimulate the tissue cells to the pro- duction of defensive substances, or antibodies. All cells or sub- stances capable of causing living tissues to form antibodies are called antigens. The most important antibodies are antitoxins, which combine with and neutralize toxins, thus rendering the latter harmless; agglutinins, which cause bacteria to clump together; Jgsins, which destroy bacteria and other cells; and opsonins, which prepare bacteria in some manner so that they are more easily ingested and destroyed by the phagocytic leucocytes. Immunity is a state of resistance to an infection. It may be actively acquired by the production of antibodies during the course of an infection, or during the process of intentional in- 154 GENERAL PATHOLOGY oculation, as in "immunization" in which animals are inoculated for the purpose of producing antitoxic and bacteriolytic sera, or as in "vaccination" or "bacterination." in which attenuated or killed cultures of bacteria are inoculated into healthy persons to cause the formation of antibodies as a matter of protection against infection, or into diseased individuals for the purpose of effect- ing a cure of the disease. Immunity may also be passively ac- quired when antitoxic sera ("antitoxins") and bacteriolytic sera ("antisera",), manufactured within the tissues of an animal or even a human being, are injected into the tissues of another in- dividual for the purpose of protection or cure. Natural immunity is not well understood, but may be defined as that which is possessed by an individual or race, not known to have experienced any of the recognized processes of protec- tion. A septicemia (or bacteremia) is a disease due to the presence of bacteria with their toxins in the blood. Thus typhoid fever, anthrax, etc.. are septicemias, as well as generalized staphylococ- cic or streptococcic infection, though surgeons are apt to limit the term "septicemia" to invasion of the blood by pyogenic organ- isms. A pyemia is a condition in which secondary (metastatic) ab- scesses appear in various organs and tissues, formed by bacterial emboli brought by way of the blood vessels or lymphatic vessels from some primary focus of suppurative inflammation. A toxemia is a diseased condition due to the absorption of the toxins of pathogenic bacteria, as in tetanus. A sapremia is a condition due to the absorption into the blood of poisonous substance formed by saprophytic bacteria growing in mortifying tissues, as in certain forms of gangrene, retained portions of placenta after parturition, etc. SUPPURATIVE DISEASES Suppuration (q.v.) or inflammation resulting in pus formation, when occurring naturally, is always the result of the invasion and activity of microorganisms. The most common pyogenic or- ganisms are the staphylococci and streptococci; less often the pneumococci, the pneumobaeilli, gonococci, the colon and typhoid bacilli; still less commonly, other microorganisms, including ame- PATHOLOGY OF [NFECTIOUS DISEASES 155 bse, may become pyogenic, ruder perfectly favorable conditions it is believed thai most, if no1 all, pathogenic bacteria may cause suppural ion. The micrococcus tetragenus and the />'. pyocyaneus are often associated with the more common pyococci in causing- suppura- tion, the latter giving a green tinge to the pus, but they rarely if ever arc I lie sole cause from the beginning to the end of the infection. The staphylococcus pyogenes aureus (cluster-forming, pus-pro- ducing golden yellow spherical organism) is the direct cause, as a rule, of localized and circumscribed inflammation and suppura- tion, such as abscesses, pustules, furuncles, carbuncles, etc. "When these cocci gain entrance into the circulation, pyemia and septicemia may result, though less often than in streptococcal in- fection. The organisms may remain dormant at times within an encapsulated inactive abscess, or in deeply seated subacute infections, as in subacute osteomyelitis, endocarditis, etc., and later become active and virulent. The presence of staphylococci in association (symbiosis) with other organisms in disease often aids the activity of the latter, as for example the influenza bacilli. Their specific toxins are intracellular, and have a decided chemo- tactic effect upon the leucocytes, attracting large numbers of these phagocytes to the seat of infection. A hemolytic substance is also formed. Although staphylococci cause the formation of antibodies, the use of antistreptococcic sera has not been very en- couraging, but the use of vaccines of killed or attenuated cul- tures has been more promising, especially in subacute or chronic staphylococcic infections. The staphylococcus pyogenes cilbus, and the staphylococcus epi- dermic] is alb us are mildly pathogenic forms, probably but slightly modified varieties of the S. pyogenes aureus. The first is often associated with the aureus variety in suppurations, or may be the sole cause in certain forms of acne. The latter inhabits the layers of the epiderm, and in the opinion of some bacteriologists is the cause of "stitch abscesses." The Streptococcus pyogenes (chain-forming, pus-producing coc- cus) varies considerably in virulence, but usually causes the more severe forms of suppurative disease, with a tendency to spread and become phlegmonous. Cellulitis, erysipelas, perios- 156 GENERAL PATHOLOGY titis, pleuritis, peritonitis, etc., as also general septicemia, are more often due to streptococci than to staphylococci. Strep- tococci are, however, also found in localized suppurations. In malignant endocarditis the Streptococcus viridans, a variety form- ing green colonies on culture media, is commonly found. In rheu- matic arthritis the Streptococcus rheumaticus is apparently the chief exciting cause. In erysipelas the Streptococcus erysipelatis is found, but this appears to be identical with, the Streptococcus pyogenes. Erysipelas, (literally "red skin") is a serous inflam- mation of the skin, usually found on the face, tending to spread from the nose outward across the cheeks, and preceded by a zone of congestion and dense infiltration which follows the lymphatic clefts. Occasionally suppuration occurs. Streptococci are often found in the throat and tonsils during infectious diseases, such as measles, scarlatina, influenza, etc. Kosenow believes that streptococci and pneumococci are merely different varieties of one species and has apparently suc- ceeded in transmuting one to the other variety under artificial conditions. In regard to toxins, antibodies, and vaccines, what was said of the staphylococci is also true in general of the streptococci. Epidemic Cerebrospinal Meningitis Epidemic cerebrospinal meningitis is a purulent inflammation of the cerebral and spinal meninges, caused by the meningococcus, or Diplococeus intracellularis meningitidis. These cocci occur in pairs, and resemble the gonococci both in morphology and in being found in groups within the leucocytes and other cells. They also sometimes occur in chains. The disease is a fibrinopurulent, less often a seropurulent lep- tomeningitis, the cerebral dura being rarely involved, although the spinal dura is often involved. The exudate is abundant in the large fissures of the brain, over the optic chiasm and sur- faces of the pons and the cerebellum. The inflammation usually follows the blood and lymph vessels into the substance of the brain and cord, often resulting in small abscesses. The fluid from a lumbar puncture nearly always contains the cocci, and the cocci have frecpiently been found in the nasal secretions of patients and of persons exposed to the disease. It is believed PATHOLOGY OP INFECTIOUS DISEASES 157 that meningeal invasion occurs by way of the lymphatic vessels from the nose. Various inflammations and degenerations are also noted in the kidneys, heart, spleen, muscles, and other tissues. Gonorrhea Gonorrhea is a purulent, catarrhal inflammation of the urethra and other mucous membranes, caused by the gonococcus or Mi- crococcus gonorrheae. This organism occurs in pairs, "biscuit- shaped" or "coffee-bean-shaped" in appearance, and found abundantly in the pus of acute gonorrhea of the urethra, less often in chronic cases, or in other locations. In acute gonor- rheal urethritis the inflammation begins at the meatus and soon spreads to the posterior parts; the mucosa is intensely red, and in about twenty-four hours or more a yellowish (sometimes greenish) exudate appears, consisting of leucocytes and des- quamated epithelium. Microscopical examination shows groups of the gonocoeci lying within the pus cells, as well as in the fluid portion of the exudate. From the original focus, other tissues are readily invaded, causing salpingitis, oophoritis, peritonitis, prostatitis, also me- tastasis to more remote tissues, as the heart and the joints (gonor- rheal endocarditis and arthritis). "Gonorrheal rheumatism" usually occurs months after the infection, is very intractable and apt to result in permanent damage to the joint, usually the knee, elbow or wrist. Ophthalmia neonatorum is an acute gonorrheal conjunctivitis contracted by the child from the mother during parturition. It is said that 10 per cent of blindness in children is due to this form of gonorrhea. Chronic gonorrhea is usually a direct continuation of an acute attack, and characterized by a constant discharge of a thin, catarrhal exudate (gleet). Ulcerous lesions, or papillomatous thickenings of the mucosa are a frequent result of chronic gonor- rhea, or there may be hyperplasia of the submucosal connective tissue with narrowing of the urethra (stricture). The most com- mon seat of stricture is the membranous urethra. 158 GENERAL PATHOLOGY The gonotoxin is intracellular, and while slight amounts of antibodies are produced, antisera are valueless, but vaccines may be useful in chronic forms of the disease. "While gonorrhea is usually contracted through sexual contact, the transmission of the disease by towels, bedding, and other contaminated articles, particularly in institutions, is probably more frequent that is generally recognized. Latent gonorrheal foci, existing long periods of time after apparent "cures" have been effected, and capable of becoming acute and transmitting Fig. 58. — Acute urethritis, showing purulent infiltration and gonococci in the cells and between the cells. (Birch-Hirschfeld.) the disease to others, are also more frequent than is generally believed. (Fig. 58.) Soft Chancre, or Chancroid Soft chancre, or chancroid, is an ulcer almost invariably found on the external genitals, due to the B. of Ducrey. It is always contracted through sexual contact, but is autoinocnlable, hence there are usually more than one ulcer. The infection begins as a red papule, which later suppurates, forming a yellowish ulcer with irregular infiltrated margins. Sometimes it becomes phage- PATHOLOGY OF [NFECTIOUS DISEASES 159 denic or serpiginous in character. The organisms travel along the lymphatic channels to the inguinal glands which also sup- purate as a rule. The disease is purely local — never systemic when uncomplicated. Mixed infection often occurs, and gono- eocci. Spirochete pallida, pyogenic cocci, and other organisms may be found in the ulcers. Pneumonia, or Pneumonitis Pneumonia is an inflammation of the essential lung tissue; viz.. the alveoli and their immediately surrounding structures. The clinical forms of pneumonia are practically always due to micro- organisms, but many different species of the latter have been found as the direct cause of the disease, and it is possible, more- over, to produce a pneumonia by the inhalation of hot steam or chemical irritants. Pneumonia, therefore, should be con- sidered as a distinct pathologic condition rather than a specific infection. Classified according to their pathologic anatomy, pneu- monias may be divided into: Lobar, Fibrinous or Croupous Pneumonia. Lobular. Catarrhal or Bronchopneumonia. Purulent or Suppurative Pneumonia. Fibroid, Interstitial or Productive Pneumonia. Tuberculous or Caseous Pneumonia. Lobar, or Croupous, Pneumonia is an acute hemorrhagic and exudative inflammation of the air cells of one or more lobes of the lungs, due usually to the pneumococcus, or Diplococcus pneu- moniae, but occasionally to streptococci, staphylococci, B. influ- enza?, the B. of Friedlander. and other organisms, either alone or in association (symbiosis I with the pneumococcus. Cold, fatigue and systemic depression of any nature act as pre- disposing causes. The lover right lobe is oftenest affected; next the lower left lobe, and rarely the apices. In "double pneu- monia" lobes in both sides of the thorax are simultaneously in- volved. There are three principal stages: (a) Congestion. — The diseased area is hyperemic, dark red. less crepitant than normal, heavy but still floating when placed in water, and the pleural surfaces are lustreless. Microscopically, the capillaries are congested, and the air cells contain a serous 160 GENERAL PATHOLOGY exudate with red and white blood cells, and a few desquamated epithelial cells. As this exudate increases in amount, coagulation sets in (few hours to a few days) thus forming the (b) Stage of Consolidation or Hepatization. — The affected area is now solid and liver-like, deep red or brownish red in color (red hepatization), is swollen, pits on pressure and sinks when placed in water. On section the cut surface is red, dry, and granular — due to plugs of fibrin projecting from the air cells. A fairly thick slice of the diseased lobe will break on bending. Microscopically the air vesicles are filled with fibrin holding in its Fig. 59. — Acute lobar pneumonia. Early stage. This single air vesicle shows conges- tion of the capillaries in the walls, and a small amount of exudates, fibrin, leucocytes, red blood cells, and exfoliated epithelium. (Delafield and Prudden.) meshes red and white cells and desquamated epithelium. The fibrin soon begins to contract causing a serous fluid to collect in the vesicles, the red cells disintegrate, the epithelial cells be- come fatty, and when these changes have advanced far enough to give the affected areas a yellow or grayish color, the name "gray hepatization" is applied. The area is still solid but less apt to break on bending, and the air cells contain a mass of fibrin which is retracted from the walls and cells, chiefly leucocytes and epithelium. (Figs. 59 and 60.) This substage (gray hepatiza- tion) does not always develop — the red hepatization passing at once into the third stage of (c) Resolution. — The affected area now softens, pitting is no PATHOLOGY OF [NFECTIOUS DISEASES 161 Longer possible and crepitation can again be elicited. On section a purulent fluid exudes. Microscopic/I! //, liquefaction necrosis, Avitli cells in different stages of disintegration are the chief features. Proliferation of epithelial cells becomes marked, thus repairing the damaged al- veolar -walls, -while the softened, emulsified contents are being absorbed by the lymphatics and in part expectorated. During the course of the disease, the lung tissues surrounding the inflamed parts are more or less emphysematous, and the pleura is usually inflamed, hence a typical pneumonia is nearly always a Fig. 60. — Acute lobar pneumonia. Later stage. The air vesicles are filled with exu- date consisting of leucocytes, fibrin, and serum with a few epithelium cells. (Delafield and Prudden.) pleuropneumonia. A blood examination shows leucocytosis. Rarely, in intense intoxications a leucopenia is present. Paren- chymatous changes in the kidneys and heart may occur due to the toxemia ; albuminuria is frequent, and the chlorides are di- minished or absent from the urine during the disease, but usually reappear in excess during convalescence. Bronchopneumonia or Lobular Pneumonia Bronchopneumonia or lobular pneumonia is an acute inflamma- tion starting in the smaller bronchioles and extending to the air cells of the lungs, in which the exudate shows little or no ten- dencv to fibrin formation. About one-half of the lobular forms 162 GENERAL PATHOLOGY of pneumonia are due to the pneumococcus, either alone or as- sociated with the organisms mentioned under croupous pneu- monia. Any of the organisms mentioned may also be the sole cause of this form of pneumonia. Bronchopneumonia is most frequent in the young and the aged, and may be secondary to measles, whooping cough, scarlatina, diphtheria, pulmonary cirrhosis, typhoid fever, etc. Grossly the pleural surface presents red or grayish areas, which correspond to the lobules or areas of the terminal bronchioles affected. In extensive cases all the lobes of both lungs may be Fig. 61. — Bronchopneumonia. Child. The wall of the small bronchus is and the lumen contains a mucopurulent exudate. The adjacent air vesicles tain a catarrhal exudate. (Delafield and Prudden.) thickened also con- involved, but not all the lobules are affected, i.e., the lobes are not uniformly affected as in lobar pneumonia. The inflamed, lobular areas usually project slightly above the surrounding sur- faces, and are surrounded by emphysematous tissue. The lung as a whole is crepitant, but the localized diseased areas are airless and sink in water. The bronchi and bronchioles contain muco- purulent exudates, and their complete obstruction sometimes leads to local areas of atelectasis. (Fig. 61.) Microscopically the alveoli are filled with a semifluid exudate containing desquamated epithelium and blood cells. The alveolar walls show round-cell infiltration and the bronchioles catarrhal bronchitis. PATHOLOGY OF [NFECTIOUS DISEASES 163 Hypostatic pneumonia is ;i bronchopneumonia, not so distinctly lobular as the ordinary form, and with an exudate thai is more fibrinous. It commonly involves the bases and posterior (de- pendent) parts of the Lungs in individuals who are confined to bed during prostrating diseases, as typhoid or chronic nephritis. When the heart action becomes feeble hypostatic congestion de- velops in the dependent parts and soon bacteria enter the con- gested part and set up a catarrhal inflammation. Aspiration pneumonia is also a form of bronchopneumonia re- sulting from the inspiration of infectious material from the upper air passages, as well as food and secretions from the mouth in eases of paralysis, in anesthesia, or from the inhalation of hot steam, chemical irritants or dust in concentrated form. The le- sions vary with the causal factors. When infectious or highly irritating matter is "aspirated," an intense catarrhal inflamma- tion with solidification results; the exudate is hemorrhagic and liable to become suppurative or necrotic. In the inhalation of dust, as in marble cutting, coal mining, etc., the catarrhal inflam- mation may be moderate in degree or absent, while the produc- tive inflammation, with a resulting fibroid pneumonia, may be the main pathologic change. Purulent pneumonia is an acute inflammation in which pyogenic bacteria, whether as a secondary infection brought by way of the bronchi, blood channels or the pleura, or as a primary in- fection, cause suppuration of the inflammatory exudate. Small miliary abscesses, or one or more large abscesses may result, a condition which is very apt to be fatal. When the abscesses break into the pleural cavity, an empyema results. The term, empyema, refers to a collection of pus in the pleural cavity how- ever produced. Fibroid pneumonia is a chronic process in which the cellular proliferation becomes permanent fibrous tissue. When this con- dition is caused by the inhalation of coal dust, iron dust, or marble dust (pneumonokoniosis) the particles penetrate the al- veolar walls and the walls of the bronchioles, and become sur- rounded by a zone of inflammatory exudate which finally or- ganizes into fibrous tissue. This form of pneumonia also occurs at times secondary to other forms of pneumonia, to syphilis, tu- berculosis, etc. When the indurated areas are extensive, con- 164 GENERAL PATHOLOGY traction with distortion of the lung follows, with obliteration of the air cells and proportionate impairment of respiration. Caseous or tuberculous pneumonia is due to the B. tuberculosis, and characterized by a filling up of the air cells and an infiltration of the interalveolar tissues with an exudate which tends to caseation instead of resolution. There are small areas of con- solidation, usually lobular, at first red (congestion), later yellow (caseation). These areas finally soften and undergo resolution, if small, or become encapsulated, or may coalesce into larger cavities, resulting in chronic pulmonary tuberculosis; if mixed infection occurs, rapid suppurative softening results and the con- dition quickly becomes fatal ("galloping consumption.") The specific or infectious granulomata are smaller or larger masses of pathologic tissue, resulting from subacute or chronic proliferative inflammatory processes, due to specific microor- ganisms, and having a tendency toward degenerative or necrotic change. The lesions are for the most part tubercles, nodules or nodes, consisting essentially of more or less typical granulation tissue, but there is no tumor in the true sense, and the term "granuloma" is deservedly falling into disuse. The lesions usually described under this heading are those found in tuberculosis, leprosy, glanders, syphilis, rhinoscleroma, actinomycosis, sporotrichosis, blastomycosis, etc. In the following pages the pathology of the lower or true bacterial diseases will be considered immediately, while those morbid conditions due to the higher bacteria and other organisms will be taken up in their proper order. Tuberculosis Tuberculosis is a disease comprising the morbid processes due to the B. tuberculosis. It affects man and practically all the lower animals, though goats, horses, dogs, and cats are relatively im- mune. Locations. — It is found in the respiratory tract, the gastroin- testinal tract (especially the lower ileum, rectum, throat and mouth), the lymph nodes, serous membranes, bones, spleen, kid- neys, adrenals, brain, middle ear, uterus with appendages, tes- ticles, bladder, and skin. Organs which are rarely affected are I'ATIlOUHiY OF IXKKCTIOCS DISEASES 165 Mii „*^ .«/: *\Y £ /$ -If *. , 5 r V;; ^•sffi'- ■■:«■>? >*?'•'. li-M $>■ :V^. J, >« 'iVo ># ■•■* .y W$8$r ■tan*' Yx» .«»*«? & ■•>■'.■"• -„;%>-, 4 W W4? I s3 ^1< Fig. 62. — Miliary tubercles in the liver, showing abundant round cells in the peripheral pails, epithelioid and giant-cells within. (Stengel and Fox.) Fig. 63. — Miliary tubercle of the human form. (Stengel and Fox.) 166 GENERAL PATHOLOGY the salivary glands, thyroid gland, the muscles, cartilages, ovaries and heart. In children the lymph nodes, serous membranes and the bones are most frequently infected. Gross Pathology. — The characteristic lesion is the miliary tu- bercle. This is a gray, semitranslucent, slightly elevated (if su- perficially located) nodule varying in size from a point scarcely visible to the naked eye to 2 mm., which merges into the sur- rounding tissue (can not be "peeled out"). The second form of tuberculous lesion is an infiltration of the tissues with epithelioid cells and other cells characteristic of the tuberculous process, but without forming distinct tubercles. When caseation sets in, the lesions become yellow (yellow miliary tubercle). (Figs. 62 and 63.) Minute Anatomy. — The bacilli (or their toxins) first cause pro- liferation of the endothelial cells of the lymph spaces, lymph capillaries and blood vessels and connective tissue of the part. These cells are large and have vesicular, poorly staining nuclei, and known as epithelioid cells. Giant cells (large multinucleated cells) may appear in the midst of the epithelioid cells, probably formed from the latter by proliferation of the nuclei without di- vision of the cytoplasm. Round cells, consisting of leucocytes and lymphocytes, surround the collection of epithelioid cells, and at this stage it may be possible at times to see the three zones usually described as consisting of an inner zone of giant cells, a middle zone of epithelioid cells and an outer zone of round cells. This is the histology of the gray tubercle ; no new blood vessels are formed, and after a variable time, the center becomes cheesy (cheesy necrosis), the cells lose their outline and the nuclei degenerate, giving the field a granular appearance, which, surrounded by cells not yet having undergone degeneration, presents the so-called "raked field" appearance. The giant cells also degenerate, and those which have undergone but partial degeneration have a crescentic outline. Giant cells are not neces- sarily present, but are characteristic of a typical tubercle. The histologic appearance of tuberculous infiltration is essen- tially the same, but there are more blood vessels in the area, and especially upon free surfaces a typical, highly vascular granula- tion tissue may be formed. PATHOLOGY OF [NFECTIOUS DISEASES 1 07 Results. When well established, the disease progresses usu- ally to a fatal termination. Many times, however, caseation may be followed by encapsulation with temporary arrest of the in- fectious process (latent foci), or by calcification, and if the dis- ease has nol progressed too far, a permanent cure is possible. When the lesions undergo liquefaction, cavities (vomica;) are formed, or, especially in cases of bone infection, cold abscesses result. Secondary tuberculosis may be set up in various parts of the body by (1) extension along lymphatic channels, (2) along nat- ural channels, as the respiratory or intestinal tract, and (3) through the blood vessels. Leprosy Leprosy is a chronic infectious disease due to the B. lepra. It occurs in two forms, the nodular (or tubercular) and the anesthetic. In the first, gray or yellowish nodules develop, vary- ing in size up to a walnut, or larger. (Fig. 64.) These occur in the skin and subcutaneous tissues of the face, exterior surfaces of the legs and arms, about the hands and other parts, and are red and inflammatory at first, but later pale and indolent. They usually break down into ulcers which slowly cicatrize, often Avith great distortion. The mucous membrane and internal organs may also rarely be affected. In the anesthetic form the lesions are less conspicuous, but the hyperesthesia, neuralgia and later atrophic ulcers make it more serious than the nodular form. Anesthesia of the parts occurs when the ulcerations develop. The two forms are often associated, and tuberculosis often fol- lows the lesions, especially those of the internal organs. Microscopically, the nodule is seen to be fibrous, somewhat vas- cular without tendency toward caseation. It is composed of epithelioid cells (proliferated endothelium and connective tissue cells) which are often vacuolated and may contain the bacilli; large degenerated cells ("lepra cells") containing many bacilli and a few more or less degenerated nuclei are always found. Giant cells are sometimes present, but far less often than in tu- berculosis. 1G8 GENERAL PATHOLOGY In the anesthetic form the bacilli grow within the sheaths of nerves, forming fusiform swellings, resembling the nodules in structure. Skin eruptions (pemphigus leprosa) often occur, also atrophy of the parts affected, and sometimes even loss of parts, as fingers or toes. Fig. C4. — Xodular leprosy. (Goldschmidt.) Syphilis, or Lues (or "Great Pox") Syphilis is an infectious disease due to the presence of the Spirochete pallida, or Treponema pallidum. 2 It occurs in three stages. 2 There is a tendency to place this organism among the protozoa. It is a rigid spiral, in many respects resembling the spirilla, but it is claimed by some observers that in reproduction longitudinal division takes place, which would place the spirochete among the animal organisms. According to Jordan {General Bacteriology, 1918), "At present the systematic position of this organism may be regarded as unsettled, although the majority of investigators incline to place it with the true bacteria, or at best in a group midway between the bacteria and protozoa.'' PATHOLOGY OF [NFECTIOUS DISEASES 169 The primary stagi Is characterized by the chancre, which appears after an incubation period of three weeks, a1 the site of u lation, as a red papule increasing in size and hardness (Hunte- li.-ni chancre). It usually presents a dry, sometimes slimy super- ficial erosion, but docs not ulcerate; is located usually upon the glans penis, prepuce, or just within the meatus; in the female, in the vagina, urethra or cervix uteri. Extragenital chancres may occur in the rectum, about the anus, in the mouth, eyes, groin ami other locations. Wherever the initial lesion occurs, local lymphadenitis devel- ops simultaneously, forming the "indolent bubo" — painless, hard and movable beneath the skin. Histologically, the chancre consists of round cell infiltration leucocytes and proliferated connective tissue cells) within the deeper layers of the skin or mucous membrane, and especially along the course of the blood vessels. There is considerable in- tercellular exudate, which coagulates, favoring* necrosis of the superficial cells (erosion). The chancre attains a maximum size in one to two weeks, from a few millimeters to a few centimeters in diameter, remains sta- tionary for three or four weeks, then slowly disappears, though the induration may persist for years. The secondary stage may follow in about six weeks, and is characterized by eruptions upon the skin and mucous mem- branes, with swelling and induration of the lymphatic glands generally. The eruptions begin as papules or macules which be- come flat tabular swellings with superficial erosion, having a dull red or coppery color on the skin, and a grayish color on the mu- cous membrane the mucous patch). These eruptions are poly- morphous in outline, are covered with a scant secretion, often offensive, sensitive to the touch, and the most contagious of syphilitic lesions. Histologically, there is round cell infiltration, with edema and necrosis of the epithelium. The papilla become abnormally large and hyperemic. These eruptions last from one to three years, then disappear, and recovery may lie effected, or the tertiary stage may follow. The tertiary stage may follow the secondary in from one to four years, or after many years, and is characterized by the presence 170 GENERAL PATHOLOGY of gummata, which are nodules varying in size from a pinhead to an orange. They occur most frequently in bones, especially tibia, sternum and skull; in internal organs, as liver, kidneys, lungs, brain and other parts. ^lacroscopically, a gumma is a hard, somewhat elastic nodule ; on section the central part is found to be gelatinous in appearance. Fibrous bands are usually seen radiating from the center to the periphery and into the surrounding tissues. Tin- hard and elastic character suggested the name "gumma," i.e., gummy tumor. The center may soften, especially when near a surface, forming ulcers which finally cicatrize. (Fig. 65.) 3: m Fig. 65. —Gummatous meningoencephalitis. (Ziegler.) Histologically, the gumma is composed of round and spindle cells and usually a few giant cells. The blood vessels are markedly thickened, and new vessels are formed. Degeneration or a form of necrosis (resembling caseation) is always seen in the center of the gumma. There are also diffuse tertiary syphilitic lesions, such as bands of connective tissue, greatly thickened, atheromatous vessel vails, with a diffuse infiltration of tissues with the characteristic round cells; often seen in the liver, spleen, kidney, heart, and nervous system. PATHOLOGY OF INFECTIOUS DISEAI 171 Glanders, or Equinia Glanders is an acute 1 or chronic infectious disease, occurring spontaneously in horses, due to the B. mallei, and occasionally communicated to man and other animals. In horses, the nasal mucosa is the usual seat of inoculation, in which slightly elevated, pea-sized nodules appear, which increase and finally break down, leaving' yellowish ragged-edged, pus-dis- charging ulcers. When these heal, characteristic, stellate scars are formed. Bronchopneumonia by aspiration of infected mate- rials from the nose or upper air passages may follow. Metastatic abscesses of internal organs often occur. The disease is often fatal, death occurring with all the symptoms of a septicemia. When the skin is particularly involved, the condition is called farcy and the nodules in the skin and subcutaneous tissues, vary- ing in size up to hazelnuts, are called f'. diph- theriae (Klebs-Loeffler bacillus), and characterized by the forma- tion of a false membrane locally, and by toxemia systemically. While the tonsils, pharynx and the nose are the common seats of the disease, the eyes, skin, middle ear, vagina, and other parts may also become infected. Symbiosis with streptococci increases the virulence of the diphtheritic bacillus. After an incubation of from 2 to 7 days, an acute fibrinous inflammation sets in, the exudate of which as it appears upon the surface undergoes coagulation necro- sis, thus forming a thick, adherent membrane — the false or diph- theritic membrane. In the larynx this membrane with the swollen and inflamed mucosa may cause fatal asphyxia, but aside from this purely mechanical condition, diphtheria becomes serious or fatal only through the toxin which is formed. The bacilli rarely invade the blood or internal organs. At necropsy are found degeneration and inflammation of the myocardium and endocardium, and ne- phritis. Bronchopneumonia is present in over 50 per cent of fatal cases, due to B. diphtheriae, to pneumococci or other organisms. During convalescence paralysis of the soft palate and other mus- cles often occurs. The use of antidiphtheritic serum (antitoxin) affords the best example of successful serotherapy in the art of therapeutics. Asiatic Cholera Asiatic cholera is an acute infectious disease characterized by a serous inflammation of the intestines and due to the Spirillum or Vibrio cholerae asiaticae, often called the "comma bacillus" of Koch. The spirilla invade the mucosa of the lower part of the ileum chiefly, also often the large bowel, causing an intense watery exuda- tion, which with the contained particles of desquamated epithelium, constitutes the "rice-water" discharges, so prominent a symptom of this disease. Postmortem examination reveals no definite or constant morbid changes, but often congestion or inflammation are noted in the affected parts, with degenerative changes in the liver, kidneys, and other organs. The spirilla do not enter the blood, but secrete a soluble toxin, which either alone or together with other toxic products accounts for the symptoms. 174 GENERAL PATHOLOGY Typhoid Fever Typhoid fever is an acute general infection of the lymphade- noid tissue of the body, with its most characteristic lesions in the lymphoid structures of the intestine, and due to B. typhosus (B. typhi abdominalis) of Eberth. The bacilli appear in the blood (a bouillon culture inoculated with blood during the first week of the disease is the most positive means of diagnosis) and in all the se- cretions and excretions, as well as in the "rose spots" which oc- cur upon the exterior early in the infection. As in Asiatic cholera, the organisms are usually ingested with food and water. After an incubation period of two or three weeks, the solitary follicles and Peyer's patches in the lower part of the ileum become congested; during the second week these become pale and enlarged, due to proliferation of the lymph- oid cells and to phagocytic endothelial cells (macrophages) and softening and necrosis are apt to take place, which during the third week results in ulceration. When the Peyer's patches ulcerate, the ulcers are longitudinally disposed with reference to the long axis of the intestine (thus differing from the tubercu- lous ulcer in the same situation which is transverse). After the third or fourth week the ulcers begin to heal.- Not all the lymph follicles or patches proceed to ulceration, and in some cases no ulcers are formed at all. In some cases the lymphoid structures of the upper colon and upper ileum are also involved. On the other hand the intestinal structures may not be involved, the in- fection electing lymphoid tissues elsewhere in the body as the seat of its activity. In typical typhoid fever, however, the in- testinal glands, the mesenteric glands, the spleen, liver, kidneys, bone marrow, and the lymphoid structures in other parts are in- volved, showing congestion, cellular infiltration, and frequently necrotic areas. The spleen is greatly enlarged (splenic tumor) in nearly all cases. The specific toxin is an endotoxin, to which the symptoms of temperature, delirium, prostration and anatomic changes are due. Agglutinins are also formed, and their presence after the first week of the disease may be shown by the Widal reaction; viz.. the clumping of the typhoid bacilli from a young culture when mixed with a minute quantity of the patient's blood serum. PATHOLOGY OF IXFI'.CTIOI - DISKASKS 175 Antisera are of qo avail therapeutically, but vaccination lias proved successful as a preventive measure. After recovery, the organisms continue to grow in the liver and oilier parts of individuals, as well as in a few persons who never had the disease in recognizable form (subinfection). Such individuals may in feet others, hence are called "typhoid car- riers." Diphtheria and a number of other infections may also be ''carried" for variable periods of time. (Fig. 66.) Paratyphoid infect ion is a mild (rarely fatal) form which is clinically almost identical with typhoid fever, but with certain pathologic differences, and due to "paratyphoid" bacilli, of Fig. 66. — Typhoid fever, showing necrosis of Peyer's patches and intense congestion of the bowel. (Modified from Kast and Rumpel.) which there are several strains, and which differ from the B. typhosus in certain cultural characteristics and in agglutinative reactions. Bacillary Dysentery Bacillary dysentery is an infectious colitis due to B. dysen- teriae (Shiga), a nonmotile member of the typhoid-colon group. It produces toxins which are probably both intracellular and ex- tracellular. Great swelling of the mucosa of the colon with muco- catarrhal inflammation are noted, and the surface of the colon becomes considerably eroded. In severe cases the inflammation becomes hemorrhagic and even necrotic, the alvine discharges varying in character with that of the inflammation. 176 GENERAL PATHOLOGY Malta Fever or Mediterranean Fever Malta fever is a specific infectious disease, clinically resembling typhoid fever, and characterized pathologically by swelling of lymphoid structures, as Fever's patches, spleen, etc., and with ulcerative inflammation of the large bowel, and due to the Micro- coccus melitensis. It is conveyed by means of the milk of infected goats, and probably in other ways. The disease is practically un- known in this country. Anthrax Anthrax is an infectious disease due to the B. anthracis, occur- ring in cattle and sheep (splenic fever) and communicated to man, in whom it is known as malignant pustuU and wool sorters' dis- ease. Inoculation of the skin causes an intense local inflammation, consisting of a rapid infiltration of the part with leucocytes, great edema and large numbers of the bacilli. Pustules form which dis- charge a bloody fluid and become covered with crusts. The pus- tules or ulcers are intractable owing to rapid invasion of surround- ing tissues by the bacilli, which also enter the blood stream, and always cause a hemorrhagic splenitis. Any internal organ may be involved in the general infection. When inhaled, as in wool sorters' disease, a severe, atypical lobu- lar pneumonia results, usually with involvement of the mediastinal tissues, endocarditis and pleurisy. A typical case of anthrax presents the most conspicuous example of septicemia or bacteremia (more specifically in this connection, a bacillemia) to be found in the study of infectious disease. Im- mense numbers of anthrax bacilli occur in the circulation, clogging the capillaries of organs and tissues, and apparently giving weight to the early theory that death was due to internal asphyxiation. Moreover no toxin, extracellular or intracellular, has been dem- onstrated. It is probable, however, that these bacilli, as all other pathogenic bacteria, form some kind of toxic substance, since death has occurred in some anthrax infections in the absence of large numbers of the bacilli in the blood vessels. Antisera have proved successful in some cases, while vaccination of cattle has been uni- formly successful as an immunizing measure. PATHOLOGY OF [NFECTIOUS DISEASES 177 Malignant Edema Malignant edema is an intense infection due to the B. edematis maligni (Koch), characterized by rapid edematous swelling- of the subcutaneous tissues with suppuration and frequently necrosis. The organism is anaerobic and does nol enter the blood stream. Infection occurs through traumatisms, and is rare. Gaseous Edema Gaseous edema or infectious emphysema is an infection due to the B. aerogenes capsulatus (Welch). It causes an edema of the tissues with gas formation at the area of inoculation, usually the subcutaneous tissues. The whole body may be invaded. Rapid necrosis is apt to follow. Postmortem examination shows gas bub- bles in the internal organs and in the blood, rendering this fluid foamy. Infection takes place through abrasions of the skin or traumatisms, as compound fractures. The infection is very grave, but fortunately not very frequent. Postmortem gaseous edema takes place by invasion of the tissues from the intestinal tract, in which the bacillus is found as a parasite. Bubonic Plague Bubonic plague is a general infection due to the B. pestis. The disease is common in the rat, ground-squirrel and other rodents, and transmitted to man by the rat flea and probably other insects. There are three forms of the disease: (a) the bubonic form, in which polyadenitis is the conspicuous feature. The bacilli are carried from the seat of inoculation to the nearest lymphatic glands which become swollen and inflamed (primary buboes). From these the bacilli are carried by the blood stream to the glands of the body generally (secondary buboes). There is a great tendency to capillary hemorrhage into the surrounding tissues, due to the action of the toxin upon the capillary walls, setting up an intense hemorrhagic inflammation (periadenitis). The glands are greatly swollen, red and hemorrhagic; later they soften and suppurate. Microscopically the blood vessels are congested, inflamed and their lumen often plugged with bacilli. The lymphoid and endothelial cells are proliferated and the bacilli fill the lymph sinuses. 178 GENERAL PATHOLOGY (b) The pneumonic form may result from the bubonic form or be directly contracted through inhalation of the virus from an- other diseased individual. A lobular form of pneumonia results, attended with marked edema and hemorrhages into the lung tissue. There is a mucopurulent bronchitis, and the peribronchial lymph glands are involved. This is the most fatal form of plague, as well as the most contagious. (c) The septicemic form is commonly the terminal condition of the bubonic and pneumonic forms, but at times plague septicemia occurs without distinct buboes or marked inflammation of the glandular tissues. In all forms the liver, kidneys, spleen and bone marrow are usually congested and enlarged, and show areas of hemorrhage, necrotic foci and the presence of the bacilli. The toxin is apparently intracellular. The use of antisera and of prophylactic vaccines has been more or less successful. Influenza Influenza is an infectious disease, often occurring in epidemics, less often in pandemics and characterized by inflammation of the respiratory tract, gastrointestinal tract, meninges and other parts. The exudate is mucopurulent, and often bloody. In 1892 Pfeiffer found in the blood and sputum of influenza patients a very small bacillus, which was named the B. influenzal and regarded as the specific cause of the disease. But the recent pandemic (1918-1919) has failed to confirm this view, the ma- jority of investigators apparently believing that the B. influenzae is merely an associated organism or secondary invader of the tis- sues. This bacillus is found in a majority of uncomplicated cases of influenza, and in the secondary pneumonia, endocarditis, otitis media, meningitis, etc., as well as in the blood. Pneumonia is the most frequent complication, and is usually an atypical and bilateral bronchopneumonia, of a more or less hemor- rhagic type. In some cases the areas involved are lobar rather than lobular in extent. The B. influenza?, pneumococci and strep- tococci, either alone or in association, are the chief causal factors of the pneumonia. PATHOLOGY OF [NPECTIOUS DISEASES 179 Epidemic Conjunctivitis Epidemic conjunctivitis ("pink eye") is a. catarrhal or muco- purulent inflammation of the conjunctivae, due to the Koch- Weeks bacillus, which resembles the B. influenza in morphology and staining reaction. Whooping Cough or Pertussis Whooping cough is a specific infectious inflammation of the upper air passages, occurring usually in childhood and character- ized by a paroxysmal, convulsive cough. A short oval bacillus Mas discovered in the bronchial exudate by Bordet and Gengou, and named B. pertussis. Later the organism was found in great numbers lying between the cilia of the tracheal and bronchial epithelium. It can be found in large numbers in the early stages of the disease, but later other organisms, especially the influenza bacillus, outgrow it. Bronchopneumonia is a frequent complica- tion of pertussis, and tuberculosis a moderately frequent sequela. Vincent's Angina Vincent's angina is an acute infectious inflammation of the tonsils, spreading to the pharynx, characterized by superficial ulceration and pseudomembrane formation, due to an anaerobic organism which in the early stage of its life history is a spindle- shaped bacillus (B. fusiform is) and later becomes a spiral form (Spirochuta vincenti) both forms appearing in the exudate and in artificial cultures. Relapsing Fever Relapsing fever is a specific infectious disease, due to the Spiro- chuta obcrmcicri, and characterized by a peculiar febrile course; viz., three or four periods of five to seven days each of high tem- perature, separated by periods of equal length, in which the tem- perature is normal or subnormal. The spirochete is usually classed among the flagellated protozoa, but Novy and Knapp have demonstrated that it has many of the characteristics of bacteria, and its classification must at present be considered as undetermined. 180 GENERAL PATHOLOGY The spleen and lymphatic glands are enlarged and often the seat of various forms of degeneration or necrosis. The organisms occur abundantly in the blood, and were discovered by Obermeier in 1873. THE HIGHER BACTERIA ( Trichomycetes, Chalamy dobacteriacese ) These are filamentous forms (see page 153) which are inter- medial e between the true bacteria and the molds. Great confu- sion prevails in the classification and nomenclature of the organ- isms, but the following varieties are usually recognized: Leptothrix — thread-like filaments, showing no branching forms. Cladothrix — thread-like filaments, showing false branching forms. Nocardia (Streptothrix) filaments, showing true branching forms. Actinomyces — radial filaments, showing true branching forms. The Nocardia form spores, which usually appear in chains; the actinomyces are further characterized by formation of club- shaped ends at the periphery of the rosette-like colony, and by the absence of spore-formation. The bacilli causing tuberculosis, diphtheria and glanders some- times exhibit branching forms, and are believed by many to be- long to the higher bacteria. Leptothrix Infections, (Leptotrichoses) The common saprophyte of the mouth (L. buccal is) may accord- ing to some observers become pathogenic and form white patches on the tonsils and other parts of the mouth. The organisms are regarded, however, by most pathologists as merely associated or- ganisms or secondary invaders. Cladothrix and Nocardia Infections or Mycoses The difference between true and false branching has not been definitely established; false branching being merely an apparent branching due to the fact that portions of fragmented filaments assume the position of branches to the main stem; hence all that can be stated definitely at present is that organisms belonging to one or the other of these groups have been found in a causal relation in abscesses of the brain, in lesions of the lungs resem- PATHOLOGY OF INFECTIOUS DISEASES 1*1 bling tuberculosis very closely, and in other Locations. Mos1 ob- servers, however, are inclined to regard the pathogenic forms as belonging to the Mocardia (or Streptothrices), while the Clado- thrices are believed to be harmless saprophytes. Actinomycosis This is a chronic infectious disease due to the Actinomyces bovis. In cattle the lower jaw is principally affected ("lumpy jaw"), le ss frequently the upper jaw, tissues of the neck, the tongue ("wooden tongue") and rarely other parts. In man the disease occurs occasionally, affecting the mouth, lungs, and ab- dominal organs. The invasion of the organism results in the formation of a hard nodule which slowly increases in size and infiltrates and destroys Fig. 67. — Actinomycosis of the tongue, a. actinomyces granule; b and c, cellular nodules; d, transverse section of muscle; <• and /, connective tissue. (Ziegler.) adjacent tissues, whether these be soft tissues or hone. In the lungs the lesions often resemble tuberculosis. Microscopically there are round cell infiltration, proliferation of connective tissue cells and formation of granulation tissue rich in leucocytes. Occasionally giant cells appear. Later suppuration and necrosis result. Some- times repair processes proceed in one portion of the affected area while softening advances in another, causing considerable dis- figurement. Diagnostically the essential feature is the presence of the para- site itself, which is visible to the naked eye as a gray or yellow "sulphur granule." These granules crushed between two glass slides are seen to be composed of one or more rosettes made up of 182 GENERAL PATHOLOGY radially disposed filaments ("ray fungus") with club-shaped bodies at the periphery, and usually coccoid in the center, which may be degeneration products or contaminating cocci. (Fig. 67.) Mycetoma, or Madura Foot of India Mycetoma, or madura foot of India, is due to the Actinomyces madurse, which grows upon certain thorns whose prick causes the development of slowly growing, marble-like hard nodules on the foot, or rarely upon the hand. These nodules suppurate in Fig. 68. — Blastomycosis. Old partially healed ulcer of the leg. (Irons and Graham.) one or two years, the pus containing white, black ("melanoid form") or rarely red granules. Blastomycosis or Saccharomycosis Blastomycosis is an infection caused by yeasts (blastomycetes) , a generic term for fungi which reproduce by budding. These cells are oval or spherical (1-40/x) and nucleated. Only a few yeasts appear to be pathogenic. The first fatal blastomycosis, reported in 1894, showed an ulcerous inflammation of the tibia, with metas- tasis to the internal organs and the lymph glands. A number of PATHOLOGY OF INFECTIOUS DISEASES 183 cases of blastomycetie dermatitis have been observed; they begin as papules which ulcerate and spread, and run a chronic and usually fatal course. (Fig. 68.) Oidiomycosis Oidiomycosis is an extremely fatal disease, so far observed eh icily in the San Joaquin Valley, California. It was at first thought to he due to protozoa, and called coccidioidal granuloma, but is now known to be due to an organism resembling both yeasts and molds. Small tumor-like growths are formed, followed by fatal generalized infection in most instances. Thrush, or Soor, is a fungus growth found in the mouth, es- pecially of bottle-fed infants. White patches, composed of the organisms and epithelial debris, form on the palate and other parts. The causal organism — oidium albicans — grows on all media, forming both buds and mycelial threads, hence is regarded by some as a yeast, and as a mold by others. Mycoses due to Molds, or Hyphomycetes Hyphomycetes, or molds, are fungi characterized by growing in long threads or filaments (hyphce), which form a felt-like mass (mycelium). The hyphae develop from single cells, often become branched, and finally at the tip of the terminal hypha? sporangia develop, which contain endospores. Some molds, however, form chains of budding exospores. Favus, or Tinea favosa is a dermatomycosis due to a mold — Achorion shoerileinii — which forms a yellowish moss-like growth on culture media. Favus is characterized by the formation of yellowish, concave, scaly crusts composed of the mold and des- quamated epithelium. The hair follicles in the diseased areas are usually penetrated by the mold. Ring*worm, or Tinea trichophytina, is a mycotic inflammation of the skin, tending to spread in a centrifugal manner, and char- acterized by the formation of grayish, crusty rings of infiltrated inflammatory tissue, the center of which tends to heal while the peripheral part advances. The hair follicles are invaded by the organism, causing looseness and brittleness of the hairs. This dermatomycosis is due to the Trichophyton, of which there are two chief varieties, the microsporon with spores 2[x to 3/i in 184 GENERAL PATHOLOGY diameter, found most frequently in ringworm of the scalp, and megalosporon with spores three times as large, found most fre- quently in ringworm of the body. The organisms are best ob- served by extracting a diseased hair in and about the root of which parallel rows of spores may be seen enclosed in delicate threads of byphae. (Fig. 69.) Tinea tonsorans affects the scalp, and occurs most frequently in children. Tinea circinata affects the body, particularly the moist folds of the skin. Tinea sycosis, or "barber's itch" is a follicular inflammation of the hairs of the beard, attended with active in- flammation and often abscesses of the sebaceous glands. Tinea 'i A A — t, ; 8 J ' A 1 ** % <* *•• . :, «». «■',> » •:»»«.! » • ^« « ' '• * . : j."".* 1 . : .**•£ *•} ft •» • r • \.-: X 1 I ♦ * • ■ SJ- I* , VJi-.^ 1 Fig. 69. — Invasion of a human hair by trichophyton: A, Points at which the parasitic fungi coming from the epidermis are elevating the cuticle of the hair and entering into its substance. Magnified 200 diameters. (Sabouraud.) versicolor, or pityriasis, due to the fungus, microsporon furfur, consists of yellowish brown patches of desquamated epithelium in the upper layers of the skin, without active inflammation or in- volvement of the hair follicles. Sporotrichosis is a subacute mycotic inflammation of the skin, and sometimes of the mucous membrane, characterized by the formation of nodules resembling gummata (syphiloid type) or cutaneous tuberculosis (tuberculoid type) and often by multiple abscesses. When the mycosis becomes generalized, affecting deeper tissues or internal organs, it is apt to be fatal. The causal agent is a Sporothrix, which in lesions has the appearance PATHOLOGY OF [NFECTIOUS DISEASES 185 of oval yeast-like bodies, but in cultures forms long mycelial tli reads. Other molds, belonging to the genera, Aspergillus, Mucor, Peni- cillium, etc., have occasionally been observed in pathologic condi- I ions, both local and general. The diagnosis of these mycoses, as in all east's of infection with the higher bacteria, yeasts and molds, pests upon the identification and demonstration of the organisms in the 1 issues. THE PROTOZOAN INFECTIONS Protozoa are unicellular animal organisms, ranging from 3 Hiiera to several centimeters in length. They contain one or more nuclei, and the cytoplasm presents an outer portion (ecto- plasm) concerned in prehension of food, excretion and locomo- tion, and a central portion (endoplasm), which is more granular and contains the digestive vacuoles and the nuclei. The major- ity of pathogenic protozoa have now been successfully cultivated. Protozoa are divided into the following classes : I. Rhizopoda (Sarcodina), which have changeable protoplasmic processes (pseudopodia). To this class belong the genera Ameba and Entamcba. II. Mastigophcra, which have flagella. The principal order is the Flagellata, to which belongs the genus Trypanosoma. III. Sporozoa, which have no flagella or cilia and which repro- duce by sporulation. Here are found the genera Plasmodium, Piroplasma and Coccidium. TV. Infusoria, which have cilia. The principal subdivision is the Ciliata, to which belongs the genus BaJantidium. Amebic Dysentery Amebic dysentery is an infectious inflammation of the mucosa and sub mucosa of the large intestine, due to the Entameoa his- tolytica, which measures 15 to 50//, and is round when at rest; its pseudopods are short and blunt, and its ectoplasm and endoplasm are well differentiated, thus differing from the Ameba coli (En- tameba coli), found in normal human intestines and regarded as harmless parasites; these are smaller and their ectoplasm and endoplasm are but slightly differentiated. The pathogenic amebre are said to pass between the epithelial cells, enter the submucosa, causing inflammatory infiltration and 186 GENERAL PATHOLOGY fibrinous exudation, leading to ulceration. The whole colon or only localized areas may he affected. The ulcers vary in size from 2 mm. to 2 cm., and have undermined edges, and yellowish red bases. The disease generally becomes chronic, and the submucosa greatly thickened. Stenosis of the colon may result from the healing and contraction of the ulcerous areas. The arnebae may enter the mesenteric blood vessels, reach the liver and cause focal necrosis or multiple abscesses, or occasionally a single large abscess. Amebae are frequently found in the mouth, in tartar of the teeth, in carious teeth, abscess of the jaw and in pyorrhea areo- laris, but their causal relation to these conditions has not been proved. Fig. 70. — Trypanosoma gambiense. (Todd.) Trypanosomiasis The trypanosomes include certain flagellates swimming free in the blood of man and animals. The cell body is elongated and averages 1.5x25/*. It has a long flagellum at the anterior end and an undulating membrane projecting from one side like a fan. Reproduction usually takes place by longitudinal fission. (Fig. 70.) The following are the more common pathogenic trypanosomes: T. evansi, causing surra in horses and cattle — transmitted by flies. T. bruci, causing nagana in horses and cattle — transmitted by tsetse flies. T. equiperdum, causing deurine ("horse syphilis'"') — transmitted by coitus. T. gambiense, causing sleeping sickness of Central Africa — transmitted by the bite of the Glossina palpalis, a fly belonging to the same genus as the tsetse fly, which causes nagana. PATHOLOGY OF [NPECTIOUS DISEAS 187 The T. gambiense measures 1 to - 17 to 25fi including the fla- gellum. Tlu> membrane usually crosses the body and motion is very active due to the screw-like rotation produced. Human trypanosomiasis occurs in two stages; in the first the organisms occur in small numbers in the blood, but may be absent for days at a time. There is slight fever and glandular enlarge- ment. After several months or even several years, the second stage begins in which the patient becomes apathetic and drowsy, emaciation progresses and finally complete coma sets in, followed by death in six or eight months from the beginning of the second stage. The organisms are found in the blood and cerebrospinal fluid in This stage. The spinal fluid is cloudy, and the postmortem findings show a meningo-encephalomyelitis and enlargement of the spleen, liver and lymphatic glands. Leishmaniases The Leishmaniases include two tropical visceral and one cuta- neous disease. Kala-azar, or dumdum fever (India and Africa) is due to the Leishmania donovani, organisms belonging to the flagel- lates and related to the trypanosomes. The disease is characterized by splenomegaly, enlarged and cirrhotic liver, both organs being filled with the parasites, progressive anemia and remittent fever, running a course of six to nine months, with a mortality of 96 per cent. Infantile kala-azar or Splenomegaly is probably identical with the above type, occurring in the Mediterranean countries. Oriental sore or delhi boil is due to Leishmania tropica and characterized by ulcerating nodules on the face and elsewhere. Malaria Malaria is a protozoan disease, characterized by paroxysms of chills, fever and sweating, and anemia due to destruction of the red blood cells. It is due to the Plasmodium or Hematozoon ma- lariae (Laveran). This protozoon has two life cycles — one in man (the intermedi- ate host) and one in the Anopheles genus of mosquito (the true or definite host). "When man is bitten by an infected mosquito, spores (or merozoites) of the Plasmodium enter his red blood 188 GENERAL PATHOLOGY cells, grow upon its substance and dissolve its hemoglobin, until the parasite becomes as large or larger than the cell, swelling the latter until only a faint ring remains. Then division (seg- mentation or sporulation) takes place, occurring more or less simultaneously in all the organisms, thus accounting for the par- oxysms of the disease. Segmentation destroys the red cell, and the young protozoa escape into the blood plasma and each enters a new red cell to produce a second generation. AVhile most of the organisms divide as just described there are some which grow to full size, destroy the red cell, but do not segmentate. These "extracellular bodies" are finally eliminated, unless a ma- larial patient be bitten by the mosquito and some of these bodies be sucked up with the blood. In the stomach of the mosquito, these bodies, which are sexually differentiated (gametocytes) find conditions favorable for sexual development ; Avhen the fe- male cell becomes fertilized, it penetrates the stomach wall and becomes encysted, and when the cyst ruptures the sporozoites migrate throughout the body of the mosquito, accumulating par- ticularly in the poison gland (a modified salivary gland) and are thus in position to be inoculated into man. Stagnant pools, swamps, etc., are not the habitat of the Plas- modium, but merely the breeding places of the mosquito. It is the female of about seven or eight species of the Anopheles genus by which infection occurs. The following features serve to distinguish the Anopheles from the common mosquito (Culex) : The Anopheles The Culex The palpae of both sexes nearly The female palpae very short, equal to proboscis. the male palpae very long. In resting on perpendicular The body is parallel to the wall. wall, the body is inclined at angle. The wings are spotted usually. Wings never spotted. The head, thorax, and body Lower part of body is joined to form a straight line. thorax at an angle. The larvae are parallel to the The larvae hang downward from surface of the water. the surface of the water. PATHOLOGY OF INFECTIOUS DISEASES 189 The Plasmodia are of three varieties: (1) P. vivax, causing" tertian fever, segmentates every 48 hours, i. e., on the third day, into 12 to 24 merozoites. When young the organisms are hyaline and actively motile (ameboid), bid as time for segmentation approaches they become granular and nonmotile. The fully grown parasite and the gametocytes are larger than the average red blood cell. (2) P. malaria', causing quartan fever, segmentates in 72 hours, into 6 to 14 merozoites (usually eight.) The young parasites are not actively motile. The fully grown forms and the gametocytes are about as large as the red blood cell. (3) P. falciparum, causing aestive-autumnal fever, a pernicious and often fatal type, occurs in two forms: (a) the quotidian which segmentates every day within the bone marrow and internal or- gans, into 6 to 16 merozoites. The young are actively motile. The fully grown forms and the gametocytes (which are crescen- tic, "half-moon" forms) are smaller than the red cell, (b) The tertian form segmentates in 48 hours. This would cause the oc- currence of irregular paroxysms, but distinct paroxysms are sel- dom seen in this form of malaria. Gametocytes with flagella may be seen in all types. The paroxysmal chills, fever and sweating are believed to be due to toxins liberated during segmentation. When two groups of P. vivax segmentate on alternate days, daily paroxysms, or "quotidian fever," results. Pathologically, destruction of the red cells, with melanemia, relative and absolute leucopenia, and liberation and alteration of the hemoglobin are the principal features. Hemoglobinuria occurs, and the internal organs, as liver, spleen, bone-marrow and brain are darkly pigmented. The spleen is enlarged in all cases, soft and friable in acute cases, and filled with infected red blood cells ; focal areas of necrosis are seen. In chronic cases the spleen may become enormous and sclerotic, with much of the pulp and follicles destroyed ("ague cake.") Texas cattle fever ("bovine malaria") characterized by acute fever and destruction of red blood cells, is due to the Piroplasma bigeminum, belonging to the Sporozoon class of parasites, which is transmitted by the cattle tick. 190 GENERAL PATHOLOGY Coccidiosis Coccidiosis, primarily a disease of rabbits and occasionally transmitted to man. is due to the Coccidium oviforme, an ovoid granular body, enclosed in a tough capsule, and measuring 15 to 20 by 20 to 40 miera. It occurs in the tissues, a daily of the liver, where it forms cyst-like nodules, containing degenerated host cells in which the parasites are embedded. They are found also in the intestinal epithelium, and sporulate after elimination from the body in the stools. Infection may occur by ingestion of the spores. The liver besides containing the specific nodules becomes cirrhotic. Other organs are rarely involved. The Balantidium coli, an infusorial parasite, has been found in the intestines of swine and occasionally of man, and various patho- logic conditions, particularly colonic diarrhea, have been attrib- uted to it. It is found in the stools and blood, is ovoidal in form (0.06 to 0.1 mm.) and covered with numerous cilia. INFECTIOUS DISEASES CAUSED BY UNDETERMINED MICROORGANISMS Measles ^Measles (Rubeola- is an acute, contagious disease, due to a filterable virus, i.e.. a microorganism small enough to pass through the pores of a porcelain filter, the filtrate causing the disease when susceptible animals are inoculated. Pathologically there is mild pharyngitis, rhinitis and conjunc- tivitis with a mottled eruption of the skin, consisting of brick- red, slightly elevated, papules, which run together to form eres- eentic patches. The skin is hypereinic and slightly swollen, par- ticularly upon the face. The eruption is followed by a powdery desquamation. Both the eruptive lesions and the desquamated scales contain the virus, and may convey the disease, this being true also of other exanthemata, or diseases attended with char- acteristic skin eruptions. In severe cases of measles bronchopneumonia and nephritis may develop. In the severe and usually fatal form — the black mea- sles — the toxemia is great, and the eruption becomes hemorrhagic and dark. PATHOLOGY OF INFECTIOUS DISEASES 191 German Measles German measles, or rubella, is a mild contagious disease, char- acterized by red punctate spots in the pharynx, followed by more or less circumscribed spots on the reddened skin, which do not fuse to form mottled patches, as in measles. Swelling of the postcervical glands is seen, and rarely there may be distinct pharyngitis, bronchitis, etc. Chicken Pox or Varicella ( Ihicken pox, or varicella, is a mild contagious disease char- acterized by a red papular eruption which becomes vesicular. The papules are usually discrete and few in number, although occasionally they are numerous and may become very large, re- sembling pemphigus. Scarlet Fever or Scarlatina Scarlet fever, or scarlatina, is an acute contagious disease char- acterized by inflammation of the mucous membrane of the nose, mouth, throat and eyes, as in measles, but usually of greater in- tensity. The lingual papillae swell and redden ("strawberry tongue"), and the throat is spotted with fine red points. The rash, first appearing upon the body and spreading to the ex- tremities, consists of small red spots which fuse as the skin swells, thus forming an intensely red, uniform erythema. Endocarditis, pericarditis and nephritis, as well as broncho- pneumonia are more frequent than in measles, and the glands of the neck often suppurate. In fatal cases focal necrosis is usually seen in the internal organs. Mumps, or Acute Epidemic Parotitis Mumps, or acute epidemic parotitis is an acute contagious in- flammation of the parotid, less often of the submaxillary salivary glands. Usually the glands on both sides are affected, resulting in extensive and painful swelling, due to a serous exudation. The salivary ducts and the contiguous lyinph glands are also usually inflamed, and metastatic orchitis and epididymitis are not in- frequent, especially in adults. 192 GENERAL PATHOLOGY Measles, rubella, varicella, scarlatina and mumps are distinctly the diseases of childhood or youth. Their pronounced contagious character results in early infection, and the usual life-long immu- nity conferred makes second infections or recurrences and in- fections in adults very infrequent. Acute Poliomyelitis, or Infantile Paralysis Acute poliomyelitis, or infantile paralysis, is a disease of child- hood when occurring sporadically, but in epidemic form appar- ently affects any age, though still more frequent among the young. It is an acute general infection characterized by diffuse cerebrospinal lesions, especially inflammation of the anterior horns of the spinal gray matter, with paralysis and wasting of the muscles, degenerative changes in the nerves, hyperplasia of lymphoid structures and degenerative changes in the liver, lungs, kidneys, and other organs. The pia mater and arachnoid are inflamed, accompanied by marked round-cell infiltration; groups of ganglion cells become in- flamed, degenerate and disappear and their nerve fibers neces- sarily degenerate. The whole cord becomes edematous. In se- vere and fatal cases the medulla, pons, cerebellum or cerebrum are similarly affected. The virus is filterable and is present in the brain, cord, spinal fluid, nasopharynx, blood and gastrointestinal contents. Inocu- lated into the brain of a monkey, the symptoms and lesions of the disease are said to result. Small bacteria-like bodies have been discovered, but their nature and relation to this disease have not been fully established. Direct transmission through the nasopharynx to the nervous system is the most probable mode of infection according to Flexner, while Rosenau reported the trans- mission from monkey to monkey by the bite of the common stable fly. One attack of poliomyelitis confers immunity. Acute Articular Rheumatism Acute articular rheumatism is probably an infectious disease and apparently due to a streptococcus, but this has not yet been definitely established. The lesions consist of an arthritis, the in- flammation involving all the structures of the joint, and often the periarticular structures. The joints are usually involved in PATHOLOGY OF INFECTIOUS DISEASES 193 succession (polyarthritis). The knee is the mosl frequently af- fected, then the ankles, elbows, and wrists. Endocarditis, peri- carditis or myocarditis are frequenl complications. Sudamina are common, accompanying the profuse sweating, and subcuta- neous nodes (or aggregations of round or spindle cells) as large as buck shot may sometimes be felt on the fingers, wrists, elbows and elsewhere. Dengue Dengue is an acute contagious disease of tropical origin, which lias invaded Europe, the United States, and South America. A mosquito is believed to be the eontagium carrier, but fomites may also transmit the disease. There is a polymorphous eruption on the body, face, and arms, which may be scarlatiniform, urticarial, vesicular or even pustular. Many of the joints become swollen one after another and painful ("break-bone fever" and "dandy fever" — terms given in allusion to the peculiar gait necessarily assumed). The muscles become painful and swollen. Prostra- tion, convulsions and coma occur in fatal cases. One attack does not confer immunity, three or four recurrences being reported. Yellow Fever, or Typhus Icteroides Yellow fever, or typhus icteroides is an acute infectious dis- ease, endemic in American tropics and contracted through the bite of a mosquito — Stegomijia calopus. The mosquito serves as a host for one of the life cycles of the microorganism, for an in- fected mosquito (one observed to draw blood from a yellow fever patient) can not infect a healthy person until after the lapse of at least 12 days. The unknown organism is in the peripheral blood only in the first three days of the disease, because a mosquito can convey the infection only when it bites the patient during that time; likewise only blood taken during that time will successfully inoculate a healthy person. The virus is filterable. One attack confers immunity. Pathologically there is fatty degeneration of the liver and acute hemorrhagic inflammation of the kidneys with degenerative changes in the parenchyma. Hemorrhages occur into the mucous and se- rous membranes : Icterus, albuminuria, hematemesis and fever with great prostration are the chief features. 194 GENERAL PATHOLOGY Typhus Fever Typhus fever, or ship or famiue fever is an acute contagious disease attended with a macular skin eruption (roseola?) later changing to copper-colored petechia?, catarrhal inflammation of the air passages, intense toxemia with high temperature and severe nervous symptoms — the latter simulating those of typhoid fever. The spleen is enlarged, soft and easily ruptured. The liver is swollen, soft and grayish. In severe cases gastrointestinal hemorrhages, ulcerations of the esophagus and acute myocardi- tis are observed. In fatal cases the blood is dark and fluid and rapidly putrefies. The virus is believed to be transmitted by the body louse, Pediculus vestimenti, or "cootie." Smallpox, or Variola Smallpox, or variola, is an acute contagious disease marked by an eruption upon the skin of hard, shot-like papules, which change in a feAv days to vesicles, and finally to pustules. These pocks may remain discrete or become confluent. Finally the exudate of the pustule dries and a necrotic crust forms. When the lesions are confined to the epidermis no deformity or "pit- ting" results, but if the corium is much involved cicatricial scars are formed. Other changes that may occur are diffuse suppurative inflammation of the skin, ulcerations of the mucous membranes, ulceration of the lymph glands, degenerative changes of the liver, kidneys, and spleen. In the virulent form, Variola purpura, or "black smallpox," hemorrhage into the lesions or pocks occurs, giving them a purple or dark color, often inky black. In this form death may ensue before the pustular or even the vesic- ular stages are reached. Infection is direct by means of the eruptive lesions, especially the dried pustular exudates, but the blood, secretions and excre- tions may all convey the virus. One attack usually confers life- long immunity, and vaccination with the virus of cowpox gives immunity for variable periods ranging from one year to many years. Foot-and-mouth Disease Foot-and-mouth disease, or epidemic stomatitis, is a contagious disease of cattle communicable to man, occurring in Europe and PATHOLOGY OF [NFECTIOUS DISEASES 195 America. There is swelling of the mucous membrane of the mouth with formation of small clear vesicles, and similar lesions on the udders and hoofs. In man the mouth and hands are usually affected. The virus is filterable. One attack gives im- munity. Infection follows the use of milk or contact with af- fected animals. Kocky Mountain Fever Eocky mountain fever is an acute contagious disease observed in Montana, Idaho, Wyoming, and Nevada. It is characterized by epistaxis, fever lasting one to two weeks, bronchitis, nephri- tis, hepatic and splenic enlargement, slight jaundice, moderate leucocytosis, muscular pains and a macular rash over the body which does not disappear upon pressure (except at the begin- ning.) The virus is transmitted by a tick, Dermacentor reticula- tus or occidentalis, and is contained in the blood, but is not filter- able. METAZOA Among the Metazoa (multicellular animal organisms) the fol- lowing parasites are of interest to the pathologist. 1. Helminthes, Vermes or Worms. — These are endoparasites, infestation with which is called Helminthiasis. They may be divided into : (A) Platyhelminthes, (Flat worms) — flat, bilaterally symmetrical, requiring two hosts for complete life cycle. Subdivided into: (a) Trematodes or Flukes — oval, leaf-like, unsegmented, having incomplete alimentary canal; majority hermaphroditic. (b) Cestodes or Tapeworms — tape-like, segmented, no alimentary canal; all hermaphrodites. The Flukes include : (1) Distomum hepaticum, or Liver Fluke. (2) " buski, or Intestinal Fluke. (3) " pulmonale, or Lung Fluke. (4) Schistosomum hematobium or Blood Fluke. The Tapeworms include: (1) Tenia solium, or Pork Tapeworm. (2) " saginata, or Beef Tapeworm. (3) Dibothriocephalus latus, Fish Tapeworm. (4) Tenia echinococcus, or Dog Tapeworm. (5) " nana, or Dwarf Tapeworm. (6) " canina, or Dog and Cat Tapeworm. 196 GENERAL PATHOLOGY (.15) Nematodes or Bound Worms — elongated, cylindrical, tapering toward ends, bisexual in nearly all cases, the female 1 icing twice as large as the male. These include: (1) Ascaris lumbricoides — Common round worm. (2) Oxyuris vermicularis — Thread or seat-worm. (3) Trichocephalus dispar — Whipworm. (4) Strongyloides Intestinalis (Anguillula). (5) Ankylostoma duodenale or Hookworm. Uncinaria ameiicana — American Hookworm. (6) Trichina spiralis. (7) Filaria medinensis — Guinea-worm. (8) " sanguinis hominis (F. bancrofti). (9) Eustrongylus gigas. II. Arthropoda (having "jointed feet"). These are epipara- sites, which cause various forms of dermatitis. Some are dis- ease carriers. (A) Arachnida — "spider-like" forms, air-breathing: (a) Acari — including mites and ticks. (i ) Mites (1) Leptus autumnalis — Harvest mite. (2) Acarus scabiei — Itch mite, (ii) Ticks (I) Dermacenter reticulatus — believed to be car- rier in Rocky Mountain Fever. (2) Margarbpus annulatus — believed to be car- rier in Texas cattle fever. (B) Insecta — having "cut into" or segmented bodies. (1) Pediculus capitis or Head louse. (2) " pubis or Crab louse. (3) " vestimenti or Body louse, "cootie." (4) Cimex lectularius or Bed bug. (5) Pulex irritans or common Flea. (6) " penetrans or Jigger, Chigger, or Chigoe. (7) " cheopis or Rat flea of India, Australia and the Phil- lipincs, believed to convey B. pestis which causes bubonic plague. Trematod.es. — The ova are deposited in water and developed into ciliated embryos (miracidia), which enter a small snail (mol- lusk) in which they develop into motile bodies (cercarise). These leave the mollusk (intermediate host), and swim about in the water, whence they may enter man (definitive host). Of the many fluke-worms the following only are important: Distomum hepaticum, or Liver fluke, is oval (8x25 mm.) hav- ing two suckers ("distomum") and a median genital pore con- taining male and female organs (hermaphrodite). The mature fluke-worm, yellowish brown or pink in color, is found in the I'\T1H>I,()<;y OF [NFECTIOUS DISEASES L97 bile duds of lierbivora, rarely in man, and if in sufficienl num- bers, will canst' obstructive inflammation of the ducts. In sheep tlic liver is often greatly degenerated ("liver rot.") (Fig. 71.) Distomum buski is the largest fluke-worm found in the human intestine (25-70 5-14 nun.); occurs chiefly in Eastern and South ern Asia. Distomum pulmonale (Paragonimus westermani) or Lung Fluke. — This is about one-third as large as I), hepatica, and /V-W^* ,/t .Vet. SERF "-■-MM. 'A -«• Fig. '1. — The common liver-fluke (Fasciola hepatica), enlarged to show the anatomic characters. (Afn-r Stiles.) found in cyst-like cavities in the lungs. It is apt to cause hemop- tysis (parasitic hemoptysis of Eastern Asia). Schistosomum hematobium, or Blood Fluke. — This worm is bi- sexual, the male measures 12x0.5 mm., and is white in color, the female, 20x0.25 mm., is white anteriorly and gray posteriorly. The female is attached to the male, lying in a groove on the ven- 198 GENERAL PATHOLOGY tral surface of the latter. They occur in the veins of the bladder and rectum (very rarely entering the general circulation), and cause local inflammation, ulceration and hematuria (Bilhar- ziasis of Africa and Asia). The ova, yellow, translucent and oval (1 mm.), may often be found in the urine or feces. The Cestodes, or Tapeworms Tenia Solium, or Pork Tapeworm. — This parasite is 2 to 4 me- ters long, occasionally much longer, and consists of a small head (1 mm.), spherical and dark brown in color, (scolex), with four disc-like suckers and a rostellum armed with a double row of hooklets (about 30) on its anterior end. The neck is thread- like and one inch long. The body (strobila) is composed of 600 Fig. 72. — Head of T:enia solium. (Mosler and Peiper.) to 900 segments (proglottides) which increase in size from the neck backward, becoming smaller again near the posterior end. The largest segments measure about 6x10 mm. Each segment (proglottis) is hermaphroditic and has a uterus with seven to fif- teen branches. Groups of segments may be discharged from the bowel at intervals, and each segment has independent motility. The ova develop in utero into embryos having six hooklets, and surrounded with a striated shell (onchosphere). When ingested by the hog, or rarely other animals, even man, the shells are dissolved in the stomach and the embryos pass into the tissues where they form cysts (cysticerci) and develop a scolex. The cysts are visible to the naked eye, and constitute the "measled" pork or other meat. When insufficiently cooked pork is eaten, the scolex or head l'ATIKtl.OGY OF INFECTIOUS DISEASES 199 attaches itself to the mucosa of the upper ileum and a tapeworm develops, reaching its full growth in about four months. (Fig. 72. Tenia Saginata or Beef Tapeworm. — This is twice as long and lias a head twice as large as the T. solium. The head has four suckers, but no rostellum or hooklets. The segments usually number over 1000, the largest measuring 7x20 mm. The uterus has 20 to 35 branches, and the ova are larger and more oval than those of T. solium; the segments also are more motile. The lar- va? are found in the muscles, liver, and lungs of the ox. Dibothriocephalus Latus or Fish Tapeworm. — This is the larg- est parasite of man. It is common in Asia and Europe, is gray- ish yellow in color, measures 5 to 9 meters in length and has 3000 to 4000 segments, short and broad in the middle but di- minishing toward either end. The head is very small, flattened, elongated and has a deep, longitudinal groove on each side. The ova have brown, operculated shells, and develop in the water to motile, ciliated embryos, provided with six hooklets, which enter an intermediate host, usually the pike, perch or other fresh- water fish. The complete life history of this worm is not known. The symptoms produced by the larger intestinal tapeworms are usually insignificant, and in the majority of instances these worms occasion no harm; however, when present in great num- bers, they may cause intestinal obstruction, and various reflex nervous symptoms, and occasionally grave anemic conditions, believed to be due to hemolytic poisons formed by the death and decomposition of portions of the worm. Tenia Echinococcus. — This is a small tapeworm, 2 to 6 mm. long, inhabiting the intestines of dogs, wolves, foxes, etc. It is composed of a head and three segments. The head is about one- third as large as that of T. solium, but otherwise resembles it in structure and equipment. The last segment alone is mature, and as large or larger than the remainder of the worm. The uterus consists of a central trunk with lateral branches. The ova are thin-shelled and resemble the ova of the pork tapeworm. When ingested by man the embryo passes to the liver, lungs and other parts, forming a cyst — the hydatid cyst. The hydatid or echinococcus cyst has a wall composed of two layers, an outer layer of elastic cuticle (ectocyst) and an inner, 200 GENERAL PATHOLOGY germinal layer, (endocyst). The entire cyst becomes encapsulated by fibrous tissue from the tissues of the host. From the inner germinal layer, bud-like "brood capsules" develop and project into the cavity of the cyst ; from the brood capsules scolices (heads with suckers and booklets) form as external growths. The inte- rior of the cyst is filled with clear fluid, nonalbuminous, but rich in sodium chloride and other salts. From the primal or "mother cysts," secondary cysts, "daugh- ter" and even "granddaughter cysts" may develop, each capable of forming brood capsules and solices. Thus from one ovum, thousands of solices may develop. Hydatid cysts vary in size from a walnut to an apple ; occasionally they grow to a very large size, especially when secondary cysts arise. When large they are apt Fig. 73. — T;ienia echinococcus, enlarged (Mosler and Peiper). to rupture into the peritoneum, lungs and other organs or struc- tures with fatal results. Small cysts may become inactive after a time, or die and be replaced with fatty, fibrous or calcareous ma- terial. (Fig. 73.) Tenia nana, or dwarf tapeworm, is one inch long, often less, occurring in rats and other animals and rarely in man. The inter- mediate host is believed to be an insect. Tenia canina is a worm found in dogs and cats, sometimes in man, especially children. It is 15 to 35 cm. long; its head has four suckers. The mature segments are reddish in color, and re- semble cucumbers in shape, hence also called T. cueumcrina. The Ascaris lumbricoides is a frequent parasite of man, par- ticularly of children. The female ascaris measures 20 - 35 cm. x 4 _ 6 mm. These Avorms are brown or pink in color, cylindrical PATHOLOGY OP INFKCTIOUS DISKASKS 201 ami nonsegmented, resembling the common earth worm in out- line. They are transversely striated and have four longitudinal ridges. The head is small, and the mouth is surrounded with three lips. The tail of the female is straight, that of the male is curved. Infestation occurs through ingestion of the ova, which develop into worms in the upper and middle portions of the ileum. Usually only a Jew worms are present at one time, and these Fig. 74. — Ascans lumbricoides : A, female; B, male; C, egg, magnified 300 diameters; b, head, magnified. (After Perls.) may cause few or no symptoms, but sometimes great numbers occur and may cause obstructive symptoms, or may migrate into the gall ducts, stomach, esophagus, trachea and nose. Fatal plugging of the pharynx has occurred. The parasite secretes irritating, volatile aldehydes and fatty acids, which may account for the anorexia and nervous manifestations that frequently oc- cur. (Fig. 74.) 202 GENERAL PATITOEOGY Oxyuris vermicularis, or Pin-worm, Thread-worm or Seat- worm. — These worms are small, white, round, the female meas- uring 10 x 0.4 mm. and having a straight posterior end, that of the male being curved. These parasites are very common in children. Infestation occurs through ingestion of the ova, and the worms mature in the small intestine. After impregnation the female descends into the rectum where the eggs are deposited. Many of the ova and worms are discharged with the feces, but some of the latter pass out per anum by their own movements, causing considerable irritation and nervous irritability. Emi- gration occurs principally at night and the parasites are often found upon the bed clothing. Trichocephalus dispar or Whipworm.^-The anterior end of this Fig. 75. — Male Trichocephalus dispar or whipworm. A large part of the cephalic end has transfixed a fold of intestinal mucosa. (Cohen.) worm is thread-like, resembling the lash of a whip, and the pos- terior part is thicker ("handle") and straight in the female, but curled in the male. The female is 45 to 50 mm. long, the male a few millimeters less. The ova incubate in water or mud. When ingested the embryo develops and matures in the cecum, occasionally entering the appendix. The worm attaches itself Im- penetrating or transfixing a fold of mucous membrane with its thin anterior end. It is a frequently encountered parasite, and usually quite harmless, but occasionally serious anemia has been ob- served. (Fig. 75.) Strongyloides intestinalis (Aguillula intestinales).— These small (2x0.30 mm.) worms occur in the upper intestinal tract in ATHOLOGT? OF INFECTIOUS DISEASES 203 association with certain forms of diarrhea in the tropics, bu1 its etiologic significance is not definitely determined. Ankylostomiasis, or Uncinariasis, is a disease due to the pres- ence of the hookworm. 11 is characterized by anemia, which in some cases resembles the pernicious type; the cells are greatly reduced in number and many nucleated red blood cells appear. Fig. 76. — Cephalic extremity of Uncinaria Duodenalis. Profile and front view. (After Leuckart-Gould.) Fig. 77. — Duodenum showing attached Uncinaria. (Specimen of Capt. C. F. Kieffer, U. S. A., presented to the Jefferson Medical College.) The Lone marrow is pale and fatty or gelatinous. The leucocytes are not increased, in fact may he decreased but the eosinophils usually rise to 15 or 25 per cent of the total leucocytes. The hookworm attaches itself to the duodenum or upper jejunum, causing the loss of blood by hemorrhage and by ab- sorption, and produces hemolysins. The patient becomes sal- 204 GENERAL PATHOLOGY low, debilitated and usually exhibits epigastric pain and tender- ness, with dyspnea and other symptoms. Children become stunted in growth. The disease prevails in tropical and subtropical countries — India, Egypt, Southern Europe, West Indies and the southern part of the United States. The hookworm or Ankylostoma duodenale is a short, white worm — brown or red when gorged with blood — its head bent back like a hook, and its mouth having six hook-like teeth. The female is 10 to 18 x 1 mm., the male being about one-third smaller, and having at its posterior end an expanded copulatory bursa. The ova when discharged incubate in moist, warm soil and the re- sulting larva? penetrate the skin of the feet of those who work in or pass through the contaminated soil. The parasite then reaches the lungs and passes by way of the trachea and the esophagus into the intestines. (Figs. 76 and 77.) The Necator Amcrieanus, or American, or New World, Hook- worm, is a separate genus, found in the southern part of the United States, South America and other parts. It is smaller in size and has plates or suckers in place of the hook-like teeth of the Old World hookworm, and its ova are larger, but it has practically the same life history and produces the same symp- toms and pathologic changes. Trichinosis (Trichiniasis) is a parasitic disease attended with painful myositis and extensive edema, due to the presence of the larva? of the Trichina spiralis. The larva? are ingested by those who eat insufficiently cooked, trichinosed pork. The larva? lie curled and encysted in the muscles, where they can remain alive for many years, and when ingested by man or other animals the capsules are digested and the embryonal worms liberated. They mature in the small intestine where the females (3 to 4 mm. long and twice the size of the males) are fecundated, after which the males die. Within a week 1000 to 2000 embryos are born, which enter the lymph and the blood streams, finally lo- cating in the muscles and become encysted, in which stage they are identical with the encysted stage in the hog. Hogs probably become infected by eating offal. In two or three days after eating diseased meat, nausea, vomit- ing, pain, and diarrhea usually occur. In the invasive stage there is fever, and in severe cases symptoms resembling typhoid fever PATHOLOGY OF I N i'l :< "I'll US DISEASES 205 are present. Acute myositis with mild or severe pain and in- terference with muscular function are always aoted, and leuco- cytosis with eosinophilia constituting 30 to 50 per cent of the total white cells is almost a pathognomonic sign. The mortality is 5 per cent, but in certain epidemics it is much higher. (Fig. 78.) Guinea-worm Disease (Dracontiasis) is a tropical disease due to the guinea-worm (dracunculiis medinensis) . Man is infected by the Cyclops (a minute fresh-water crustacean) and the em- bryos develop in the intestinal tract; after fecundation the male dies and the female enters the tissues through which it slowly migrates, finally (8 to 16 months) reaching the region of the an- kles, where vesicles or ulcers form, through which the worm dis- charges her embryos periodically, after which it passes from the ,;-' : ' Fig. 78. — Trichina spiralis with its connective-tissue covering: a, early stage; b, calci- fied. (Leuckart.) body through the same lesions and dies. The embryos enter the cyclops as their intermediate host. Filariasis is a disease caused by various filaria, whose larvae are found in the blood, while the parent worms are found in the tissues, the inner blood and lymphatic vessels and lymph glands. The Filaria bancrofti (F. sanguinis hominis nocturna) is a white, uniformly cylindrical worm, the female having a curved tail and the male a spiral tail. The female gives birth to larva? (0.3 mm. x8ju) which pass into the lymph stream, thence into the blood and may be seen in samples secured at night (or in daytime if the patient sleeps during the day) as small, snake-like worms whose active movements agitate the red corpuscles. In the day- time they recede into the lungs and larger blood vessels. These larvae (microfilaria) may remain in man for years, being unable to become mature worms until they enter a suitable intermediate 206 GENERAL PATHOLOGY host — the Culex genus of mosquito, which may occur when a pa- tient is bitten during a time when the larva? are in the peripheral blood. In the mosquito the larvae undergo several developmental changes and finally pass into the proboscis whence they may be inoculated into man. Pathologically the filaria may occasion no symptoms, though eosinophilia is always present, but in other cases the parent worms, which lie curled up in the larger lymphatic vessels, trunks or even the thoracic duct cause obstruction of the vessels, lead- ing to distention of tributary vessels; secondary inflammatory thickening may occur, with distention and rupture of the lym- phatics of the kidneys, bladder or other structures, causing hematochyluria, or of the scrotum, causing chylocele, etc. "When very extensive the obstruction may extend to the peripheral lym- ?M -t ^ ■ o Q._. m - Fig. 79. — Filaria embryo, alive in the blood. (F. P. Henry.) phatics with great distention of the tissues, known as Elephan- tiasis, which usually affects the lower limbs, scrotum, and less often other parts. (Fig. 79.) The Eustrongylus gigas is a brownish or red worm (the female may be 100 cm. long) which is found in the pelvis of the kidney, ureters and bladder of cattle and rarely of man, causing dilata- tion of these structures with atrophy of their substance. Leptus Autumnalis is a name applied to the larvae of the harvest mite and other mites; they possess a suctorial proboscis with which they penetrate the skin and cause greater or less irrita- tion. Acarus scabiei, or Itch-mite, is a pale, spheroidal body with bristly legs. The male (0.2 to 0.3 mm.) lives upon the surface of the skin, but the female (0.3 to 0.4 mm.) after impregnation burrows into the epiderm (thus becoming an endoparasite tern- PATHOLOGY OF INFECTIOUS DIM \ 207 porarily) laying her eggs al intervals in the epidermal tunnel, which appears as a dark line about one centimeter long, ami oftenest located between the fingers, on the wrists, elbows, axilla?, etc. Vesicles and sometimes pustules form along the course of the burrow. The ova hatch in a few days, forming six-legged larva;. (Fig. 80.) The pathologic manifestations produced by the Insecta may be summarized in the statement that some of them cause more or Fig. 80. — Female acarus (after Anderson). less annoyance by injecting an irritating salivary secretion when they bite, which occasionally causes eczema, but more often leads to secondary bacterial infection due to the scratching in- duced by the itching. The female jigger (Pulex penetrans) after impregnation bur- rows beneath the skin, as does the Acarus scabiei, especially be- tween the toes, where she lays her eggs, causing inflammation and often ulceration. CHAPTER IX 1 MALFORMATIONS The term "malformation" is used to designate an abnormal de- viation from the usual structure of parts or organs and is the result of errors or accidents in the process of development. The study of malformations, therefore, is primarily the study of embryology, because they occur during the process of intra- uterine development. While we have as yet no classification that is entirely satis- factory, the following is perhaps the best for the student. 1. Malformations by Excess. — The excess may be simply a re- dundant foreskin or a supernumerary digit, or it may be an al- most completely formed individual {double monster). Gigantism also comes under this head. 2. Malformations by Defect include those due to arrest of the normal process of development, and they fall into three groups: (a) Those due to defective development in the posterior median line. (b) Those due to defective development in the anterior me- dian line, including the structures of the umbilical cord. (c) Miscellaneous defects involving chiefly the internal or- gans. 3. Malformations by Perversion include those cases in which the development has been irregular or disorderly. Malformations by Excess In Double Monsters the duplication may be anything from an arm or leg to the entire body. In the latter event, if the de- velopment of the individuals is equal, two well-formed children result {homologous twins) ; but if one is stronger than the other, it develops at the expense of the weaker, which shrivels up or x This chapter has been written by J. Waller Reeves, M.D., formerly Trofessor of General Pathology in the Dental Department of the University of Southern California. 208 MALFORMATIONS 209 only partially develops. When there are two individuals, they are usually united by corresponding parts, and the monster is named according to the location of the union; For example, when it is at the head, craniopagus; at the sternum, stemopagus; at the xiphoid, xiphopagus (Siamese twins); etc. Malformations by Defect (a) Malformations Due to Defective Development in the Pos- terior Median Line. — 1. Those due to failure of the neural groove to form the neural canal. (a) Ancncephalocclc, in which all the brain is missing. (b) Open spina bifiela, an absence of all the structures covering the medullary canal. These two forms are incompatible with life, and of little in- terest. (c) A minor degree of spina bifiela. These cases show a tumor in the lumbar region, which may contain: (1) a cavity continuous with the central canal and surrounded by all the structures of the cord {syringomyelocele) ; (2) part of the cord with its membranes (myelonieningocele) ; or (3) only the cord membranes (menin- gocele). (d) Similar pouches in connection with defects in the cranium, Avhieh may contain (1) a cavity continuous with one of the ven- tricles and surrounded by brain tissue and the membranes (en- eephalocele) ; (2) brain tissue and . membranes (encephalomenin- gocele) ; or (3) membranes only (meningocele). 2. Malformations occurring after the cranium and spinal canal are formed. (a) Microencephalia (small brain) and micromyelia. (b) Irregular defects of the cortex. (c) Hydrocephalus, in which there is an abnormal increase in the amount of fluid in the ventricles (internal hydrocephalus) or surrounding the brain (external hydrocephalus). The cranium may reach an enormous size. (b) Malformations Due to Defective Development in the An- terior Median Line. — 1. Irregularities in the fusion of the maxillary and nasal proc- esses. 210 GENERAL PATHOLOGY Harelip and cleft palate, which will bt taken up in detail later. 2. Irregularities in tht closing of the branchial clefts. Fistula in the neck. 3. Umbilical ht rnia. 4. Meckel's diverticulum is formed by the persistence of the omphalomesenteric duct, and is given off from the ileum between L c \ >4) \ B ) _*i j V ^A X* } \ i Fig. 81. Fig. 82. (After His.) C, frontonasal process; B, Fig. 81. — Head of fetus at end of fifth week, maxillary process; A, mandibular processes. Fig. 82. — Head of fetus in the seventh week. (After His ) A, the now united man- dibular processes; B, the maxillary process; C, frontonasal process; D, lateral nasal proc- ess; E, globular processes attached to the nasal part of the frontonasal process. The central nasal processes are separated from the lateral on each side by the lateral nasal grooves, which represent the anterior nares. 12 and 36 inches from its lower end. It is present in about 2 per cent of persons. 5. Yesiced fistula, the bladder opening through the anterior ab- dominal wall. 6. Epispadias, the urethra opening above the penis. 7. Hypospadias, in which the urethral opening is on the under surface of the penis or through the scrotum. 8. Imperforate anus. MALFORMATIONS 211 (c) Miscellaneous Defects. — One or both kidneys may be tab- ulated or horseshoe-shaped, the testieles undescended, viscera transposed, etc. The various forms of clubfoot, intrauterine amputations and congenital hip dislocation may also he classed under this head. Malformations of Perversion are too numerous and varied to be described in detail. Fig. 84. — Almost complete single harelip Fig. 85. — Diagram of median hare- lip. (After Blair.) Harelip and Cleft Palate These malformations are due to a failure of complete union of the maxillary and nasal processes. (Figs. 81 and 82.) Harelip involves the upper lip, and is usually, though not al- ways, complete, through the entire lip into the nostril. It may be single or double, and is very rarely in the median line. It may or may not be associated with cleft palate. Figs. 83'. 84, and 85.) Cleft palate may involve the soft palate only, or both hard and soft palates, and may be either single or double. The va- rious forms are shown in Figs. 86 and 87. 212 GENERAL PATHOLOGY Fig. 86. — Cleft of the hard and soft palate. (Federspiel.) Fig. 87. — Complete double cleft in an infant. (Blair.) PART II DENTAL PATHOLOGY CHAPTER X INTRODUCTION Dental pathology is the study of dental and oral disease in all of its aspects. Dental and oral disease is any structural or phys- iologic deviation from the normal in the hard tissues of the teeth, in the pulp, in the peridental membrane, in the supporting os- seous structures (i.e., the alveolar process), in the gingivae and gums, in the soft tissue lining of the mouth, and in the salivary glands. The study of the anatomic changes in cells, as the results of disease-producing influences, is concerned with morbid anatomy and morbid histology, or as generally termed, pathologic anatomy. The study of altered function resulting from abnormal degrees of irritation of any kind is concerned with morbid or pathologic physiology. We shall endeavor throughout the book to discuss dental diseases from both viewpoints. The conditions giving rise to disease, whether predisposing or exciting, are included in the study of etiology, which has refer- ence to the cause, or group of causes which give rise to ana- tomic or physiologic deviations from the normal. Predisposing and Exciting Causes If man were to live a better regulated life than is generally possible in this age of intense physical and mental needs, par- ticularly so in regard to proper diet, clothing, ventilation, ex- ercise, rest, both physical and mental, and sleep — doubtless the toll of disease would be much less than is actually the case. The functions of the tissues and organs of the body would be car- 213 214 DENTAL PATHOLOGY ried on, after the stage of maturity had been reached, in such a way as to make up for functional disuse without undue stress on any of the body structures, and this state of functional balance would be accompanied by the expression of a maximum of power on the part of the cells and fluids of the body to resist bacterial infection. The vital resistance would be at its highest. As it is, the degree of vital resistance varies frequently, at times being high (i.e., nonreceptivity to bacterial infections), and at others below par, or low (i.e., receptivity to bacterial infection). A de- gree of vital resistance below the maximum for a given individual predisposes to and makes possible the onset of disease. Lowered Vital Resistance The conditions which lower vital resistance are improper cloth- ing, extremes of temperature, errors of diet in either quantity or quality of food, faulty metabolism (defective assimilation, elimination or both), excessive use of alcoholic beverages, poor ventilation of living quarters, continued dampness, mechanical and thermal irritation, foci of chronic infection, chemical poisons, addiction to drug forming habits, anatomic abnormalities, men- tal depression, etc. In the presence of any one or more of the foregoing conditions the power of the human organism to ward off a bacterial invasion is minimized, and the microorganisms which first enter any portion of the body, being enabled to prop- agate the infection soon acquires a degree of virulence which is manifested in various kinds and degrees of cell degeneration or death. Vital resistance below par renders the individual sus- ceptible to disease. Exciting Causes "While some of the conditions enumerated under the heading of predisposing causes play an important role in the development of disease of bacterial origin, it is to be borne in mind, however, that there are diseases whose etiology can not be directly as- sociated with the presence of bacteria. It is then that abnormal food supply, sudden extremes in temperature, mechanical forces, chemical poisons, congenital anatomic deviations, and changes in the external or internal secretions — all of these without bac- terial infection, have to be included in the group of exciting INTRODUCTION 215 causes. Thai is to say, any one or more of the nonbacterial factors may incite a diseased state regardless of any bacterial activity. In the so-called diseases of metabolism, for instance, pathogenic bacteria are, strictly speaking, no1 concerned, and it' concerned, are secondary to the primary etiologic causes. The condition of 1 lie individual will depend upon the normal or ab- normal assimilation of f 1. this being governed by the quality and quantity of the digestive secretions. Again, pathogenic bacteria are excluded as causative factors in such pathologic con- ditions as rickets, myxedema, cretinism, exophthalmic goiter, Addison's disease, hyperglycemia, diabetes, arteriosclerosis, val- vular disorders, i Predisposing' Causes of Dental Disease In diseases of the teeth and associated structures, the predispos- ing cause may be found in an impairnu nt of circulatory activity. This is often brought about by the existence of a systemic dis- order. Consequently, that which from the standpoint of the phy- sician is the manifestation of an exciting cause — disease — from that of the dentist it must be considered as the predisposing cause of the dental and oral disorder. We know, for instance, that after the removal of all sources of irritation to the peridental membrane, alveolar process, and gingivae in a case of true pyor- rhea alveolaris, not infrequently the pathologic process con- tinues. The structures concerned at no time develop the max- imum of vital resistance necessary to overcome the bacterial ele- ment concerned in the process. This lessened resistance in the supporting tissues may be the result of abnormal circulation fol- lowing, for instance, some error of metabolism. This would be caused, for example, by the presence in the stomach of an in- sufficient amount of hydrochloric acid (hypochlorhydria). From the physician's standpoint hypochlorhydria is the exciting or direct cause of the digestive disorder to which it has given rise, while from the dentist's standpoint, hypochlorhydria is only the predisposing cause of the dental disorder, for the reason that it has brought about errors of metabolism which prevent the de- velopment of a sufficient degree of vital resistance in the in- vesting tissues of the teeth and retard or prevent the eradication of the infectious processes around the teeth. Any systemic con- 216 DENTAL PATHOLOGY dition which is a deviation from the normal, and which is the result of a combination of exciting causes, may become the pre- disposing cause of a dental or oral disease. Disease, general or dental, itself is not a separate entity, out may be defined as abnormality in structure, in function, or in both com- bineel. 1 The general division of disease into organic and functional, im- plying in the former case alteration of cellular structure, and in the latter alteration of physiologic function without alteration of structure, is of doubtful value in its application to general dis- ease and to dental and oral disease. It is true that physiologic derangement may exist without any apparent structural changes, but then it is more probable that cellular changes have taken place which it is not possible to locate and analyze because of as yet a relatively imperfect pathologic technic. The conception of modern pathology, general and dental, is almost exclusively anatomic, i.e., structural changes in the cells. The changed ap- pearance of an organ which results from the changes in its cells; the study of the retrograde changes in the cells themselves by means of the microscope; the changes in the body secretions; the nature of the body excretions — these are some of the most im- portant phases in the study of pathology, whether general or dental. Gross pathology studies macroscopic changes only. Prior to the promulgation of the cell theory of disease, the study of pathology consisted almost exclusively in the observa- tion of gross anatomic changes, and in the manifestations of pathologic physiology. The conclusion that disease is the result of the sum total of the changes which take place in the individual cells consecpient upon the continued influence of irritation, ab- normal in character or amount, marks the beginning of a logical conception of general and dental pathology. 1 Stengel and Fox: Text-book of Pathology, Philadelphia, W. B. Saunders. CHAPTER XI ENAMEL, DENTIN, AND CEMENTTJM Normal Histologic Considerations It being impossible to appreciate deviations in the substance of the enamel, dentin, or cementum, — the hard tissues of the teeth — in the pulp, or in the bony or soft investing structures, without previous clear conceptions of these tissues when within the limits of normality, it becomes advisable to review the his- tology of all of them beginning with that of the enamel. We shall consider also the relation of the latter to the dentin and cementum, bearing in mind that the study of the normal charac- teristics of these tissues is undertaken as a means of facilitating the comprehension of the pathologic processes which may con- cern them. Normal Enamel The enamel, the hardest tissue of the body, is a specialized form of calcined epithelial tissue of ectodermic origin, which surrounds the crown of the tooth in its entirety and extends to the gingival line. Here it is covered by the unattached gingiva? for a distance of several millimeters. It varies in thickness from the gingival line, where it is the thinnest, to the occlusal or in- cising edges where it is the thickest. The increase in thickness is gradual and particularly Avell marked at such areas of the tooth as arc usually subjected to strong and continued friction and stress during mastication. The greater the stress to which an area of crown surface is subjected, the thicker and more resistant will be the enamel on such an area, not because of any difference in chemical composition, but because of a peculiar arrangement of the enamel rods to meet the requirements of great stress. Per- fection in development throughout the enamel is rarely encoun- tered so that in describing this tissue our aim will be to describe the microscopic appearance of an average specimen falling within the limits of normality. (Figs. 88 and 89.) 217 218 DENTAL PATHOLOGY Fig. SS. — Area of normal dentin and enamel, a, dentin; b, enamel; c, c', dentoenamel junction; e, dentinal tubuli; /, series of interglobular spaces faintly reproduced. ENAMEL, DENTIN, AND CEMENT! M 219 The components <>!' enamel are the enamel rods and the confut- ing or interprismatic substance, the latter being the binding ma- terial which holds the rods together. This substance, like the enamel rods, of ectodermic origin, is a calcified stratified-squa- limus epithelium. The rods are five- or six-sided and from three and one-half to four and one-half microns in Length. Some of the rods may he traced from the dentoenamel junction to the surface of the crown of the tooth. The cementing substance is Fig. 89. — Area of normal dentin and enamel from ground section of area near apex of incisor of man. a, dentin, showing dentinal tubules; b, enamel; c, crack in enamel made in grinding. more susceptible to the action of dilute acids than the enamel rods, so that if a section of enamel be subjected to dilute hy- drochloric or lactic acid, until the cementing substance is in part dissolved, a clear differentiation between enamel rods and ce- menting substance will be obtained. This is due to the fact that upon the removal of the cementing substance a greater dif- ference in the indices of refraction of the enamel rods and the decreased cementing substance between them will have been es- 220 DENTAL PATHOLOGY tahlished Fiy. DO... Examination of a ground section of a tooth with a 16 mm. objective does not render possible the detection of the physical peculiarities of the individual rods or of the ce- menting substance. With a higher magnification, in a longi- tudinal section the individual rods appear as a series of striations of alternating dark and light areas. It is with difficulty that a rod can be traced microscopically from its free end to the dento- enamel junction. Upon the axial surfaces the rods are more or less parallel to each other and mosl of them, according to Noyes, extend from the dentin to the free surface of the enamel. 1 That 'Hl^k. .6 Fig. 90.— Contrast between norma! enamel at a and a' ', and decalcified enamel at b and b'. they extend as single rods to the free surface of the enamel must he concluded largely from observation in cleaving enamel in the preparation of cavities for the reception of fillings. Mi- croscopically ii is practically futile to attempt to trace the rods across the section as single rods. The majority ( _,i' sections that have been examined })y the author show the tendency toward parallelism of the rods on the axial surfaces, but, on the other hand, do not show many rods traceable uninterruptedly from within to the free surface of the enamel (Fig. 91). Woyes: Dental Histology and Embryology, Philadelphia, Lea & Febiger. ENAMEL, DENTIN, AND CEMENTUM 221 Another peculiarity of enamel, within the bounds of nor- mality arc the bands of Betzius. These are better seen upon ex- amination with a low-power objective and appear as brownish striations which mark the beginning and completion of the cal- cification of sections of enamel structure. They are the boundary lines between calcification installments, and hence have been ap- propriately named by the descriptive term incremental Inns b' Fig. 91. — Ground section. Dentoenamel junction. The character of the granular layer of Tomes is unusually well shown. The hearing which this laver has upon the progress of caries should not be overlooked. This section also shows the tendency at parallelism of the enamel rods; a, a', enamel; b.b', dentin; c, c' , granular layer. (Noyes). The portions of enamel included between the dento- enamel junction and a hand of Retzius, and between the bands themselves, represent synchronous calcification installments (Fig. 92). These bands of brownish color, when viewed under a low or high amplification, run obliquely across the lengths of the enamel rods from the dentoenamel junction on one side to the 222 DENTAL PATHOLOGY dentoenamel junction on the opposite (from mesial to distal sur- faces) in the incisal region and in the cusps of bicuspids and molars. Beyond these regions they run from the dentoenamel junction to the surface of the enamel. They mark the strata of enamel in the order of their calcification. They begin at the dentoenamel junction in the region of the incisal area, and ter- a -d' J I c Pig. 92. — Ground section, longitudinal, showing the prevailing mode of junction of enamel and cementum. Inasmuch as the calcification of the enamel is completed before that of the cementum begins, the latter tissue either overlaps the enamel or the joint is of the butt type. The lines of Retzius are also seen. a. a', dentin; b,b', enamel; c, c' , cementum. In the enamel the lines running obliquely from the dentin to the free sur- face of the enamel are the lines of Retzius d, d' ; line of junction between enamel and cementum, the latter overlapping the enamel, seen at c. minate, after following a curved course, at some other point in the dentoenamel junction. Sections of enamel when examined under a low power with direct light occasionally exhibit markings or bands running at right angles to the dentin. These are the lines of Shreger and are due to "alternating uniform curvatures of the prismatic ENAMEL, DENTIN, AND CEMENTUM 223 bundles." They embody no significance, histologic and path- ologic. Recently Lodge 2 lias made an interesting study of the cause of the presence of these lines, lie has found, by superimposing two wire screens and viewing them over a white surface or by sub- dued transmitted light or by placing together two layers of a silk fabric, that the lines of Shreger can be simulated. The lines of Shreger are due, according to Lodge, to "net" effects pro- duced by light falling upon the cut enamel prisms, the optical densities varying according as the meshes of these nets are in apposition or in interference. The lines are difficult to see where the section is cut absolutely parallel to the long axis of the enamel rods, but are plainly observable when sections of the same enamel are made at 45° or more to the first-made sections. Chemically, the enamel is composed mainly of salts of calcium, with a trace of salts of magnesium, and other salts in smaller proportions. This may be outlined as follows : Calcium phosphate and fluoride 89.82% Calcium carbonate 4.37% Magnesium phosphate 1.34% Other salts .88% Organic matter 3.59% 100%' It possesses a peculiar luster, to which it owes its names. The word enamel is derived from the old French word esmail, this in turn being derived from the Latin smaltum, a term first given to a vitreous compound when fused upon a metallic surface. The surfaces of the enamel upon all the aspects of the tooth are not normally smooth, but on the contrary the enamel is "traversed on its vertical aspect by minute ridges separated from each other by corresponding 'furrows' which run parallel to each other in a direction at right angles to the long axis of the tooth. These horizontal lines are in some cases large enough to be visible to the naked eye, and must have been noticed oc- casionally by many who, like myself [Pickerill], thought at first that they were either caused by attrition or were a microscopic form of hypoplasia." 3 =Lodge. E. Ballard: Dental Cosmos, lix, 1087. _ „,.,,,.. r, o 3 Pickerill: The Prevention of Dental Caries and Oral Sepsis, Philadelphia, b. b. White & Co. 224 DENTAL PATHOLOGY This investigator has named these horizontal lines "the imbri- cation lines of the enamel" (Figs. 93 and 94). These horizontal lines are widest and the furrows between them deepest at a Fig. 93. -Imbrication lines on lower incisor of sclerotic type (Pickerill.) Fig. 94. — Imbrication lines on lower incisor of malacotic type (Pickerill.) point two-thirds the distance from the neck of the tooth to the cutting or occlusal surface. In the teeth of the uncivilized races in which dental caries is so much less frequent than in the teeth of the modern races, the imbrication lines are less marked. In ENAMEL, DENTIN, A.ND CEMENTUM 225 fact, he says, the enamel of the teeth of the primitive races is more lustrous, and the imbrication Lines arc so feeble that they .•an qo1 be brough.1 out by the graphite method of staining. In- asmuch as the more susceptible to caries a tooth is, the more marked arc the imbrication lines and the deeper are the fur- rows between them, the conclusion is reached that the character of the external surface of the enamel as to the presence of mi- croscopic CEMENTUM L'L'M Fig. 98. — A field of dentinal tubules. At a, b, and c individual tubules are plainly visible. Fig. 99. — Transverse section of dentin. The dentinal tubules are cut somewhat diagonally. 230 DENTAL PATHOLOGY the odontoblastic layer of the pulp; of a matrix, the dentin matrix, or substance occupying the spaces between the tubules; and of the sheaths of Newman, which may be sheaths of the fibrillae lying in apposition with the tubular wall or a substance more resisting to acids than the dentin matrix, and located immediately outside the tuhuli. The substance which makes up the sheaths of New- man is probably elastin, soluble only in concentrated acids or caustic alkalies, but digestible by bacterial ferments. Dentin is hard, though elastic, usually of a yellowish white color and of a slight degree of translucency. In the crown por- tion of the dentin the tubuli run a wavy course from the dento- enamel junction to the walls of the pulp chamber, and being disposed everywhere in a more or less perpendicular direction to the external surface of the tooth, radiate in various directions. In the root portion of the dentin they run for a distance only, an almost straight course at practically right angles to the long axis of the tcoth. but as the apical third of the root is approached, their direction becomes apical and a radial effect is produced. The diameter of the tubules is greater on the pulp end than on the enamel or cementum end and are in closer proximity to each other where they are the wider in diameter. The tubules anas- tomose with one another, these anastomoses being more marked in the root than in the crown. In the incisors, in the middle of the incisal region of the crown, the tubules run a course almost parallel with the long axis of the tooth, maintaining this for a short distance toward the mesio-incisal and disto-incisal angles. They then assume a course which becomes less and less oblique, until the junction of the lower with the middle third of the root, where the course of the tubules is practically at right angles to the long axis of the tooth. The tubules follow the same relative direction upon the labial and lingual and mesial and distal as- pects of the tooth in its entire length. In the incisal region, if a mesiodistal section be examined, the tubuli will be found to run from the dentoenamel junction toward the pulp chamber in a fan-like arrangement. In molars and bicuspids the tubules form an arrangement something like this: Beginning at the enamel-cementum junction and toward the occlusal aspect the tubules sweep toward the pulp chamber describing a double curve. The curve near the dento- ENAMEL, DENTIN, AND CEMENTUM 231 enamel junction presents its convex surfi toward tlie occlusal and its concave surface inward the apex. The curve a1 the rool canal wall is less marked, the concave aspect being directed toward the occlusal and the convex toward the apex. The tubules in relation to the cusp present a typical wheat-sheaf arrangement. The granular layer of Tomes, so-called because of its having been Fig. 100. — Interglobular spaces of Czerrr.ack in the dentin. Evidences of periods of arrestment of calcification of the dentinal tubules. The presence of a large number of these spaces would render more rapid the progress of caries in the areas in which they are located, by reason of the greater penetrability of the tissue to the acid end products of fermentation, a, a', a", interglobular spaces of Czermack. first described by Sir John Tomes, represents a system of inter- communication among the tubules at the dentin-cementum and dentoenamel lines. It is more marked at the dentin-cementum line than it is in the crown portion of the tooth. These spaces, produced by the widening out of the tubules, are filled with pro- toplasmic matter and are responsible for the increased sensitive- 232 DENTAL PATHOLOGY ness of dentin in these areas. Into the spaces of the granular layer in the root or crown portions of the tooth the tubules empty, so to speak, and in some instances they have been observed to pass beyond for some distance into the cementum and the enamel. Practically every specimen of enamel shows that here and there dentinal tubules penetrate its substance for a clearly perceptible distance, a condition which may render very much less unreasona- ble the observed fact that occasionally teeth are encountered where enamel responds to stimuli. b' c' ■ f£' y* * ,\suwHnaHH| 4 b — >4 KHbHBhj^H a Fig. 101. — Longitudinal ground section of tooth showing fields of dentin at a, a' and enamel at b, b' . ~ In the body of the dentin at some distance from the dentoenamel junction and the granular layer at c, c' large numbers of interglobular spaces are seen at d, d' . The granular layer of Tomes should not be confused with the interglobular spaces (Figs. 100 and 101), which are located in the body of the dentin at some distance from the granular layer. These spaces are more marked in the crown portion of the dentin and in the gingival third of the root, and are, beyond certain limits, evidences of hypoplastic phenomena (imperfect develop- ment) of the dentin matrix and dentinal tubnles. They are plainly visible in ground sections with a high or low power. ENAMEL, DENTIN, AND CEMENTUM 233 In fresh specimens they are filled with calcified or semi-calcified dentin matrix, or protoplasm. A few tubules may pass through the space. In old specimens the spaces appear dark, being filled with debris from the grinding process. They have been called interglobular spaces, (i. e., spaces between globules) for the rea- son thai similar outlines can be made by zones of spheres. Within certain limits as to size and number, the interglobular spaces may be considered as not abnormal characteristics of den- tin. Every specimen of dentin, however, is, strictly speaking, not a normal one if considered from the standpoint of the inter- globular spaces, for these must be viewed as evidences of tem- porary arrestments of development. The chemical composition of dentin may be outlined as fol- lows : Calcium phosphate, 66% Calcium carbonate, 3 to 4% Magnesium phosphate, 1 to 2% Organic matter, 27 to 28% 100% Cementum It is that bone-like tissue which envelops the root of the tooth in its entirety and which, beginning as a slender covering at the enamel line, gradually increases in thickness until the apical re- gion is reached, where it is the thickest. The cementum is de- veloped from the fibrous envelope of the tooth follicle — the so- called follicular wall. It differs from bone in that it does not contain any Haversian systems ; in that it possesses no blood or nerve supply of its own, but depends exclusively for its nutrition and innervation upon the peridental membrane; and in that from the pathological standpoint, it has no reparative power, except in so far as this occurs through the agency of the peridental mem- brane. The cementum is deposited in layers, the deposition of a new layer not beginning until the previous one is completely calcined. These layers, or lamellae, are distinguishable under low and high amplifications and represent the incremental lines of the cementum (Figs. 102 and 103). Within its substances are found the lacunae or spaces containing active cells from the follic- ular wall — the ccmcntoblasts, which became encapsulated during the calcification process. From the lacuna? a considerable num.- 234 DENTAL PATHOLOGY ber of small canals lead out, and these communicate "with similar small canals from other lacuna?. These small canals are the canaliculi and they, as well as the lacunce, as has been stated, are in healthy eementum filled with protoplasmic matter (Fig. 104). The matrix is granular in some locations and fibrous in others. In decalcified specimens in which the organic portion of the ee- mentum is adherent to the dentin, the fibrous character of the ma- trix is plainly visible in some localities. As the eementum calcifies, r -fi m Fig. 102. — Transverse ground section at the apical region of a root. In the apical region and in root bifurcations and trifurcations the eementum is the thickest. The lamellae or layers of eementum may here be seen especially at a; the dentin at b; and the root canal at c. through the agency of the eementoblasts in the peridental-mem- brane-to-be, some of the fibers of the latter tissue in its em- bryonic stage become encased in the eementum (Fig. 105). They are to be found, as seen in Fig. 105, not in proximity to the granular layer, but at some distance therefrom in eementum rather younger in development. The similarity in development between eementum and subperiosteal bone lends credence to our belief that the fibrous appearance of the eementum matrix is due to I \ will.. DENTIN, Wl> CEMENTU \l 235 the deposition of inorganic salts in a fibrous framework, and al s0 to the Pad that wherever calcification is not carried on to full completion the semicalcified libers persisl as such. These fibers bear to cementum the same relationship in genesis as Shar- pey's fibers do to bone. The lacuna of variable size and shape are practically absenl in the thin portion of the cementum (Figs. 106 and 107), but are to Fig 103— Transverse ground section of tooth at the beginning of apical third of root. Observe that here the thickness of cementum is markedly less than what it is farther apically. a, a' lamellae of cementum; b, dentin; c, root canal. be found in considerable numbers wherever the cementum is thick and in hypercementosis. They are located in areas nearer the dentin, as shown in Fig. 108, but may also be found equidis- tant from the granular layer and the external cementum surface (Fig. 109). The lacuna? are particularly abundant in the apical region and in the bifurcations and trifurcations of molars (Fig. 110). The layers of cementum next to the peridental membrane and those next to the dentin as a general rule contain fewer 236 DENTAL PATHOLOGY lacunas than those in the central portion. In hypercementozed specimens the lacunae are distributed throughout the tissue with- out regard to form, number, or arrangement. The tissue is Fig. 104. — Thick area of cementum in the bifurcation of the roots of a molar, showing lacuna" and canaliculi and intercommunication of canaliculi. characterized, however, by the presence of large numbers of lacunae. The form and size of the lacunae vary within certain limits in the same tooth, and the canaliculi branch out in ENAMEL, DENTIN, AND CEMENTUM 237 c\i:\ti.\, and ci;\ii:\ti \i a b 289 rf' a.. Fig. 10S. — Longitudinal ground section of cementum showing lacunae in areas near dentin at a; fibers of peridental membrane incased in the cementum at b. The granu- lar layer is seen at c; the width of cementum is from d, d' . I'ig. 109. — Longitudinal ground section in ginghal third showing at a, lacunas and canal iculi equidistant from granular layer at b, b' , and external cementum surface at c. 240 DENTAL PATHOLOGY the fully formed cementum the processes of the cementum cor- puscles undoubtedly anastomose with those of the peridental membrane, with each other, and with the processes of the granu- lar layer just within the dentin. 8 Fig. 110. — The cementum in the apical region of the roots of an upper first bicuspid. The section did not involve the root canal. The dark spots represent the lacunae. The chemical composition of cementum according to von Bibra is as follows : Calcium phosphate, 48.73% Calcium carbonate, 7.22% Magnesium phosphate, 0.99% Soluble salts, 0.82% Organic matter, 42.24% 100.00% If this analysis is compared to that of bone, it will be seen that cementum contains 18.90 per cent more organic matter than bone, and 8.94 per cent less inorganic matter. s Andrews, R. R.: Calcification, Dental Cosmos, January, 1912. CHAPTER X 1 1 DEVELOPMENT OF THE TEETH From the fiftieth to the sixtieth day of intrauterine life the first step in the development of the teeth becomes evident. At this time a thickening of the stratum malpighii of the oral epithelium along the peripheral area of the jaws is to he observed. This thickening of the oral epithelium progresses in the direction of the under- lying connective tissue and constitutes the dental hand or ridge (Figs. Ill and 112). The dental groove, a term frequently en- countered in connection with the embryology of the teeth, can refer only to the appearance of a transverse vertical section of a developing jaw where it will be seen that the underlying con- nective tissue has been scooped out, so to speak, the groove be- ing filled with masses of epithelial cells — the epithelial band — a term which more accurately describes the early stages of tooth embryology than the term dental ridge. If we picture, as sug- gested by Magitot, 1 a rope of epithelial cells snugly fitting into a depression in the connective tissue, it will facilitate a correct conception of the dental hand and d ratal groove, the band being the epithelial rope and the dental groove being the grooved bed in which the rope rests. The dental band is convex externally and concave internally. From the concave surface, about mid- way between the apex and the base of the band, an epithelial pro- jection — the dental lamina,— grows out lingually almost at right angles to the vertical diameter of the band. This projection does not occur at any one particular locality, but extends along the entire length of the band. A shelf growing out at right angles to the band will explain better the relationship of the dental lamina to the dental band. From each of twelve points on the dental lamina, in each jaw, an epithelial cord grows out, at first in a horizontal direction to- J Legros, Ch., and Magitot, V..: Dental Follicle. 241 242 DENTAL PATHOLOGY ward the lingual aspect of the primitive jaw, and then in a di- rection almost at right angles from the lamina. Of these cords, the anterior ten are destined to form the enamel organs of the de- ciduous teeth, and the posterior two, those of the permanent first molars, of each arch. The epithelial cord is composed of epithe- ^iaf^H Fig. 111. — First evidence of tooth development. The stratified squamous epithelium is seen dipping into the subadjacent connective tissue and forming the dental band or ridge. a, epithelial band progressing in the direction of the underlying connective tissue; b, b' , and b" , thickened epithelial layer; c, underlying connective tissue. DEVELOPMENT OF THE TEETH 243 lial cells from the lamina, and the latter, in turn, from the periph- eral cells of the dental hand. As each epithelial cord, which is an outgrowth of the dental lamina, proceeds downward and somewhat lingually, and after obtaining a certain length, it un- dergoes characteristic changes which materialize about the ninth \ J Fig. 112. — A slightly later stage than in the preceding illustration showing the begin- ning of the invagination of the epithelial cord which will result in the formation of the four layers of the enamel organ, a, epithelial cells from the more superficial or older strata of the Malpighian layer; b, younger strata from Malpighian layer from which dipping of epithelium occurs; c. epithelial cord beginning to undergo the invagination which will result in the formation of the four distinct groups of cells of the enamel or- gan; d, condensation of underlying connective tissue. 244 DENTAL PATHOLOGY week of embryonal life. These changes result in the eventual formation of the enamel organ. There occurs an upward invagination in the case of the lower enamel organs, and a downward invagination in the upper, which progresses until a hood-shaped organ has resulted which sur- rounds a condensation of connective tissue cells (the dentin-forming organ, or dental papilla). The enamel organ as now constituted .•'vf&Vjiy! mi \ b Fig. 113. — The four sets of cells of the enamel organ; a, the internal or the layer of the ameloblasts; b, cells of the stratum intermedium; c, cells of the stellate reticulum, and d, of the external layer. Portions of the follicular sac are seen at c, surrounding the dental papilla and enamel organ; from the follicular wall the cementum and alveolar process will develop. will consist of an external layer of epithelial cells; of an internal layer, which is formed from the invagination of the outer layer of the enamel hud; of a layer of cells in close contact with the inner aspect of the internal layer — the stratum intermedium; and of a number of stellate cells occupying the space between the external and internal layers — the stellate reticulum (Fig. 113). The stra- tum intermedium and the stellate reticulum originate from the inner cells of the dental lamina, and these in turn from the inner DEVELOPMENT OF THE TEETH 245 cells of the dental band. The internal Layer consists of the enamel building cells ameloblasts, or enameloblasts ; the external Layer begins to show signs of an atrophic process prior to the completion of the enamel; and the cells of the stratum inter- medium and those of the stellate reticulum are probably concerned in supplying the ameloblasts with such nutritional elements as are required by them during enamel formation. In other words, and to present a mental sketch of the germ, the enamel or- gan is a double hood containing between the external hood and the internal hood the cells of the stratum intermedium and stel- late reticulum, the double hood enclosing a specialized mass of embryonal connective tissue cells — the dental papilla, or dentin- forming organ. For a time the enamel organ remains connected to the dental lamina by means of a slender corcl of epithelial cells designated as the epithelial cord. It gradually atrophies, and by the time the thirteenth week of embryonal life has been reached, the cord is ruptured and the tooth follicle proceeds in its de- velopmental work independent of any connection with the oral epithelium. The enamel organ of all the deciduous teeth may be said to ap- pear about the eighth week of embryonic life; the dental papilla about the ninth week ; the follicular wall which encircles the tooth follicle, (i. e., enamel organ and dental papilla), rises from the base of the dental papilla and appears at the tenth week; the follicle closure and simultaneous rupture of the cord occurs about the thirteenth week; and the formation of dentin begins about the sixteenth week. 2 The enamel buds of the permanent teeth, with the exception of tin first, second and- third molars, begin to develop about the sixteenth week from the epithelial cord of the corresponding temporary tooth, the process of development being analogous to that of the temporary teeth. The first molars develop from in- dependent invaginations of the dental ridge about the fifteenth week of intrauterine life in exactly the same way as do the de- ciduous teeth (see above) ; the second molars develop from an offshoot of the epithelial cord of the first molar, about the third : Legros, Ch , and Magitot, E. : Chronology of the Dental Follicle in Man. Trans- lation by M. S. Dean. 246 DENTAL PATHOLOGY month after birth ; and the third molars develop from offshoots of the second molar, about the second or third year after birth. The calcification of the enamel proceeds from within outwards, while that of the dentin from without inwards. A divergence of opinion exists in regard to the process by which enamel is cal- cified, particularly so concerning the ultimate fate of the cells of the enamel organ. Aside from the facts that the internal epithelial layer of the enamel organ is the enamel-building layer ; that the cells of the stratum intermedium are probably substitu- tion enamel cells (i.e., they replace functionally exhausted amelo- blasts) ; and that the cells of the stellate reticulum are the agen- cies of nourishment to the active enamel-building cells — nothing based upon actual observations has so far been brought out that could be considered otherwise than as mere theories. The amelo- blasts are elongated cells which become more or less hexagonal by mutual apposition. 3 They are in close relation to the large round cells of the stratum intermedium. The cells of the stellate reticulum are connected among themselves by means of processes, a reticulated appearance being the result. The cells of the ex- ternal layer, after the cells of the stellate reticulum have atro- phied, coalesce with those of the internal layer and persist for some time after the eruption of the teeth as Nasmyth 's membrane. The enamel begins to form on the deciduous teeth about the seven- teenth week of embryonic life, ending about the sixth month after birth. On the permanent teeth it begins to form at birth or slightly before birth, and ends about the twelfth year on the crown of the third molar. 4 Dentin As has been previously noted, the dental papilla, or dentin- form- ing organ, makes its appearance about the ninth week, or ap- proximately a few days after the beginning of the formation of the dental groove by the inward growth of the dental band. The dental papilla ( dentin-f orming organ, dental bulb) is a mass of embryonal connective-tissue cells (Fig. 114), whose peripheral cells assume a quasicolumnar shape and arrange themselves in a fairly regular way. The cells have a well-defined nucleus 3 Tomes: Dental Anatomv, Philadelphia, P. Blakiston's Son & Co. 4 Andrews, R. R.: Dental Cosmos, 1912. MA ELOPMENT OF THE TEETB 247 occupying a position in the interna] third of the cell toward the denial papilla, and differ in appearance as to whether dentin is being actively produced or not. During active dentinification the ends of the odontoblasts next the already formed dentin are Fig. 114. — Same stage of development as seen in the preceding illustration. The fol- licular sac which springs from the base of the dental papilla is seen surrounding the de- veloping organ, a, follicular wall; b, dental papilla; c, internal or ameloblastic layer. expanded; at periods of arrested dentinification the cells seem longer and their ends more slender and rounded. The process of calcification of dentin (dentinification) which precedes that 248 DENTAL PATHOLOGY of enamel calcification (amelification) by a few days advances from without inwards, the odontoblasts probably discharging the calcific material so as to envelop the protoplasmic process with which each odontoblast is provided at its external end. As cal- cification proceeds, a gradual recession of the odontoblasts oc- curs, and simultaneously with this there is an elongation of their external protoplasmic processes which, occupying the lumen of the tubes thus formed, become the dentinal fibers, or fibrilhc, or fibers of Tomes. It is not at all improbable that the intt rt nbular substance (den- tin matrix) is the result of the calcification of cells from the nths after birth 40th week (birthl 30th week embryo 18th week embryo 17th week embryo Fig. 115. — Calcification of the deciduous teeth. (Peirce.) Fig. 116. — Calcification of the permanent teeth. (Teirce.) dental papilla, this process being likewise presided over by the odontoblasts. Cementum and Peridental Membrane As will be remembered, about the tenth week of embryonic life there are seen to grow out from the base of each dental papilla certain cells which become the fibrous envelope of the tooth germ (follicular wall) (Fig. 114). This closes simultaneously with the severance of the cord about the thirteenth week. This fibrous layer has a dual function: the cells of the outer layer are con- DEVELOPMENT OP THE TE] ill 2 l!» eerned in the building up of the osseous structure of the alveolar process, those of the inner layer being concerned in the building of cementum. It should be added here, however, thai a line of demarcation between the externa] and internal layer is prac- tically an impossibility. At the time of eruption of t he teeth through the gums there still remain portions of the tooth root, cementum, and alveolar process to develop. The alveolar proc- ess is produced simultaneously with the cementum in order to provide for the means of retention of the tooth in the jaw. The process of root development is best studied from the diagrams (Figs. 115 and 116). CHAPTER XIII HYPOPLASIA, MICROSCOPIC AND MACROSCOPIC In the discussion of hypoplasia in its microscopic and macro- scopic aspects we aim to describe abnormalities of the teeth in structure, size, form and number. The term atrophy will not be used for the reason that in its general acceptance it conveys the thought of retrograde changes after an organ has attained its full growth, atrophy being defined as the series of changes taking place in a fully formed organ leading to a loss of weight, size and function consequent upon such causes as overuse, disuse, excessive pressure, faulty diet, and nutritional and trophic dis- turbances. Excess of waste over assimilation leads to atrophy. The teeth, barring pathologic conditions and the physiologic wearing away of their occlusal surfaces, remain unchanged throughout the life of the individual. They are not subject to retrogressive changes through overuse or lack of use, (exclud- ing, of course, the manifestations of these conditions upon the peridental membrane, which is not, strictly speaking, an integral part of the tooth, but accessory thereto), and neither are the hard tissues improved in quality, to much of an extent, 1 after they have become calcified. Enamel and dentin have no power of repair. AVe exclude from this consideration such calcifications as take place in the dentinal tubules as a normal process with advancing age, or as the result of pathologic influences. Also are excluded increases in the thickness of eementum of a strictly pathologic character, and the increases of eementum in certain areas, or the resorptions in others which take place continuously until such time as the entire complement of teeth has erupted and the occlusion for the given individual has become perma- nently established. All changes in the eementum, constructive or destructive in character, are governed, as will be studied later in the text, by either functional changes in the peridental mem- brane or by the influence of osteoclastic (cementoclastic) cells. 1 See discussion of enamel on page 226. 250 BYPOPLASIA. MICROSCOPIC A.ND MACROSCOPIC 251 As the size, form, and structure — the latter up to certain limits — of the crowns of teeth appear after their eruption, so will they remain unaltered through life, except, of course, as the result of disease processes. DENTAL HYPOPLASIA Enamel, Dentin, and Cementum Imperfect or insufficient development of a part resulting from abnormal influences during- intrauterine life, or during develop- Fig. 117. — Hypoplastic defects of the enamel. Incomplete calcification of the fissures and faulty development of the ena.mel rods in the area of a cusp, a, incomplete fusion of the cusps of a bicuspid resulting in a defecting calcified fissure; b. disturbance in the arrangement of the enamel rods. The histological characters of the enamel rods in the area at b, are wanting. mental periods after birth, is classified as hypoplasia. Under this heading the study of developmental defects of the enamel, den- tin, and cementum will be undertaken. Etiology. — By hypoplasia of the teeth is meant incomplete, de- fective or misdirected development of the tissues of the teeth. These developmental faults may be only microscopic, or both 252 DENTAL PATHOLOGY microscopic and macroscopic in character, and are dependent for their production upon unbalanced nutritional processes affect- ing the dental follicle at any time from the beginning of its for- mation to the completed development of the tooth, which is marked by the calcification of the apical portion of the root Fig. IIS. — Hypoplastic defect of the enamel. Int ision of the cusps molar producing a defective fissure as shown at c. Areas of normal enamel at a, a' : a small area of normal dentin at b. and the establishment of the apical foramen as it will persist with whatever changes may occur in its diameter throughout the life of the tooth. The inorganic salts which enter into the formation of the enamel are not carried to the enamel organ in sufficient amounts as the result of faulty metabolism or of a diet poor in inorganic salts. Again, it may result from a defective combination EYPOPLASIA, MICROSCOPIC AND MACROSCOPIC 253 between the inorganic salts and the albuminous binding sub- stance. The periods of nutritional insufficiency may be due to path- ologic conditions in the mother which will affecl the deciduous teeth, directly, or in the advanced stages of development by hav- ing induced in the infanl changes affecting its physiological ac- tivities. It is well to remember in this connection that the be- ginning of calcification of these teeth is included in the period from the sixteenth to the twentieth week of intrauterine life. Disturbances in the mother interfering with the nutritional proc- esses in the fetus may. in some instances, affect the first per- manent molar, as the calcification of ibis tooth is known to begin in some cases one or two months before birth. The transmission from mother to fetus of certain systemic intoxications, particu- larly syphilis, may result in hypoplasia of certain teetli whose calcification does not begin until after birth. Concerning con- ditions after birth, it can be stated that any disease or deviation from the normal in the child may result in temporary arrests of calcification of the enamel and dentin, or in defective calci- fication; but particularly important are the exanthematous fevers — measles, chicken pox. scarlet fever, smallpox, etc. — which may leave a hypoplastic impression upon the enamel and dentin. A rise in temperature of whatever origin, if it persists for as little as a few days, may leave its permanent impress upon the teeth. Infectious processes in the roots of the deciduous teeth may cause changes in the underlying permanent tooth sac: resulting in de- fective calcification. 2 Developmental defects of enamel affect certain areas of as many teeth as are in process of development at the time the nu- tritional errors were taking place. It is in this way that, knowing the chronology of tooth development, and in particular that of calcification of the enamel, it is a comparatively easy matter to ascertain the period in the life of the embryo or after birth when these disturbances of nutrition occurred. Histologically these defects in the enamel are due to insuffi- ciency in the number of enamel rods, imperfect calcification of the rods, and likewise to deviations in the quantity or quality or •Turner, T. S.: Transactions Odontological Society of Great Britain, XXXVJT, in Bennett's Dental Surgery. 254 DENTAL PATHOLOGY .2 orS E-s l-'S U o m £ « "j3 \S.S o :.<= 3 .. O 0JT3 r"l J3 3 ij-. 3 a.** 3 ■ 3 &<«* O f-i w O " r3 *0J rt 0) 3 g- «o O Vh O 3 u E5 «33 s o be"- 1 - 1 c c c c" s 3 s 3 o o o o J> oooo SSES-5 SEES \£> O O O -C ^i-^ooo Hi-tCQg £ C\) <\) CM rO CO ~* ON >-l VO r-l CM o o Si •? • ■8*1! — § rt E >£ g fa fa fa 23 1-1 TO .3 c C£ o 3 *" b be 4J C * « ■< *S u CJ c J^ 1-1 CI 5 t> "-S 4J^ 5E u.jj . ~ u U '-' CM 5 u u - " -z 3 — la ^ ^^ EEEE C S V rt _rt 3 3 . o. +4 d c d^j d *i d c - E, - a *j| — -r m ■S-ra-o — — Mtfl ■J/ v; — ^ N CM "' rHNWr^ro S ~ 1) m j. 2 ~ V o — a es u at ■s _ -= 3 u > a> * > 3 ■.J 3-D OJ T3 3 a D T3 to a> D V -S h ^ s > c '5" o-% 1/ u ■3.Q K n U v rt -j. HI V - §■ - (J ~- 5 u » * o ^ 5 u - u - '-' 1> u o 4J nt ~ fi — j: V ■~ V — rt — UOpiJUap JU3UBIUJ3J BYPOPLASIA, MICROSCOPIC AND MACROSCOPIC 255 both of the cementing substance (Figs. 117, 118, 11!), and 120). Two interesting specimens of marked enamel hypoplasia are shown in Pigs. 11!' and 120. As previously stated, the histologic defect may be so intense as to give rise to a macroscopic defect visible on the external enamel surface, such being the case with the specimen under consideration. In Fig. 120 a disturbance in the disposition of the enamel rods has occurred. The rods, in- stead of following the perpendicular direction to the surface, as -b' Fig. 119. — Hypoplasia of the enamel producing an external macroscopic defect on the labial surface of an incisor. At o is observed the area of disturbed enamel rod calci- fication; the enamel rods that are present are of a low grade of calcification and stunted in their growth and the interprismatic substance is not present in sufficient amounts. Normal enamel is seen at b and b' : normal dentin at c and c' , and defects in the calci- fication of the dentin in the form of interglobular spaces at d. is the case in approximal surfaces, appear wavy and very irregu- lar in their course and faulty in their calcification. The more marked cases show a deficiency or absence of enamel, and the surface of the tooth is irregular and rough. 3 (Fig. 119.) Cases of complete or partial absence of enamel are also occa- sionally encountered. This form of exaggerated enamel hypo- 3 Bennett: Dental Surgery, New York, Win. Wood & Co. 256 DENTAL PATHOLOGY plasia is designated under the term of enamel agenesia (Fig. 121). Systemic disturbances of a severe type undoubtedly occur at the calcification period of the affected teeth. In the dentin, hypoplastic defects arc represented by imperfect tubular formation, incomplete tubular calcification, and defects in the dentin matrix (Fig. 122). These hypoplastic changes are manifested in the shape of an increase in the size and number of the interglobular spaces. These Fig. 120. — Hypoplasia of the enamel in the approximal surface of an incisor. At a. a' enamel rods which do not follow the direction of normal enamel rods in these loca- tions are seen. Also the abrupt decrease in the thickness of the enamel, from left to right of the picture should be observed. spaces are found in the dentin throughout the entire extent of the tooth, but are more prominent near the enamel. They represent stages of arrested activity of the odontoblastic layer. Any patho- logic influence strong enough to produce hypoplasia of the enamel will likewise produce arrested calcification in certain areas of the dentin. The formation of tubules will come to a standstill, and upon the recovery of the formative organ the formation of tubules will begin at some distance from the point where growth had stopped. The sections of organic matrix which undergo partial BYPOPLASIA, MICROSCOPIC AND MACROSCOPIC 257 Fig. 121. — A case of enamel agenesia. All the deciduous teeth are affected. The dentin is nowhere protected by enamel and is of a yellowish color typical of dentin when - 1 to the fluids of the mouth and to extraneous substances. m'...-d V ;M Fig. 122. — Decalcified section showing a multitude of interglobular spaces. These are areas of incomplete develoDment and calcification of the dentin matrix and dentinal tubuli. a, cementum (hyaline); b, normal dentin; c,d,e,f, interglobular spaces of Czermak. 258 DENTAL PATHOLOGY calcification, or do not undergo any calcification at all, constitute the interglobular spaces first described by Czermak after whom they are named the interglobular spaces of Czermak. Examples of hypoplasia of the deciduous teeth are rare: when it occurs it is located high in the crowns toward the gingival mar- gin, the occlusal surfaces being almost invariably normal. The reason for this lies in the fact that the period of greatest suscepti- bility to abnormal influences in utero, so far as the teeth are con- cerned, is during the last month or two of intrauterine life, and reaches to the beginning of the second year after birth. On the other hand, hypoplasia of the permanent teeth is relatively frequent in some teeth, while others are rarely affected ; e.g., the bicuspids and second molars are seldom the seat of hypoplasia, while the third molars upper and lower are frequently the seat of defective development affecting the crown or roots of the tooth, or both, and is in practically all instances the result of obstructions in the path of their eruption. Pathologic Anatomy. — In the study of structural hypoplasia of the enamel or dentin any deviation from the appearance of mi- croscopic sections which are within the limits of normality is to be considered as a developmental (hypoplastic) defect. By this we mean that the enamel should have a uniform appearance, and the rods under high magnification should show the transverse markings indicative of the method of individual rod formation (Figs. 88 and 89). In the case of the enamel, the lack of cement- ing substance produces the white spots so frequently encoun- tered, also spots from the faintest to the deepest shade of brown. Two cases of extensive enamel hypoplasia are reported by the late Dr. G. V. Black 4 in which a general absence of cementing substance was responsible for an enamel which was white, chalky, and easily disintegrated. In these places the enamel is so easily disturbed or penetrated by means of a cutting instrument that an explorer, after the surface has been penetrated, will in some ex- aggerated cases convey a sense of chalkiness. These white spots may or may not affect the entire thickness of enamel. Patho- logically these are significant defects because of their offering favorable areas for the rapid spread of caries. Imperfect enamel calcification is frequently encountered in the fissures of molars and 4 Black, G. V.: Operative Dentistry, i. HYPOPLASIA, MICROSCOPIC AND MACROSCOPU 259 Fig. 123. Fig. 123. — Hypoplasia of the enamel in the shape of a slight reddish brown discoloration. Fig. 124. Fig. 124. — Hypoplasia of the enamel in the shape of intense reddish brown discoloration. Fig. 125. — A case of brown stain affecting the enamel on the labial surfaces of the central and lateral incisors only. bicuspids, and in the lingual pit of the upper central and lateral incisors, when the pit is present; in the linguogingival ridge of the upper cuspid, when fissured or grooved ; in the buccal groove of the upper first molar. In these locations the defect is due to incomplete closure of the fissure. 260 DENTAL PATHOLOGY Fig. 126. — A slight hypoplasia of the enamel on the labial surface of an upper cuspid. Fig. 1 -27. — Hypoplasia of the enamel on the labial surface of an upper cuspid. Fig"; 128. — Hypoplasia of the enamel on the Fig. 129. — Hypoplasia of the enamel labial surfaces of upper left and upper right in an upper left central incisor. The lateral incisors, semilunar in shape. enamel is tr'ansversed by horizontal and vertical depressions of a brown Ci ill il'. The formation of rods has been insufficient to produce a smooth bridging over or closure of the fissure. A large number of sec- tions which have been examined in the course of our studies show frequently the presence of calcified amorphous bodies in these defective fissures. In the milder forms of hypoplasia the bands HYPOPLASIA, MICROSCOPIC AND MACROSCOPIC 261 of Retzius appear larger and are of a deeper brown color than is the case in normal specimens, testifying to a lack of uniform cal- cification of the rods in their long diameter. The enamel being Fig. 130. — Hypoplasia of the enamel in Fig. 131. — Hypoplasia in the crown of a an upper right lateral incisor. lower molar. The enamel is studded everywhere with soft chalky spots (chalky- enamel ). Fig. 132. — Hypoplasia of the crown of an upper molar. The enamel, as in the previous picture, con- tains a large number of chalkv areas. Fig. 133. — Hypoplasia of the enamel in upper rcclars. The extent of the faulty development is shown externally by an extreme irregularity of surface upon the occlusal and approx- imal aspects of the teeth. deposited in segments represented by the bands of Ketzius. it stands to reason that any disturbance which will affect the proc- ess of enamel formation will be represented by variations from 262 DENTAL PATHOLOGY the normal throughout the segment of enamel in the course of deposition. Inasmuch as insufficient or imperfect enamel forma- tion is the result of a temporary arrest of activity throughout the extent of the ameloblastic layer, it consequently follows that all enamel that would have been formed, in the absence of disturb- Fig. 134. — Hypoplasia of Ihe enamel in lower molars. The occlusal and approximal sur- faces, as in previous specimen are extremely irregular. Fig. 135. — Hypoplasia of the enamel in Fig. 136. — Hypoplasia of the enamel in an upper cuspid. Several faint lines run- an upper central. The band in the cen- ning horizontally across the enamel mar ter of the crown is the dividing line he- the appearance of the crown. tween two periods of hypoplasia which oc- curred at different times. The incisal third, the gingival third, and the "band" are the normal enamel areas of the tooth. ing factors, is affected. While this view is upheld by a number of pathologic investigators, instances have come under our own ob- servation in which the defective formation has not followed a segment or band of Retzius in its entirety, but has manifested it- HYPOPLASIA, MICROSCOPIC AND MACROSCOPIC 263 self in the shape of a relative preponderance of cementing sub- stance throughout the depth of several segments in the direction of the enamel rods. The greater amount of cementing substance at the sacrifice of the number of enamel rods is characterized microscopically by dark, cloudy areas surrounded by enamel rods of normal appearance. This increase in the depth of color is be- lieved to be due to tin 1 presence of actual pigment. 8 Developmental defects in the enamel and dentin, when pro- nounced, give rise to conspicuous malformations of the crown which may range from the slightest brownish discoloration, as seen in Fig. 123, to most marked broien spots in the enamel as seen in Pigs. 124 and 125, and from the faintest chalky whiteness in the enamel, as seen in Fig. 126, to as pronounced a hypoplasia as seen in Figs. 127 to 134. Again, from a faint line or lines in the enamel (Fig. 135) sufficiently pronounced to mar its appearance to as wide a banel as that shown in Fig. 136. In other cases several grooves may be present in the labial side of the crown, and in still others the hypoplastic defects assume a rough granular or pitted appearance — the granular elefect of the enamel. The pit form of enamel defect consists of either one single pit surrounded by healthy enamel structure, or of a series of pits ; the former may be located anywhere on the enamel surface, the latter in the lower half of the crown near the incisal edge in the case of the incisors or cuspids or near the occlusal surface in the ease of the bicuspids or molars. The more pronounced develop- mental defects will be discussed under the heading of macroscopic deformities of the teeth in the following chapter. 5 Xoyes: Dental Histology and Embryology, Philadelphia, I.ca & Febiger. CHAPTER XIV MACROSCOPIC DEFORMITIES OF THE TEETH Macroscopic deviations from the normal may affect the crown, the root, and botli the crown and the root of one tooth, of several teeth, or of all the teeth in the same month. These macroscopic deviations may be so slight as to require careful examination in order to detect them. In these cases the external appearance of the tooth is slightly affected and the physiologic function not at all. In other instances the deviation from the normal is so ex- tensive as to mar the appearance of the toolh to the point of ren- dering its identification difficult and its physiologic function incom- plete. Gross deviations in size may affect one or more teeth, or all of the teeth in both arches. It is not unusual to find that one tooth is larger or smaller in relation to the other units of the same arch, and again that all the teeth in both arches are either too small or too large in relation to the size of the mouth and to facial contour. The upper central incisors and canines, the lower second bicuspid and the third molars, upper and lower, are frequently out of harmony with their fellows in the arch. Other types of abnor- malities in size consist in a disproportion in the size of the crown and root, as is seen in the case of central incisors with abnor- mally short roots and upper cuspids with abnormally long or short roots. Under a different heading will be studied those ab- normalities affecting the number of teeth in the arch, i.e., the presence of supernumerary teeth, and the congenital absence of one or more units from the dental arch. Abnormalities of Form Affecting the Crowns and Roots of the Permanent Teeth Central Incisors. — The most important macroscopic defects in the central incisors are those which affect the cervicolingual ridge. This ridge may be either insufficiently developed or over- developed to such an extent as to result in the presence of a pseudo- cusp (Figs. 137 and 138). The division of the cervicolingual ridge 264 \l \( ROSCOPIC DEFORMITIES OF THE TEETH 265 by ;i nearly central fissure, as seen in some instances, results in the presence <>f two cervicolingual ridges— a mesiolingual ;m]>er incisors. ground see ion of an incisor with an overdeveloped cervicolingual ridge simulating a cusp, is seen. An extra root arising from the lingual aspect is another abnormality that may affect this tooth. 'Bennett: Dental Surgery, New York, Win. Wood & Co. 266 DENTAL PATHOLOGY A disproportion between the size of a crown and its root may exist. The central incisors may be the seat of severe hypoplasia. (Figs. 141, 142, and 143.) The root only may be imperfectly developed (Fig. 144). A ground section shows normal microscopic characteristics, notwithstanding the macroscopic root deformity Fig. 140.— Photomicrograph of a central incisor with an overdeveloped cervicolingual ridge simulating a cusp, a, dentin; b, enamel; c, hypoplastic defect of the enamel in the under surface of the cervicolingual ridge. (Fig. 145). A hypoplastic defect of the middle lobe of the central incisor, the so-called Hutchinson's notch, is shown in Fig. 146. The upper central incisors are in some instances much larger in size in proportion to their neighbors. When present, this ab- MACROSCOPIC DEFORMITIES OF THE TEETH 207 normality in size generally affects both, 2 the right and left cen- tral incisors. Upper central incisors willi abnormally short roots are some- times encountered. Fig. 141. — Severe hypoplasia of upper Fig. 142. — Severe form of hypoplasia in central incisor, embodying the microscopic upper incisor, embodying the microscopic and macroscopic forms. and macroscopic forms. Fig. 143.— Severe form of hypoplasia in Fig. 144.— Hypoplasia of the root of an upper incisor involving the crown and upper incisor. the root. The lower central incisors arc rarely the seat of abnormalities. Lateral Incisors. — The upper lateral incisors may be the seat -P.urchard and Inglis: Dental Pathology and Therapeutics, Philadelphia, I.ea & Febiger. 268 DENTAL PATHOLOGY of macroscopic defects of the same character as found in the central incisors, i. e., underdevelopment or overdevelopment of the eervicolingual ridge and the presence of an additional root. The lower lateral incisors art 1 rarely the seat of abnormalities. The upper lateral incisor is frequently the seat of marked macro- scopic aberrations, the crown assuming various shapes, in addi- ng. 145. — Ground section of specimen shown in Fig. 144. It shows normal microscopic characteristics, notwithstanding the gross root deformity. tion to a disproportion between the size of the crown and that of the root. A peg-shaped lateral is occasionally encountered (Fig-. 147). The root of the upper lateral incisor may he de- flected labially, as seen in Fig. 14S. Upper lateral incisors are sometimes found with abnormally deep eervicolingual ridges and a median fissure two-thirds across their vertical diameters, A MACROSCOPIC DEFORMITIES OP THE TEETH 269 lower lateral incisor with a prong-like process on the lingual Mii-fact' is seen in Pig. 149. The lower lateral may have two roots and two root en mils i Fig, L50). The two roots may he well formed and independent of one Fig. 146. — Hypoplasia of the incisal Fig. 147. — Peg-shaped upper lateral in- third of an upper incisor. A so-called cisor. As the length of the picture is Hutchinson's tooth. The middle lobe is twice the actual length of the tooth it does incompletely developed upon the incisal not convey a clear idea of the diminu- aspect. tiveness of the tooth. Fig. 148. — An upper right lateral in- cisor mesial view with a labial deflec- tion of its root. Fig. '49 — A prong-like process on the lin- gual surface of the lower lateral incisor at a. another, or the deformity may consist of the bifurcation of its normal root at the apical third. Cuspids. — With the exception of a disproportion in the size of this tooth as com] tared with the other teeth in the same arch. the cuspid is rarely the seat of macroscopic defects, although 270 DENTAL PATH' rdevelopment of the cervicolingual ridge may be encountered, and in some instances it i^ so marked as to simulate a lingual Two ere hypoplasia of the crown of an upper id are seen in Figs. 151 and 152. A series of short-rooted upper cuspids is shown in Fig. 153. A series of long-rooted upper cuspids is shown in Fig. lo4. The deflection, if there is any. of the root of the upper cuspid is as a Fig. 150. Fig. 151. Fig. : r j. Fig. 150. — Lower lateral incisor, with two roots. Fig. 151. — Severe hypoplasia of upper cuspid. (Microscopic and macroscopic defects.) Fig. 152. — A marked case of enamel and dentin hypoplasia ("microscopic and macro- scopic defects) in upper right cuspid the result of an exanthematous fever from which the patient suffered at the time at which the tooth was being calcified. The defect and incomplete development has affected both the enamel and dentin. general rule in a distal direction Fig. 155 . but it may be in a mesial direction, as shown in Fig. 156. TIih occurrence of two-rooted lower cuspids is not rare. S mens of this type of malformation are shown in Figs. 157 and 158. The lower cuspid may have an abnormally short root. A supernumerary root in a lower cuspid occasionally occurs (Fig. 159). A severe hypoplasia of a lower cuspid is seen in Fig. 160. MACROSCOPIC DEFORMITIES OP TEK TEETH 271 Bicuspids. — The upper first bicuspid may have a crown with three cusps and a trifurcated root as shown in Figs. 161 and 162; also, instead of the usual bifurcated root it may have a single root with two canals and two apical foramina, or one root with one sin- gle canal constricted mesiodistally. In the upper second bicuspid, when the root is bifurcated, the two branches may be united by a Fig. 153. — A series of upper cuspids with unusually short roots. Fig. 154. — A series of upper cuspids with abnormally long roots. band of cementum for some distance from the bifurcation to the apices of the roots, as shown in Fig. 163. The lingual root of the upper first bicuspid may be deflected to the extent shown in Fig. 164. The root of the upper second bicuspid may be abnormally small and stubby, dividing into two branches in the apical region, as shown in Fig. 165. In the case of three-rooted upper bicuspids 272 DENTAL PATHOLOGY Fig. 155. — Distal deflection of an ni> per right cuspid. Fig. 156. — A marked deflection to the mesial in an upper right cuspid. Fig. 157. — Lower cuspids with two roots. MACROSCOPIC DKFOKMITIES OF THE TEETB 273 Fig. 158. Radiogram of a lower righl cuspid with two roots Fig. 159. — Supernumer Fig. 160.— Marked hy- ary root in lower cuspid. poplasia of the crown ot a lower cuspid. Fig. 161. — Upper first bicuspid with three mots. Fig. 162. — Upper right Fig. 163.— An upper Fig. 164.— An upper first bicuspid with three second bicuspid with a bi- first bicuspid with marked roots. furcated root. deflection of the lingua! root. 271 DENTAL I'A'l HOLOGY the disposition of the roots may assume either one of two relation- ships: (a) there may be presenl a mesiobu<-r;il, ;i distobuccal and a lingual rool (Fig. 161) ; or (b) one rool may be on the buccal as- pect and the other two on the lingual asju-ei of the tooth, as shown in Pig. 166. There may exisl a disproportion between the crown of the npper first bicuspid and its root. as shown in Pig. 167. A Pig 165. Bifurcation of ,: Pig. 166. An upper bicuspid witli an up bicuspid. is placed buccally and two lingually. Fig. 167. — An upper lirM Bicuspid with an ab- normally long root. Pig. 168. A hypoplaa tic upper bicuspid. Fig. 1 69. Proi d( fli ction ' of an upper bicuspid. hypoplastic upper bicuspid, probably the first, is seen in Pig. 168, and in Pig. 169 a view of an upper bicuspid with a marked deflee- i ion of the root. The upper second bicuspid may presenl variations affecting the Dumber and size of its roots. As a general rule this tooth has bu1 one root and our canal, the latter having its longest diameter in a buccolingual direction. Deviation from this type may consist in MACKosconc DEFORMITIES OF THE TEETH 275 Fig. 170. Upper left e< I bicuspid ; dispropor lion between the size "i the crown and that of the root I ■" i k • 171. — An upper second bicuspid with a dispi oportionately small root. Pig. 172.— A lower first bicuspid with two roots. Fig, 173. — Lower sec- ond bicuspid with two roots. The lingual root is partly hidden behind the buccal. Fig. 17 l. — A lower first bicuspid w ith a mai ked de flection of its roots. Fig. 175.— Distal deflec- tion of the root of the lower righl first bicuspid. 276 DENTAL PATHOLOGY Fig. 176. — Disproportion between the size of the crowns and roots of lower second bicuspids. Also deflection of the roots rendering practically impossible the proper treatment and filling of the root canal. Fig. 177. — Hooked root in lower bicuspid. Fig: 178. — Disproportion be' the crown and root of a lower second bicuspid. ween Pig. 179. — Disproportion between the sizr right of t lie crown and that of the root and deflec- tions of the root of lower first bicuspids. MACROSCOPIC DEFORMITIES or THE TEETH 277 the presence of two or three foots, each with its respective rod ca- nal. Disproportion between the size of the crOwn and thai of the toot of the upper second bicuspid is seen ill Pigs. 170 and 171. The lower first bicuspid may have a lingual cusp larger or smaller than the average type of lingual cusp for this tooth. The Fig. ISO. — Hypoplasia of the lingual cusp of a Inner first bicuspid. Pig. 1S1 licuspid. -A hypoplastic tower second Fig. 182. — Lower left second bicuspid with six cusps. Lingual and occlusal views, simulating an abnormal lower third. A, buccal aspect; D, occlusal aspect. lingual cusp of the lower first bicuspid is even in normal speci- mens markedly smaller than the buccal cusp, but in some abnormal specimens it is nothing more than a rudimentary cusp. The lin- gual surface of the crown may be free from fissures, or the lin- gual cusp may be bordered on the mesial and distal by a fissure which, beginning near the mesial and distal marginal ridges, reaches over onto the lingual surface. Also, first and second lower 278 DENTAL PATHOLOGY bicuspids with two roots and tivo distinct root canals are occasion- ally found. A lower first bicuspid with two roots is a rare ab- normality (Fig. 172). A lower right second bicuspid with two Fig. 1 S3. — The roots of an upper molar Fig. 184. — An upper second molar with united by bands of cementum. its three roots fused together by means of cementum. Fig. 185. — Upper left third molar with Fig. 186. — An upper first molar with badly deflected, fused and hypercemen- hooked roots, tosed roots. roots is seen in Fig. 171?. In these cases the roots may be fused for a section of their length by means of a band of cementum or throughout the length of the roots. A marked deflection of the MACROSCOPIC PEFOKMITIKS OP Till', 'III II I 279 root of tlif lower firsl bicuspid is sometimes found, as shown in Fig. 174. The deflection in this case was toward the lingual. A distal deflection of the root of the lower first bicuspid is seen in Pig. 175. A disproportion between the size of the crown and that of the root of the lower second bicuspid, and a deflection of the root.is seen in Pig. 176. A hooked root in a lower bicuspid ren- dering impossible successful root canal treatment and filling is shown in Fig. 177. Disproportion betwet n tht si:e of the crown and that of the root is not an infrequent occurrence in the case of the lower bicuspids. The root is proportionately either considerably longer or shorter Fig. 187. — Deflection to buccal ami dis- tal roots of upper first molar. Fig. 188. — A supernumerary root upper molar. than the crown, or vice versa (Figs. 178 and 179). The dispropor- tionately long root may be either deflected, or hypercementosed, or both. These root deflections and the fact that the abnormally long root not infrequently has a very slender termination, render diffi- cult, if not impossible, the treatment and filling of the root canal. Hypercementosis of the abnormally long root of a lower first bi- cuspid is not an uncommon phenomenon. The lower second bicuspid may present a disproportion between the crowm and the root. The root may be either too short or too long. The root may be extremely deflected, usually to the left. Figs. 180, 181, and 182 are reproductions of hypoplastic lower bicuspids. 280 DENTAL PATHOLOGY First Molars. — A not infrequent macroscopic abnormality in the upper first molars is the presence of a cusp between the mesial and lingua] cusps in the gingival margin. An elevation in some Fig. 1X9. — T.ower right first molar with Supernumerary root on the lingual aspect. Fig. 190. — Supernumerary root on disto- buccal aspect of a lower first molar. Fig. 191.— A lower firsl molar with a supernumer- ary root between the me- sial and distal roots on the lingual aspect. Fig. 192. — A lower first molar with three roots. The supernumer- ary springs from the dis- tal root. Fig. 193. — A lower first molar with three roots; su- pernumerary root on inci- sal aspect. portion of the occlusal surface simulating an additional cusp is another form of abnormality found in this tooth. The roots of the first molar are generally well developed and independent of one another. There is, however, in some cases, a fusion of the two MACROSCOPIC DEFORMITIES OF THE TEETH lis] buccal roots, or of one buccal root with the lingual root, or of the three roots, the Latter being a rare occurrence. These fusions are due to a growth of cementum between the roots (Figs. 183, 1*4, and 185). The roots of the upper firsl and second molars may be markedly deflected and hooked ! Figs. 186 and 187)-. A diminutive supernumerary root may be presenl on an upper molar Pig. 188). The lower first molar is sometimes minus the distal buccal cusp. Tomes found this cusp absent in 18 per cent of a series of skulls examined by him. 4 The abnormalities of this tooth consist in the presence of a super- Fig. 194. — Four well-developed roots in lower left second molar. Fig. 195. — A hypoplastic lower third molar. numerary root in relation with the distal root (Fig. 189). This extra root is usually located on the lingual aspect of the tooth, but may be also found on the buccal aspect of the tooth (Fig. 190). In Fig. 191 is seen a lower first molar with an extra root be- tween the mesial and distal roots on the lingual aspect. A lower first molar with a bifurcated distal root is seen in Fig. 192. A lower first molar with a supernumerary root in relation to the mesial root is seen in Fig. 193. Second Molars. — The upper second molar may be a three- in- stead of a four-cusped tooth, in which case the crown is of a ■•Bennett: Loc cit 282 DENTAL PATHOLOGY quasitriangular shape, and the roots are completely fused by means of cementum. The three roots of this tooth are frequently subject to abnormal variations. The lower second molar is, how- Fig-. 196. — Dwarfed upper third molar. Fig. 197. — Dwarfed lower third molars. Fig. 198. — Dwarfed upper third molar. ever, less frequently the seat of abnormal development than the first molar. The roots may converge at their apices. 5 A lower second molar may present four well-developed roots (Fig. 194). B Barrett : Loc. cit. MACROSCOPIC PKFOKMITIKN OF THE TEETH \is:\ Third Molars.— -The third molar is frequently the scat of ab- normal development. Prom Ihe almosl perfect upper and lower third molars closely resembling their respective second molars, every type of deviation is found, even down to the dwarfed molar. Fig. 199. — Hypoplastic upper third molars. Fig. 200. — Marked deviation of the roots of an upper third molar. Fig. 201. — Upper third molars with double deflection of the buccal roots and single de- flection of the lingual roots. The lower third molar may present a fairly well-developed crown having three short roots fused together, as shown in Fig. 195. It may also present a supernumerary root located between the mesial and the distal roots. The upper and lower third molars may he 284 DENTAL PATHOLOGY as insufficiently developed as shown in Figs. 196, 197, and 198. In Figs. 199 and 200 are shown upper third molars with marked developmental deviations. An upper third molar with double deflection of the buccal roots is shown at Fig. 201. The upper third molars may exhibit roots so badly curved as to render any attempt at root canal treatment absolutely impossible. A supernumerary root may be present, springing from the base of the lingual root. Lower third molars are, as a rule, possessed of roots which are deflected distally to various extents. The mesial and distal roots may be single deflected cones, terminating in a very slender tip, or the distal root may be a single deflected cone and the mesial root bifurcated — an incomplete fusion of the mesiobuccal and mesiolingual roots. The mesial and distal roots may be fused into one single cone in which the lines of fusion make it possible to segregate them. The fusion in such cases may be complete or only partial, a space being present between the bifurcation and the beginning of fusion. "When the two roots are fused, the joined apices may or may not be deflected to the distal. Oc- casionally a lower third molar is encountered with two roots which, bifurcating near the apex, give the tooth the appearance of having four roots. The mesial root, whether bifurcated or not, may be proportionately much shorter than the distal root. A rootlet may occasionally be found between the two roots upon their lingual aspect. Geminated Teeth By geminated teeth is meant the fusion of two or more teeth by means of enamel or cementum. During the developmental period it is probable that distortion by pressure of the enamel organs of the fused teeth takes place, and again, this distortion or misplacement may affect the developing roots only, in which case the crowns will lie separated from one another, but the roots will be fused or united by means of cementum. The fusion or gemination of teeth may affect either the deciduous or the permanent teeth. Fig. 202 shows two deciduous incisors erupted with their roots fused to one another by means of cementum. Fig. .MACKosconc ltKFOKMlTIES OF THE TEETH 285 203 shows an upper central and Lateral incisor erupted fused to one another \'<>v a distance of aboul one-third the length of their roots from their apices to an imaginary line of junction between the apical third and gingival two-thirds. In Pig. 204 a molar Fig. 202. — Geminated deciduous incisors. Fig. 203. — Geminated up- per central and lateral inci- sors. Fig. 204. — Geminated molar and bicuspid; possibly two bicuspids. Fig. 205. — Geminated and third molars. upper seconi and bicuspid, possibly two bicuspids, are shown, the crowns and one half of the roots being fused together. In Figs. 205, 206, and 207 upper second and third molars are shown fused to one another in their roots. Distortions and displacements of portions of the enamel organ 286 DENTAL PATHOLOGY result occasionally in the presence of enamel tissue in abnormal locations. In Fig. 208 is seen a rounded mass of enamel tissue {enamel pearl) in a concavity on the lingual root of an upper Fig. 206. — Geminated upper second and third molars. Fig. 207. — Geminated upper second and third molars. Fig. 208. — Enamel pearl on upper left second molar located in the concavity on the lingual root which shows a tendency toward bifurca- tion. 209. — Enamel pearl in upper right first molar. left second molar, and in Fig. 209 is seen an enamel pearl in an upper right molar at the neck of the tooth. CHAPTER XV ABNORMALITIES IN THE NUMBER OF TEETH Supernumerary Teeth Abnormalities of number in excess, i. e., supernumerary teeth, are encountered more frequently than abnormalities due to the absence of teeth. A supernumerary tooth may be of abnormal Fig. J 10. — A peg-shaped supernumerary tooth between the upper central incisors. Fig. 211. — Two tuberculated supernumerary incisors in the same arch. form or may have a normal appearance, usually that of one of its immediate neighbors. A supernumerary peg-shaped tooth is 287 288 DENTAL PATHOLOGY Fig. 212. — A tuberculated supernumerary tooth between the incisors. The left central incisor is not shown in this view as it was located lingually. Fig. 213. — A peg-shaped supernumerary tooth located lingually to the upper incisors. Fig. 214. — A supernumerary central in perfect alignment between normal incisors. si PERN1 MERAR1 TEETH 2K!J at limes round between the two een.1 ral incisors, causing a very un- sightly malformation (Fig. 210). One or two supernumerary tu- berculated incisors may be present in the same arch (Figs. 211 and Fig. 215. — A supernumerary upper incisor fused to the normal central incisor. Fig. 216. — Supernumerary molar between the upper second anil third molars. Fig. 217. — A fourth molar in place. 212). A peg-shaped supernumerary tooth may be located imme- diately behind one of the normal incisors, the latter being forced out of normal alignment (Fig. 213). The supernumerary incisor may 290 DENTAL PATHOLOGY also be of normal form ; Fig. 214 shows a case in which five in- cisors were present, each tooth having attained practically normal development. A supernumerary upper right lateral incisor of normal form may be located lingually from the central incisors. A supernumerary incisor may erupt fused to either one of the normal incisors (Fig. 215). In the molar region a reversion of type, as exemplified by the presence of a fourth molar on both sides of each arch, is not infrequently observed. The supernu- merary molar may be smaller in relation to its fellows, but still of somewhat regular form (Fig. 216). In Fig. 217 is shown a super- numerary molar (fourth molar) occupying a position distal to the third molar. A unicuspid tooth is sometimes found occupy- ing a position between the first and second molars on the buccal side. CHAPTER XVI ABNORMALITIES IX THE NUMBER OF TEETH Absence of Teeth Etiology. — The absence of teeth from the arch may be due to the noneruption of fully calcified teeth; to nonevolution of the tooth germ; to the failure of calcification processes in the dental follicle; to injury to the developing tooth germ from traumatism or infectious processes: to the accidental removal of the permanent tooth germ by the extraction of the deciduous tooth; to the trans- formation of the tooth germ into an odontoma. 1 Whenever a calcified tooth does not erupt, it is a case of in- carceration or impaction according as to whether the path lead- ing to normal position in the arch is free or obstructed. This ab- normality affects the third molars, upper and lower, the upper second bicuspids, the upper laterals and upper and lower cuspids with greater frequency than other teeth. Incarceration of a permanent tooth is sometimes associated with the retention of the corresponding deciduous tooth until later in life than normal, and occasionally even throughout the life of the individual (Figs. 218 and 219). The influence of heredity in these abnormalities of number is veil shown in the case of the upper laterals', this tooth bein Fig. 232. — Multiple sulciform erosions, general, and involving the bicuspids. (Cavallaro.) Fig. 233. — Lingual aspects of preceding illustrations. Hutchinson's teeth. (Cavallaro.) 3 Cavallaro, Joseph: L,oc. cit. 302 DENTAL PATHOLOGY abraded incisal edge. It usually affects both central incisors, one central alone rarely being affected. Fournier, cited by Cavallaro, has reported a case of congenital syphilis in which the cutting edges of the upper central incisors, the lower central incisors, and one cuspid had "well-marked crescentic notches." The Hutchinson sign refers particularly to the semilunar or crescentic notch on the incisal edge in the upper or lower, or both, central and lateral incisors and cuspids. The dental apparatus may be affected in many other ways as Fig. 234. — Hutchinson teeth. Honeycomb erosions. (Cavallaro. ) the result of nutritional disturbances induced by the presence or introduction of the syphilitic virus into the child (Figs. 231 to 236). To this source, among many others, but not exclusively, may be traced the tardy decalcification of the deciduous teeth, and the correspondingly late eruption of their permanent suc- cessors; the absence of certain teeth, such as the upper lateral incisors, or the lower bicuspids; the development of a tooth in an abnormal location, i.e., under the tongue, in the maxillary sinus, in Trill. \ son s ti;i:th and syphilitic stigmata 303 in the hard palate, vomer, nasal fossae, sphenoid, inferior orbital margin, stomach, ovaries, and in dermoid cysts; supernumerary teeth; underdevelopment of the jaws; and V-shaped palate, cleft palate, and harelip. 4 Cavallaro considers that the Hutchinson's semilunar notching, particularly of the incisors, is "pathognomonic of hereditary syphilis in at least 50 per cent of cases," and as his opinion is Fig. 235. — Hutchinson teeth. Microdontism. (Cavallaro.) Fig. 236. — Complete congenital absence of teeth in the upper arch. (Cavallaro.) sustained by Fournier, whose experience as a syphilographer is far-reaching, statements to the contrary by observers of only limited experience should carry very little weight. Cavallaro 's conclusions here follow : 5 "1. In heredosyphilitics the following various dental stigmata are found : erosions of the crown, cuspal erosion, and Hutchin- son's teeth; white sulci; white marks; delay of development and 4 Loc. cit. 5 Cavallaro, Joseph: Syphilis in Relation to Dentition, Dental Cosmos, February, 1909. 304 DENTAL PATHOLOGY eruption; dental infantilism; microdontism ; amorphism; per- sistence of the deciduous teeth; anomalies of structure, shape, number, direction, arrangement and color ; vulnerability of the dental system; ectopia (malpositions'), total or partial absence of teeth, wearing away, premature caries, premature loss of teeth, spaces between teeth (diastema), and the following maxillary stigmata : malocclusion, defective articulation of the dental arches, prognathism, ogival palate and cleft palate. "2. The dental stigmata are the most frequent characteristic, being persistent and indelible among the stigmata of hereditary syphilis. "3. The erosions are systematic; they occupy the same level on homologous teeth, and a different one on teeth of a different order (showing their relative periods of calcification). Besides, they have a marked predilection for some teeth (Hutchinson's erosion in the upper centrals, horizontal grooves in the lower in- cisors, and cuspal atrophy in the canines and first molars). "4. The dental stigmata do not belong exclusively to the sec- ond, but are also frequently found in the first dentition. Some cases of dental stigmata in the third generation have been re- corded. "5. The cup-shaped, or honeycomb, erosion on the deciduous molars, especially on the second, is very frequent. "6. The dental alterations as found in idiots, backward chil- dren, etc., represent a type quite different from those found in hereditary syphilitic subjects. Hutchinson's teeth, the systemic, lesions, the horizontal grooves, dental infantilism, and the cup- shaped erosion in the deciduous molars, are peculiar to hereditary syphilitic subjects, while in idiots the vertical grooves are noted. "7. The dental stigmata are rarely found alone (we have ob- served only three out of fifty-six eases) ; they are generally as- sociated with other stigmata of the head or with other general concomitant stigmata. "8. A relationship between the factors of Hutchinson's triad (a syndrome of congenital syphilis — Hutchinson teeth, otitis media, and diffuse interstitial keratitis), especially between the dental and the ocular lesions, is very frequently found. ''In fifty-six cases of dental lesions ocular lesions were found thirty-five times, and auricular lesions twelve times. Hutchinson's teeth and syphilitic stigmata 305 "9. The anatomic and pathologic examination of the dental follicles of syphilitic teeth furnishes us with the following char- acteristic symptoms: constrictions, which clinically eorrespond to the euspal atrophies; alterations of the enamel and dentin, in- terprismatic spaces, interglobular spaces, rounded islands, granu- lations due to an inhibitory disturbance which acted upon the tissues during the period of development. "10. In the dental follicles of macerated and doubtless syphi- litic fetuses the following alterations have been found: Endo- vasculitis. perivasculitis, hemorrhage and parvicellular infiltra- tion. "11. Tin' Spirochete pallida is abundantly found in the dental follicle near the so-called dentinal cap. in proximity to the ves- sels, and in their Avails. "12. The dental stigmata depend upon a general morbid cause, which manifests its inhibitory action during the period of development of the tooth, i.e., the second half of intrauterine life and the first months of extrauterine life. Such a morbid general cause can be only syphilis. "13. The presence of vascular alterations and of the Spirocheta pallida in the dental tissues leads us to believe that the dental stigmata are of syphilitic nature and not of indirect syphilitic origin only. "14. The dental stigmata are of great importance for the diag- nosis of hereditary syphilis, indicating the disease even before the appearance of other stigmata. "Hutchinson's teeth, the euspal atrophy of the first perma- nent molar, the multiple systemic lesions of the second dentition, the multiple and systemic lesions of the first dentition, especially the cup-shaped erosions of the molars, are pathognomonic of hereditary syphilis. In twenty-three out of fifty-six cases Hutch- inson's teeth have been found. "15. The maxillary alterations, although frequently found in hereditary syphilitic subjects, do not possess an absolute diag- nostic value. "16. The specific treatment is always to be suggested in hered- itary syphilitic children with dental stigmata, even if these stigmata are found alone and unassoeiated with other syphilitic or dystrophic stigmata. CHAPTER XYIII DENTAL CARIES Historical Data The destruction of the hard tissues of the tooth, commonly called caries, or decay, has been the subject of considerable specu- lation as to its etiology and pathology in ancient, as well as com- paratively modern times. Scores of theories are on record in the literature of the subject, some writers having adhered to as many as two or three of them, all to be discarded upon the publication by W. D. Miller of his epoch-making writings on the production of caries in vitro. The Egyptian skulls of the period around 450 b. c. show no evidence of any systematized attempt having been made in those prehistoric times at filling cavities of decay, although a few skulls have been unearthed with gold incrustations in the occlusal surfaces, leading to the supposition that some of the an- cient Egyptians had some inkling as to the need of repairing by artificial means the destruction wrought by caries. By inference it may be concluded that not even the earliest of races were free from the ravages of dental decay. Hippocrates, a Greek physician, who lived some five centuries before Christ, thought that caries was a manifestation of "stagnation of depraved juices." This theory, or a modification of it, persisted for centuries, even up to the end of the eighteenth century. A certain phlegm under the roots of teeth was considered by him as the cause of caries. But particularly interesting is his statement that food debris is a cause of caries which attacks the weakest and less adherent teeth. As late as the latter part of the eighteenth century this theory was exploited by Bourdet (1757), by Benj. Bell (1787), and Serre (1788). 1 Cornelius Celsus, the Roman physician, born some twenty-five years before the Christian era, was aware of the existence of a malady which caused the formation of cavities in the teeth. 1 Miller, W. D.: Microorganisms of the Human Mouth, S. S. White Dental Mfg. Co., Philadelphia. 306 DENTAL CAK 1 1 B 307 Scribonius Largus, a contemporary of Emperor Claudius, 2 in tlic middle of the firsl century was the author of a conception of caries which persisted for centuries: It was to worms which grew in the teeth and gnawed away their substance that the cause of the disease was attributed. The worm theory of caries was accepted and promulgated by Musitanus of Naples (1635-1711), Krauter- mann (1766-1854), and Ringelmann (1821). 3 In this connection Scribonius admonished that "there are those who pretend that the forceps is the only remedy for odontalgia. Nevertheless, be- t'.>re resorting to this extreme measure, other means can be uti- lized. When a portion of the tooth is decayed, I advise that it be scratched with the excavator (scalprum medicinale). The opera- tion is not painful and the remainder of the tooth will render the same service as the whole tooth. If the pain persists, one should have recourse to collutories, to substances to be chewed, to fumiga- tions, to dentifrices." The art of filling teeth with metallic substances was unknown to the Romans; but. on the other hand, they advised filling the cavities with a powder made of the excrements of mice or the livers of lizards and covering the filling with wax. Archigenes, toward the end of the first century, was particularly concerned in devising remedies against odontalgia, and combina- tions to be introduced into carious teeth, doubtless to control the pain associated with pulpitis. Galen, a physician who lived in the year 131 a.d., and later on Acetious of Amida. in 550 a.d., believed that caries was caused by disturbances of nutrition which produced vicious humors which should be allowed to desiccate. Again, that caries was the result of an inflammation of the dentin was advanced by Galen, Eus- tachius (1571), John Hunter (1788), Joseph Fox (1806), and Thos. Bell (1831.) 4 The inflammation theory of caries was revived in 1889 by Heitzman, Bodecker. and Frank Abbott of New York. In the Middle Ages. Rhazes, born in Persia in 850 a.d., thought of caries as a process similar to the understanding which they had at that time of the gradual destruction of bone (caries of bone). Rhazes knew that acids had a destructive action upon the teeth. 2 Lemerle, L : Xotice sur L'Histore de 1' Art Dentaire. 3 Miller: Loc. cit. 4 Miller: Loc. cit. 308 DENTAL PATHOLOGY Ali Abbas 5 aboul the year L094, a.d., in a voluminous treatise of medicine, mentions a number of diseases of the teeth, with cor- rosion, or caries, among them. Avicenna 980-1037), a Persian physician, the author of the Canon, and recognized by his contemporaries as the "prince" of physicians, attributed destructive action to the dentifrices of thai time, claiming that their eausticity injured the substance of the teeth. He also admonished his readers thai the narcotics used for toothache injured the teeth. Avicenna formulated certain rules for the prevention of dental disease. [f e recommended that certain articles of food which he conceived as being capable of undergoing putrefaction be eliminated from the diet, viz.. fish and milk: avoidance of too hot or too cold beverages, particu- larly one after the other; avoidance of chewing hard substances, such as hour or sticky foods, viz.. figs and sweets; avoidance of meats which injure the teeth; avoidance of contrivances for pick- ing the teeth: and as a remedy againsl dental ills, rubbing them with honey and burnt salt. Abulcasis, the author of the Altasrif, a treatise on surgery which appeared at the beginning of the tAvelfth century, devotes several sections of the book to dental disease. Giovanni d' Arcoli (John Arculannus), professor at Bologna. studied the means of arresting the ravages of caries. He recom- mended cleaning the cavity with acids and filling it with sheets of gold. Arculannus was apparently the first to suggest the fill- ing of teeth with gold foil in the year 1450. In 1470 John Pla- tearius, professor at Pisa, revived the worm theory of caries. This was the theory accepted by Tlyff. who lived in the latter part uf the fifteenth century and died about 1571. Lazare Riviere 5 of Montpellier, professor of chemistry, also appears to have ad- hered to the worm theory of caries and recommended certain substances to destroy them. Ambroise Pare, a famous French physician and surgeon of the sixteenth century, discusses cer- tain diseases of the teeth in a book published in 1560; but his theories of caries are just as impossible as those of his prede- cessors, whose views we have already recorded. lie leans to- ward the theory of vicious humors as expounded by Hippoc- 5 Lemcrlc, L. : Notice sur 1' Ilistoire de 1' Art Dentaire. DENTAL CARIES 300 rates and Galen twenty and fourteen centuries, respectively, previously. Pierre Fauchard, a French dentist and writer who lived in the latter pari of the seventeenth and the first part of the eighteenth century (1728), made efforts to find the worms that had been considered by his predecessors as the cause of decay, hut he, as well as Pfaff, a German dentist (1756), failed to locate these animalcules, and abandoned the worm theory. Thereafter, to Fauchard, "caries was produced by a humor which finds its way into the osseous fibers of the tooth, or by a depraved saliva, or by rough foods, or by certain eroding substances placed upon the teeth to cure or bleach them. The internal causes are contained in the blood by making- it less fluid and causing it to form ob- structions in the vessels of small diameter. The teeth are more subject to caries than the other bones of the body because their tissues are closer together, which explains their obstruction and strangulation." The putrefaction theory of decay was described by Pfaff, but, of course, we know now that a tooth may remain for any length of time in a putrefying mass without the enamel being thereby affected. The electrical theory of decay was also in vogue for some time, and was championed by Bridgeman before the Odon- tological Society of Great Britain in 1861. John Hunter (1728- 1793), in his famous book published in 1771, in which he dis- cusses the anatomy and diseases of the teeth, admits that caries is a disease of obscure origin and not caused by external irrita- tion or chemical processes. Neither Jourdain (1734-1816), writer and dentist, nor Bourdet (1757), writer and dentist, added anything to the notions in vogue in those times concerning caries. Berdmore, in 1771, was the first to investigate the action of nitric and sulphuric acids upon the teeth ; to sour food and to acids an injurious action had been attributed back in 1677 by Paseh. One of the most pro- lific writers upon the subject of the chemical cause of caries was Magitot. Tomes, in 1873, reached the noteworthy conclusion that caries is the effect of external causes in which so-called vital forces play no part ; and that caries is due to the action of acids that have been generated by fermentation in the mouth; but at that time Tomes attributed no importance to the agencies through 310 DENTAL PATHOLOGY which this acid was generated in the mouth. In more recent times Jonathan Taft was a strong advocate of the chemical theory. Magitot was able to produce artificial cavities in extracted teeth by the action of the products of the fermentation of sugar, as well as with several acids. The chemical theory alone, however, does not explain all the phenomena concerned in dental caries. The chemicoparasitic theory, the one to which we adhere today, was brought out to some extent by Leber and Rottenstein in 1867. W. J. Milles and A. S. Underwood, in 1881, before the Dental Section of the International Medical Congress of London, reported in a paper on the "Nature of Dental Caries" the constant pres- ence of microorganism in tooth decay, and the widening of the tubules produced by microorganisms. Milles and Underwood should be credited with the first microscopic demonstration of the bacterial causation of dental caries. Their opinion was to the effect that the acid that dissolved the enamel was secreted by the bacteria. It remained for Miller to clarify the situation, which he did following a series of painstaking investigations resulting in the production of artificial caries in the laboratory identical in etiology and pathologic lesion with caries as it develops in the teeth of man. Miller's theory, as accepted today, is to the effect that caries of the enamel consists in its entirety of the dissolution of the enamel by lactic acid formed in situ by th( fermentation of carbohydrates which adhere to the surface of the enamel; and that caries of den- tin and cementum consists of two distinct steps: (1) the dissolu- tion of the inorganic salts from these tissues, and, (2) a subsequent action by proteolytic bacterial enzymes upon the organic constit- uent of the dentin and cementum of the tooth. CHAPTEE XIX DENTAL CARIES (Cont'd) General Considerations Dental caries is the most widely distributed disease of mankind. Peoples of all countries and races are subject to its ravages, -and have been for all time, since caries lesions have been discovered in exhumed skulls of all ages. In some localities and among certain peoples it occurs with greater frequency and intensity than in others, but everywhere it is to be found. It has been estimated that from 85 to 95 per cent of the people of the civilized races suffer from caries. There seems to exist a direct relation between the progress of civilization and the increase in the prevalence of dental caries. In the less civilized and barbaric tribes the prevalence of caries is small; in the highly civilized peoples the percentage rises tremen- dously. In prehistoric times the percentage of carious teeth varied from as low as 2 per cent, or less, to about 7 per cent ; in contem- poraneous times, and among the most highly civilized people, par- ticularly, the percentage rises to 95 per cent and even higher. "With the advance in civilization there has occurred a gradual, though radical change in the dietaries of men, and whereas, in prehistoric and ancient times the character of the food was such as to act as a cleanser or detergent of tooth surfaces, and as a stimulus to the growth of the jaws leading to regularity of position of the teeth in the arch, in modern times the food, being of the soft and mushy variety, has a tendency to become lodged upon the surface of the enamel, and affords little stimulation to the development of the jaws. The consequence is that the teeth are malposed in the arch and strongly predisposed to dental caries. Pickerill attributes the immunity to caries among the uncivilized tribes of the world not to an excessive protein diet and a small carbohydrate intake — for he tells us that the dietaries of the uncivilized tribes do not necessarily consist of protein substances only, but that they are decidedly of a mixed character. He attributes the immunity from caries to the 311 312 DENTAL PATHOLOGY use of salivary stimulants — fruits with their fruit acids, acid or pungent plants, sour foods, etc. — and masticatories, viz., gums of different trees which, when chewed, stimulate the flow of saliva and therefore increase diastatic action. No importance is attributed hy Pickerill to the use of coarse fibrous foods as detergents in the case of the immune races, for again he assures us that in the case of the Maori, and other similar races, nearly all food is steamed, thus considerably reducing its toughness. Be that as it may, wo. are, however, satisfied that the character of the food per se is of paramount importance in maintaining the surface of the enamel free from the sticky coatings so evident in mouths of the caries sus- ceptibles. The views of Bunting 6 are here quoted in corroboration of the belief that the nature of the foods ingested has a bearing upon the production of dental caries. He says, "It is very evident that certain forms of carbohydrates have a greater tendency to stick to the teeth than others. The soft sticky varieties of sugars and cooked starches, which are slowly soluble, are especially liable to retention, and form favorable pabulum for acid fermentation. That the continued and copious diet of such substances is favor- able to caries can not be doubted. The mouths of candy-makers, millers, and children who eat largely of sweets, are strong in the corroboration of this view. And conversely, we know that the Eskimo and the meat-eating tribes of South America, who have little or no carbohydrate in their diet are, as a race, remarkably free from caries." The presence of salivary stimulants in the diet of the immune races, and their absence from the diet of the civilized races, un- doubtedly plays an important, but not exclusive, role in the deter- mination of susceptibility and immunity. Pickerill, whose investi- gations on the dietaries of the immune and susceptible races in their relation to dental caries constitute a most complete and depend- able study on the subject, traces the lack of immunity — the high susceptibility to dental caries — to dietaries which contain an abundance of food articles which act as salivary depressants and which are of Ititjh potential acidity. Some of his conclusions con- cerning the prevalence of caries among the civilized and uncivi- lized races are quoted here in further elucidation of the subject: 1. That the number of persons affected with dental caries who e Bunting: Journal of the National Dental Association. DENTAL CARIES 313 live under uncivilized or "natural" conditions is comparatively small varying from 1 to 20. S per cent, while in civilized modern races the percentage is as high as 98 per cent, the increase being at Least 77.4 per cent. 2. That the number of teeth affected with caries in each individ- ual is far less in those leading natural lives than in those leading artificial or highly civilized lives, in the former varying from 2 to 7 per cent, while in the latter it has become as high as from 15 to 52 per cent, showing a maximum increase of 45 per cent. 3. That in the British races, which have been subject to the in- fluence of civilization for nearly 2,000 years, the increase in the percentage of caries is about 79 per cent. This corresponds closely to the difference in percentage given above in 1. 4. That in the Maori race, which has been subject to the in- fluences of civilization for only seventy or eighty years at the very most, but has only become "civilized" in habits quite re- cently, the increase is 93 per cent. (But against this apparently high figure has to be set the fact that the incidence of caries in each mouth is comparatively low.) Caries is a disease which has kept up its ratio of increase with advancing civilization. J. R. Mummery, 7 for instance, tells us that in the series of skulls of the primitive races examined by him the percentage which showed carious teeth varied from 1.4 in the Eskimo to 20.8 in the negro (slaves) ; in the civilized races this ratio has increased tremendously. In English and Scotch school boys and girls, in a series of 10,500 individuals, the presence of carious teeth was found in 86 per cent of the cases; in the children of Leith the percentage was 98.60. The percentage among American school children, while not nearly so large as among European school children, is nevertheless alarm- ingly high. In a series of cases examined by Emerson, out of 1478 children from one to fifteen years of age, 81.2 per cent had carious teeth. In this percentage, namely 1200 children, 5996 decayed teeth were found, which is an average of 5.0 teeth for each one of the 1200 children, or 4.7 teeth for each one of the 1478 individuals examined. These children were not suffering from any acute disease, although their general health was failing on account transactions of the Odontological Society of Great Britain. 314 DENTAL PATHOLOGY of sickness during the winter previous to the examination, and also on account of various forms of malnutrition, anemia, and general debility, all doubtless traceable to the oral infection present. Of 634 cases over fifteen years of age, also in indifferent health, probably on account of unhygienic living, only 19, or 3.0 per cent, had no defective teeth; this leaves 615, or 97 per cent, in whom were found 4022 decayed teeth, or an average of 6.5 teeth for each of the 634 children examined. In this same group of 634 individuals, 1655 teeth were missing, and in addition 1444 artificial teeth were present, making a total of 3099 teeth which had been presumably removed for advanced caries, or an average of 4.8 per cent for each one of the 634. There are so many factors which favor the development and progress of caries that where some are lacking, others are pres- ent to favor its progress. From the time a tooth makes its ap- pearance through the gum, and throughout the life of the in- dividual, it is exposed to the conditions which bring about caries, although, of course, there are periods when the teeth are more susceptible to caries than at others, as well as periods of com- plete, or almost complete, immunity. The amount and composi- tion of the saliva ; the position of the teeth in the arch and their relation to their antagonists; the structural peculiarities of the enamel and of the dentin; the character of the diet; the general health status; and the degree of hygienic care, if any — these alone or in combinations, are at the bottom of the caries problem. There was a time when it was assumed that cleanliness of the teeth was the most powerful and only weapon in the prevention of caries; but today we must conclude, in the face of observations that have been made in this and other countries, that the constitu- tional factor can not be altogether eliminated from the discussion of the subject any more than it can from pyorrhea alveola ris, or from diseases of the eye, throat, nose, skin, etc. These ob- servations concerned themselves with the marked tendency to dental caries in some mouths which were maintained at all times in a state of scrupulous cleanliness, as well as with the absence of caries in certain other instances of badly neglected mouths. The chemicobacterial theory of Miller, promulgated by him in 1882, has stood the test of scientific inquiry all this time ; and while it explains the modus operandi of dental caries with scientific DENTAL CARIES 315 exactness, still, certain important phases of the problem of dental caries remain as yet to be explored. We know how a tooth decays in the presence of carbohydrate deposits upon its surfaces, with their subsequent fermentation, with lactic acid as the end-prod- uct; but we do not know why caries is rampant in some mouths and absent in others, under apparently identical conditions of health, diet, climate, living quarters, dental hygiene, etc. Is it the composition of the salivary secretion? The evidences ad- duced so far concerning the individual constituents of the saliva in the role of induction or prevention of caries, does not clear the question to any great extent. The sulphocyanate content, for instance, bears no relation to the subject, as shown by Gies, Howe, Bunting, and others. Bearing on the question of the immunizing properties of the saliva, Miller's studies throw considerable light on certain phases of the question, although with negative results. Considering a possible similarity between the hemolytic power of the blood serum and the substances which are introduced into the body when the individual is immunized, experiments were conducted in order to ascertain whether the saliva has any hemolytic action. These experiments show that fresh saliva brings about an im- mediate total solution of blood cells, but that this action is not due to any substance contained in the saliva, but to its water content, as proved by the fact that 0.75 per cent of sodium chloride, when added to the saliva (i.e., an isotonic saliva solu- tion), does not hemolyze the red blood cells of the rabbit. That the saliva has practically no antiseptic power whatsoever, has also been conclusively shown, inasmuch as microorganisms re- tain their virulence in the presence of human saliva. Miller also attacked the problem of caries immunity and susceptibility from the standpoint of the number of bacteria in the mouth, but his experiments show that the saliva of those immune to caries con- tains almost as many organisms as the saliva of those having moderate caries, or even those who are highly susceptible to the process. He says: "The saliva of immunes develops, in the presence of carbohydrates in and out of the mouth, on an average, a little less acid than that of highly susceptible persons. The 316 DENTAL PATHOLOGY difference is, however, not constant, and is not sufficiently marked to account for the marked difference of susceptibility." 1 This conclusion has been corroborated by Bunting, who like- wise found very little difference in the amounts of acids formed in the saliva of immunes versus that of susceptibles. Bunting expresses his conclusion by stating that the ability to ferment carbohydrates varies in different individuals, as well as in the same individual, but that this rate of fermentation bears no ap- parent relation to the caries susceptibility. 9 The observations of Miller have been confirmed by Lothrop un- der the direction of Gies, the distinguished biological chemist of Columbia University. "The results obtained," says Lothrop, "show that there is acid production regardless of the condition of the mouth and teeth of the individual from whom the cul- ture was obtained." Further, as to whether the bacteria from susceptible mouths ean extract more lime salts from the tooth than the bacteria from immune mouths, has also been the sub- ject of his investigation, and he has found that cultures of bac- teria from a case of perfect immunity extracted practically as much calcium as any culture from decay cases. 10 The quantity of the saliva undoubtedly plays an important role. People with scanty saliva, almost dry mouths, and dry mouths, are more susceptible to the ravages of caries. This is probably due to the fact that in the presence of a scanty saliva the sur- faces of the teeth are not freed of sticky, starchy deposits and in superficial cavities the amount of saliva is not sufficient to dilute the acid products of fermentation, which remain in a con- centrated form, more rapidly dissolving the enamel. In more or less dry mouths food collects upon the surfaces of the teeth. and particularly in the interproximal spaces, remains undisturbed, undergoes fermentation, and soon the lactic acid end product dis- solves the enamel. But again, viscosity of the saliva, viz.. whether it is watery or thick and sticky, does not seem to correspond in a constant way with susceptibility to, or immunity from, caries. A thick saliva has been found in mouths free from caries, and a thin secretion s Miller, W. D.: Dental Cosmos, xlv, 689. "Bunting: Bulletin ot the National Dental Association, October, 1914. lu Lothrop, Alfred P : The Oral Microorganisms: A Bacterio-Chemical study of Den- tal Caries, Journal of the Allied Dental Societies. DENTAL CARIES 317 in mouths in which caries was rampant, although, in the majority of instances in months in which the teeth are being rapidly disinte- grated through caries the saliva is thick and ropy, and, vice versa, a thin and watery saliva is secreted in moid lis not so sus- ceptible to caries. Michaels found in the saliva a carbohydrate which he supposed to be glycogen, and supposed that the saliva of many individuals susceptible to dental caries contained such a carbohydrate. This view was controverted by Miller, although he was inclined to be- lieve that an acid fermentation of mucin is a possibility, and per- haps is accountable for the development of cervical caries. In recent years Gies, 11 after an exhaustive investigation into the composition of the saliva in its relation to the development of caries, has shown that the assumption that saliva may contain glycogen in sufficient amounts to become a factor in the produc- tion of caries is not supported by scientific evidence. But, on the other hand, his experiments with mucin, as carried out with the collaboration of Loewe, indicate that this glucoprotein dis- solves calcium from the tribasic calcium phosphate, and that it is highly probable that mucin is able to dissolve calcium from enamel. The foregoing considerations are intended for the purpose of preparing the reader for a discussion of the predisposing causes of dental caries. Predisposing - Causes There are those conditions of the individual teeth or of their environment which favor the development of caries. The predis- posing causes are separate and independent from the exciting causes and, contrary to the latter, are not entirely external to the tooth. Hence, it is that hypoplastic defects of the enamel, either macroscopic or microscopic, and of the dentin; the amount and composition of the saliva; the position of the teeth in the arch; the overlapping of the teeth or having broad contacts; the diet as ivell as the age; the character of the bacterial flora; and the proper hygiene of the mouth and teeth — these are some of the fac- tors which may influence the development and progress of caries. "Gies, William J.: Biochemical Studies of Saliva and Teeth, Journal of the Allied Dental Societies, 1914. !18 DENTAL PATHOLOGY Hypoplastic enamel defects predispose to caries in two ways: (1) by affording places of retention for food debris; and (2) by presenting areas of tissue lacking in normal protectiveness by reason of the absence or defectiveness of the interprismatic substance and of the enamel, or again by presenting areas Fig. 237. — Defective fissure in a molar. The dark area from a lo a represents imperfect calcification. There were no external evidences of dental caries, although at b, decal- cification has started. There is lack of interprismatic substance in the dark area as well as between the enamel rods beyond the dark area. Probably as high a proportion as 80 per cent of the fissures of permanent molars and bicuspids are defective. Invariably Nature's effort to close the fissure is accomplished by depositing an amorphous calcific mass in the bottom of the fissure. In this mass enamel rods are sometimes to be de- tected. of decreased enamel thickness. It is a rarity to find a perfect fis- sure in the molars and oicuspids, for surely at least nine out of every ten molars examined clinically and microscopically show plainly these defects (Fig. 237). No break may exist in the con- tinuity of the enamel in the apex of the fissure, while on the other DENTAL CARIES 319 band, these fissures may be so deep that they almost reach to the dentin at the dentoenamel junction and afford excellent me- chanical retention for fermentable food particles. In such loca- tions the acid end produd (lactic acid) remains undisturbed and undiluted, and caries progresses more rapidly than in other loca- l ions. The necessity for careful and frequent supervision of these teeth by the dentist with the purpose of arresting the caries process from its inception or, what is most to he preferred, of pre- venting it altogether, can not he too strongly emphasized in the minds of the laity. But defects in the enamel are not restricted to the fissures of bicuspids and molars, nor to pits in the lingual surfaces of in- cisors, nor to irregularities of surface in any of the aspects of a tooth. Predisposing causes are likewise to be found in defects due to insufficiency of structure; e.g., the chalky spots or those of different shades of brown, which are the result of the partial or almost complete absence of interprismatic (binding) substance with a low grade calcification of the enamel rods. A pit on the labial surface of an incisor is not, however, as a general rule, a location of choice for the onset of caries, for the reason that the enamel rods may be so disposed in the depression— in a mesh- like arrangement— as to offer a fair degree of obstruction to the action of the acid end product of carbohydrate fermentation. Teeth whose dentin has an abundance of interglobular spaces are predisposed to a wide spreading of caries. Malposition of one, several, or of all the teeth in the arch predisposes to caries by favoring the lodgment and retention of fermentable food par- ticles. ''The amount of foodstuffs," says Bunting, "which are retained about the teeth is in direct relation to the character and function of the masticatory apparatus. In case the dental arch is composed of well-formed and well-placed teeth, all of which are in good occlusion with their antagonists, the food may be finely divided, and finding no favorable place for lodgment, it will be washed out of the mouth and swallowed. Such a set of teeth may be said to be 'self-cleansing.' On the other hand, the poorly formed teeth and teeth which are irregularly arranged and in abnormal occlusion, tend to offer retention for foodstuffs, and are less likely to be self-cleansing. In the regular spaces between such teeth, in flat interproximal spaces, and in wedge- 320 DENTAL PATHOLOGY or V-shaped areas formed by the overlapping of teeth, food will lie wedged and retained until it has been either removed me- chanically or destroyed by bacterial action." In fact, any surface of any tooth which is inaccessible to the toothbrush or to friction during mastication is a favorite place for the onset of caries. The bearing of the diet on the develop- ment of caries, as has already been indicated, is obvious. The consumption in abundance of starchy and sweet foods is a strong predisposing factor of caries; and vice versa, a diet poor in these carbohydrates, but consisting of meats to a large extent, is conducive to restricted caries. Among the Gruachos of the pam- pas of Argentina, who subsist mainly on meat, caries is prac- tically absent, while among the aborigines of Chile, where the diet is mixed, caries is present in a relatively large proportion. The Eskimos, certain meat-eating tribes of North American In- dians. Icelanders, and Lapps, are almost entirely exempt from caries. 12 Age is a predisposing factor of caries to the extent that dur- ing the early years of life, and up to around the twentieth year, the greatest susceptibility to dental caries exists mainly on ac- count of insufficient mouth hygiene by children and the young, and infrequent examinations by the dentist. Pregnancy is proba- bly a predisposing factor of caries, but exclusively by virtue of the neglect of brushing the teeth incident to the woman's general condition. That osteomalacia of pregnancy affects the teeth has never been proved; but, on the other hand, inflammations of the gingiva and gums, which occur during pregnancy, again by rea- son of neglect of the toilet of the mouth and teeth, predispose to caries by the loosening or retraction of these tissues from the neck of the tooth with the consequent exposure of the enamel near and at the neck of the tooth and of the cementum to the in- fluence of carbohydrate fermentation. The flabbiness and re- traction of the soft tissues around the necks of the teeth favor the retention of food particles. In the order of their importance the predisposing causes were listed by ATiller as follows: 1. The structure of the teeth [i.e.. poorly developed, soft, porous '-.Miller, \V. D.: Loc. cit. DENTAL CARIES 321 teeth, with many large (dentinal) [interglobular spaces] makes for a high predisposition to caries. 2. Abnormally deep fissures or blind holes (foramina ceca) in molars and upper lateral incisors, especially in cases where the enamel also is poorly developed. 3. Fissures and cracks in the enamel. 4. Crowded or irregularly placed teeth. 5. Recession or loosening of the gums. 6. Pregnancy. 7. Heredity. 8. Various general diseases by imparting an acid reaction to the oral secretions, such as rheumatism, gout, diabetes, gastro- enteritis, dyspepsia, cancer of the stomach, scrofula, rachitis, and tuberculosis. CHAPTER XX PATHOLOGIC PROCESSES IN DENTAL CARIES Dental caries is a molecular disintegration of the hard tissues of the tooth by chemicoiacterial agencies. It is a process whose etiologic factors are external to the tooth, and which consists of two distinct steps in the case of both dentin and ceinentum: viz., (1) the disintegration of the inorganic matter by lactic acid, the result of carbohydrate fermentation, and (2) the destruc- tion of the organic matter by the action of peptonizing bacterial enzymes. The dissolution of the enamel, which is the first stage of caries, results from the fermentation of carbohydrate food by the direct action of bacterial enzymes. The enamel con- taining only a minute portion of organic matter, its disintegra- tion occurs exclusive of any peptonizing action. The enzymes of mouth bacteria possess the property of splitting monosaccharides into lactic acid. The starches are acted upon in the mouth by the amylolytic enzyme, ptyalin, and converted into maltose, a disac- charide. The starches taken into the mouth as food have the general formula (C G H 10 O' 3 ) x, the x standing for an unknown multiple. The action is one of hydrolysis, and may be expressed as follows: Starch 2C 6 H,„0- -f H 2 + ptyalin — C^BLO,, (maltose). Cj.H^O,, -)- H,0 -\ r bacterial enzyme=z 2C 6 H 12 6 (glucose, or dextrose). This conversion of starch into maltose takes place in different steps: 1. Starch, which gives a blue color with iodine. 2. Soluble starch or amylodextrin, which gives a blue color with iodine. 3. Erythrodextrin, which gives a red color with iodine. 4. a — Acroo dextrin (no color with iodine). 5. /? — Acroo dextrin (no color with iodine). • 6. y — Acroo dextrin, and possibly other dextrins. 7. Maltose. 322 l'ATI[()l,o<;i< I'KOCESSES IX DENTAL CARIES :;l':; Maltose, C^ILJ ),,, becomes hydrolyxed in the presence of one molecule of water into I ! 12 H 24 12 and, bacterial enzyme being avail- able, this is split into glucose (dextrose) 2C 6 IT,J),., which again, in the presence of a bacterial enzy , is split into lactic acid, to wi1 : 2C 6 H 12 6 = 4C 3 H 6 3 (lactic acid). The degrees of fermentation of certain carbohydrates by bac- teria have been exhaustively investigated by Gies and Kligler. 1 "Glucose was fermented by practically all the strains secured from dental deposits. Lactose and sucrose were attacked less regularly, though by larger majorities of these strains. The bac- terial strains tested by the authors in this series of investigations numbered four hundred and twenty-six. The accompanying table embodies the result of these investigations. SUGARS FERMENTED GLUCOSE LACTOSE SUCROSE GLUCOSE GLUCOSE GLUCOSE ONLY ALSO ALSO LACTOSE SUCROSE GLUCOSE LACTOSE AND SUCROSE INDIVID- UALLY Number of bac- terial strains tested 426 Percentage of the strains that induced fermentation 99.5 ::si; 326 426 15 386 '.26 16 322 56 "The relative fermentability of certain sugars in equivalent volumes by typical oral bacteria, as measured by the resultant amounts of acid, has also been determined by Gies and Kligler. "The test media were made from meat infusions according to the standard methods and included the addition of one per cent of the sugar to be tested. The titrations were made with N/ 20 sodium hydroxide solution, phenolphthalein serving as the in- dicator. The results as expressed in the following table are in terms of the number of cubic centimeters of normal hydroxide solution necessary to neutralize 100 c.c. of the culture medium, 1 Chemical Studies of the Relations of Oral Microorganisms to Dental Caries, Journal of the Allied Dental Societies, December, 1915. Because of the scientific value of these observations they are quoted in full with the consent of Professor Gies. 32-1 DENTAL PATHOLOGY each value representing average acidity produced by the dif- ferent representatives of a given species under approximately equal conditions of incubation of each form : TYPE OF ORGANISM GLUCOSE SUCROSE MALTOSE LACTOSE D. rlavus 2.5 2.6 2.7 0.6 Staphylococcus 4.5 2.5 3.1 4.5 Streptococcus 4.2 4.2 — 4.0 B. acidophilus 5.6 0.9 5.4 5.8 C. placoides 3.2 4.3 3.7 0.5 L. buecalis 3.9 0.5 2.7 0.4 Actinomyces 1.9 0.2 0.4 0.6 "According to Kligler the recently isolated strains of staphy- lococci, streptococci, and bacillus acidophilus, represent the most active acid-producers. The average results of the staphy- lococcus are 4.8, streptococcus 4.8, and B. acidophilus 7.0. "It appears from the foregoing experiments that glucose and maltose are more rapidly fermented in general than sucrose and lactose, also thai the amounts of acids produced from the sugars used were fairly constant in most cases for each type of bacteria. The B. acidophilus is capable of elaborating and withstanding a greater amount of acid than that produced and resisted by any of the other types." It is well to remember in connection with the process of car- bohydrate fermentation, as bearing upon the production of dental caries, that we have to deal with monosaccharides or sim- ple sugars, disaccharides or double sugars, and polysaccharides or multiple sugars. The monosaccharides, C^HjoO^. are directly split by bacteria into C 3 H (; 3 (lactic acid). The monosaccharides, or hexoses. are the sugars found in fruits, honey, and in sugar of milk as a derivative of lactose. These are glucose, dextrose, and grape sugar, levulose, fructose, and galactose. Dextrose, lev- ulose and galactose are fermentable by yeasts and by any num- ber of bacterial enzymes such as are constantly present in the mouth. Glucose is a thick syrup obtained from corn starch by the ac- tion of dilute sulphuric acid. The corn starch and dilute acid are heated together, the acid first converting the starch into grape sugar. The excess of acid is removed by treatment with PATHOLOGIC PROCI>>!> IX MENTAL CARIES 325 ehalk. The filtered solution is either evaporated to syrup and sold as "glucose" or evaporated to dryness and sold as grape sugar (Simon). Dextrose is found in honey. Levulose and fructose occur in sweet fruits and honey, and galactose in sugar of milk. The disaccharides or saccharoses comprise principally the sug- ars obtained from cane sugar (saccharose), from beet sugar (sac- charose), and from milk (lactose). Their general formula is CioHooO^. In the process of hydrolysis one molecule of the disac- eharide takes up one molecule of water and splits into two mono- saccharide molecules, thus G 1 & s 11 + JI 2 = 2CJl li O a . To the list of disaccharides should he added maltose and isomaltose — end products in the hydrolysis of starch. The polysaccharides are starch, glycogen, dextrin, inulin and cellulose. It is with starch that we are distinctly concerned in the study of dental caries. This polysaccharide is insoluble in cold water, alcohol, and ether. It conies in the form of an amor- phous, white, tasteless powder, or in masses. It is unabsorbable as such, but must first be hydrolyzed into maltose and then into dextrose through the action of an organized or unorganized en- zyme, in either case the intermediate products of the hydrolysis being the same. Starch is widely distributed in nature, being found in the seeds of cereals and leguminosa?. and in the' stems, roots and seeds of nearly all plants. From starch down to the production of lactic acid the chemical reactions involved are ex- pressed as follows: STAECH Maltose 2C B H 10 O 5 + HX> — ptyalin = C^H^O,,. . Maltose Dextrose C^H^O^ + H 2 -f maltase enzyme = 2C 6 H ]2 O c . Dextrose Lactic Acid 2C,.H 1 ,0 1 . — B. enzyme = 4C,H,.C\. The dissolution of the interprismatic substance or of the enamel rods, or of both, is followed by the penetration into the dentinal tubules of the acid end product of fermentation and of bac- teria which have the power of dissolving ( peptonizing) the or- ganic matrix of the dentin. As the enamel is penetrated and the decalcifying agent reaches the dentoenamel junction the process spreads laterally with a rapidity proportionate to the prominence 326 DENTAL PATHOLOGY of the granular layer. The more marked the latter ; i.e., the greater the size of the expansions into which the tubules open, the more rapid and greater will be the lateral involvement at the dento- enamel junction. The area of involvement at the dentoenamel junction, because of the facility with which bacteria will travel along this line, is greater than the area of involvement in the dentin toward the pulp. It is for this reason that the carious process in the dentin assumes a conical shape or, as expressed by Black, the tendency is to the formation of a conical area of decay with the point of the cone toward the pulp of the tooth and its base at the dentoenamel junction (Fig. 238). In the presence of wide tubular expansions Fig. 238. — Typical conical form of penetration of caries into the dentin; the base of the cone is at the dentoenamel junction while the apex of the cone is toward the pulp. (('.. V. Black.) at the dentoenamel junction — the granular layer — the amount of calcified matter to be acted upon by lactic acid will be proportion- ately decreased, so that caries will advance rapidly and a greater area of underlying dentin will become involved. Caries in a fis- sure, after the dentoenamel junction has been reached, and when an excessive granular layer is present, will advance more quickly laterally than in depth into the dentin, and this lateral caries will then advance toward the enamel undermining the enamel cap over a considerable area. The calcium salts of the dentin are dissolved by the lactic acid and the remaining tough, cartilaginous matrix is then acted upon by peptonizing bacterial enzymes. The bacteria penetrate the PATHOLOGIC I'KooLSKKX IN DENTAL CARIES 327 y if v ' ^ . Fig. 239. — Microorganisms in the structure of the dentin. (Miller.) Fig. 240. — Microorganisms in the structure of the dentin. (Miller.) 328 DENTAL PATHOLOGY dentinal tubules as soon as access to them is secured by the dis- solution of the overlying enamel (Figs. 239-242). Here they can be seen in considerable numbers and occasionally the tubules ap- pear distended, evidently as the result of the action of the or- ganisms upon the decalcified or quasidecalcified structure of the tubules. Black was of the opinion that microorganisms do not penetrate into the dentinal tubules until the calcium salts have been dissolved for a short distance in advance of the bacteria. If, now, decalcification should proceed in an external direction from the dentoenamel junction, and coincidentally in an internal direction into the dentin, a cavity of considerable size will be formed having a very small opening externally. The lateral prog- ress of caries at the dentoenamel junction is designated as lateral caries, and the progress of caries from the lateral involve- ment back into the enamel is backward curies. The tendency for caries to spread rapidly as above described is not the case in all instances, as the decalcification of the enamel and dentin, and liquefaction of the organic dentin matrix, may be a slow process from the beginning — a long time elapsing until a fair-sized cavity is formed. The involvement of the dentin, unless proper treat- ment by filling is instituted, will continue until most of the crown is broken down. If the decay advances along the dento- enamel junction and from there several paths of decalcification develop into the enamel and the dentin, the support to the ename, rods is removed and these will soon break down, the top of the crown will collapse, and the enamel rods will be washed away by the saliva. The decay advances toward the pulp, in some cases painful symptoms developing as the result of pulp irritation, while in others no painful manifestations occur until such time as it is too late to save the pulp or even the tooth. The formation of lactic acid in the deeper structures of the dentin is explained by the late G. Y. Black on the basis of os- mosis and dialysis. The sugar, as it is formed in the mouth by the fermentation of starches, or the sugars that are taken into the mouth as food and are there split into simple sugars, are dialyzed into the deeper structures of the dentin. Here they are further split into lactic acid by the bacterial enzymes of such PATHOLOGIC PROCESSES IV DENTAL CARIES 329 ^?* V- ."*** Fig. 241 — Microorganisms in the structure of the dentin. (Miller.) Fig. 242. — Microorganisms in the structure of the dentin. (Miller.) 330 DENTAL PATHOLOGY bacteria as have previously penetrated into the tubules, or which are in the deeper layers of the decalcified dentin matrix in prox- imity to as yet sound dentin. By the same process of dialysis the inorganic salts of the dentin which combine with lactic acid to form calcium lactates or calcium lactophosphates, find their way into the saliva. CHAPTER XXI CARIES OF THE ENAMEL Etiology and Pathologic Anatomy- It develops upon the enamel in spots or areas which favor the attachment of bacteria which, as the result of their activity in a carbohydrate medium, produce lactic acid. This dissolves first the interprismatic substance between the enamel rods, and then the rods themselves. This incidence is easily demonstrated upon free fragments of enamel when the dissolution of the inter- prismatic substance by lactic acid or any other acid brings into view the outlines of the individual enamel rods by establishing a greater margin of difference between the refractiveness of the rods and that of the interprismatic substance, the rods standing separated from each other at their free ends (Fig. 243). The bacteria which induce the fermentation of carbohydrates upon the surface of the enamel are supposed to become collected under a protecting gelatinous mass which the late G. V. Black and J. Leon Williams have considered to be essential in the de- velopment of caries. These coatings of gelatinous consistence, designated by Black as gelatinous plaques, were by him inter- preted as the product of bacterial activity. The slimy deposits which form upon the surfaces of the teeth, particularly during sleep and in the mouth not properly cared for, are not the plaques described by Black. The mucinous plaque is not the result of the precipitation of mucin, as thought by many, for the reason that mucin precipitates in the form of flakes which do not adhere to the enamel. The formation of the plaque from mucin is a purely physical process. Black considered the plaque as an essential factor in the retention of bacteria upon tooth sur- faces and also in the localization of the products of carbohydrate fermentation. The plaque is not, however, considered by Kirk 1 as essential in the progress of caries, and again, Hopewell-Smith J Kirk, E. C. : A Consideration of the Question of Susceptibility and Immunity to Dental Caries, Dental Cosmos, 1910, xli, 729. 331 332 DENTAL PATHOLOGY is of the opinion that the mysterious plaque is nothing more than fragmentary remains of Nasmyth's membrane. Gies has sug- gested the use of weak solutions of organic acids as mouth washes and mouth cleansers on the assumption that the precipitation of mucin in flakes, and their consequent elimination in the saliva, would prevent the formation of the mucinous plaque. Bunting tells us that the plaques and films which form upon the teeth are not of the same character in their composition. He says that some Fig. 243. — Artificial decalcification of the enamel by one per cent hydrochloric acid sim- ulating caries, a. dentin; b, sound enamel; c, artificially decalcified enamel. forms of plaque which occur in certain mouths have the property of favoring caries and making it possible, while in other cases films are formed which are protective in their nature and which do not favor acid fermentation in their substance. The disappearance of the cementing substance leads to the falling and washing away of the enamel rods (Fig. 244). The first symptom of caries of the enamel is a whitened spot pro- CARIES OF THE ENAMEL 333 Fig. 244.— Caries of enamel at the deepest portion of the cavity. In the dentin the lightest area at a, is the transparent zone of Tomes. At b, in the transparent zone tubular calcification had not been so marked. A wall of enamel at c, surrounds the cavity shown at d; a mass of decalcified broken-down enamel is shown at e f g and h 334 DENTAL PATHOLOGY duced by the dissolution of the cementing substance. Here the enamel feels chalky and soft to the explorer. Localization of caries of the enamel is, in the order of frequency, in the follow- ing areas of the tooth: 2 1. (a) Pits or fissures in the occlusal surfaces of bicuspids and molars. (b) In the buccal surfaces of molars. (c) In the lingual surfaces of molars. (d) Occasionally the lingual surfaces of the upper incisors. 2. In the proximal surfaces of all the teeth. 3. In the gingival third of the buccal or labial surfaces of all the teeth, and rarely in the lingual surfaces. Certain discolorations upon the approximal surfaces of molars and bicuspids are probably the result of the penetration of a slightly decalcified enamel by extraneous substance from the saliva. The discolorations in fissures of bicuspids and molars is attributed by Hopewell-Smith to color changes in a persisting Nasmyth's membrane by certain microorganisms, to wit: B. fluorescens liquefaciens. In occlusal surfaces caries develops in fissures and pits because here the friction of mastication is unable to keep these locations clean. Once food debris becomes lodged in a pit or fissure, it un- dergoes fermentation, with the result that the interprismatic sub- stance and rods are dissolved. The occlusal surfaces are sub- jected to considerable friction during mastication. The lingual surfaces of the upper and lower teeth are kept clean by the fric- tion of the tongue, and the buccal surfaces are likewise main- tained in a relative degree of cleanliness by the friction of the cheeks and lips. As a general proposition it may be said that the beginning of caries is located in areas which are not ordinarily subjected to friction, either by the cheeks, lips, tongue or during mastication. Seldom, if ever, do the prominent lines of a tooth — those which are frequently cleaned by either muscle friction, the toothbrush, or the food itself during mastication — become the original seat of caries. Rather, it is the points on the surfaces of teeth that offer a place of concealment for food or bacteria that are first attacked in caries. The process of caries is limited by the 2 Black, G. V.: Pathology of the Hard Tissues of the Tooth, vol. i. CARIES OF Tin: i;\a.mi.i, 335 position of normal gum (issue, by friction in mastication, by mus- cle friction, and by artificial cleaning. Fig. 245. — Caries of enamel in proximal surfaces. It has progressed in the direction of the enamel rods. All of the dark area (marked X) is carious enamel, the decalcifica- tion having affected the interprismatic substance, which is practically dissolved away, the individual rods can be distinguished without difficulty. The area marked E is sound enamel. In this specimen caries bad progressed part way through the enamel. (G. V. Black.) In the approximal surface caries of the enamel exhibits a tend- ency to follow the lengths of the enamel rods, but this is by no means a constant tendency. Many a microscopic section re- ddb DENTAL PATHOLOGY veals the fact that caries is likely to progress across the long axis of the rods after a certain area of enamel has become de- calcified (Figs. 245 and 246). In pits, also, the progress is oc- casionally across the lengths of the rods (Fig. 247). The pit may not show externally any evidence of caries, but upon examination t lie explorer will detect an opening, and caries Fig. 246. — Caries of enamel in a proximal surface in which caries has made c< erable progress. D, dentin, E, enamel (sound), X, carious enamel, the dentoenamel junction is seen between D and B. (G. V. Black.,) will be found to have penetrated the thickness of the enamel and to have spread across the lengths of the enamel rods toward the dentoenamel junction. In proximal surfaces the predisposing cause of caries is to be found in the failure of the septal tissues to completely fill the interproximal space. Under normal conditions the septal tis- CARIES OF THE EN \ \li:i. 337 sues will fill this almost to tin atacl point, and the food glides over them so that none, or only very small particles, becomes lodged under them. Under conditions which bring about inflam- matory disturbances of the septal tissues, causing them to recede, food becomes lodged in the spaces and caries begins there, be- cause that portion of the enamel which was previously protected is now exposed to the influence of carbohydrate fermentation. In pits and fissures caries advances frequently across the lengths of the enamel rods. The outline of the caries process in these localities is more or less conical, with the apex of the cone Fig. 247. — Caries of enamel in a pit. The whiteness in the enamel around the pit is caused by the dissolution of the interprismatic substance. Caries has advanced across the long diameter of the enamel rods. (G. V. Black.) at the bottom of the pit or fissure, and the base at the dento- enamel junction (Figs. 248 and 249). In these cases it is not unusual to find the enamel thoroughly undermined, with the opening into such a cavity very minute. Food which accumu- lates in a pit or fissure is not readily disturbed, so that any acid produced there by the fermentation of carbohydrates has ample time to dissolve the rods even before the dentin has been penetrated, because it remains slightly diluted, being not readily washed away by the saliva. A strong predisposing cause of caries in the approximal surfaces of incisors is to be found in an inflammation of the septal tis- sues. Their natural rounded form is destroyed, or the tissue 338 DENTAL PATHOLOGY shrinks from its normal position, — in either event producing a space between the septal tissues and the approximal surfaces of the teeth in which food accumulates and undergoes fermentation. The incidence of caries here is usually in a very small spot, the whitened surface of the enamel marking the location at which Fig. J48. — Progress of enamel caries in a molar. The dark area represents the portion of the enamel that has been decalcified by the lactic acid end-product of carbohydrate fermentation, a, dentin; b, b, dentoenamel junction; c, partly decalcified enamel; d, com- pletely decalcified enamel, c, sound enamel; /, interior of cavity. the cementing substance has been dissolved away. Then the advance of caries is exactly the reverse of what occurs in pits or fissures; that is to say, the penetration is in the shape of a cone with the base on the surface and the apex toward the dento- enamel junction. The central portion of the cone is in close CARIES OF THE ENAMEL 339 proximity to the dentin, and it is there that the dentin is first affected by the acid of caries. The tendency in the approximal surfaces of bicuspids and Fig. 249. — 'Progress of enamel caries in a molar. A greater enlargement of the same section shown in Fig. 247. molars is for the carious process to begin at some point and spread in a buccal and lingual direction. Spreading toward the occlusal is apparently the exception. 3 3 Black, G. V.: Operative Dentistry, i. CHAPTER XXII CARIES OF DENTIN AND CEMENTUM Etiology and Pathologic Anatomy Following the decalcification of enamel by the acids which result from the fermentation of carbohydrates, the dentin be- Fig. 250.— Caries of dentin showing decalcification of the organic constituents and conversion into a soft cartilaginous mass. a. pulp chamber; b, b, decalcified dentin which lias been converted into a soft cartilaginous mass. comes involved. In the dentin conditions are present which make for a difference from the process of caries in the enamel. The decalcification of the dentin— that is to say, its conversion into 340 CARIES OF DENTIN AND CEM1 \Ti \l :;n a tough cartilaginous substance — is ■ designated as the softening of tli<' dentin (Figs. 250 and 251). It is the resull of the dissolu- tion of the inorganic salt constituents of the tissue. This soft b Fig. 251. — Caries of dentin showing decalcification of the inorganic constituents anil conversion into a soft cartilaginous mass; a, interior of cavity; b, decalcified dentin which has been converted into a soft cartilaginous mass. mass may be easily peeled off, and when compressed, discharges a small quantity of liquid of a strong acid reaction (Miller). 342 DENTAL PATHOLOGY The softening of the dentin is followed by a partial or complete liquefaction of the organic matrix. This organic matrix is the cartilaginous substance which remains after decalcification has been effected and which upon disintegration or liquefaction leads Fig. 252. — Undermining caries; destruction of tooth substance from within. (W. D. Miller.) to the formation of a cavity. Decayed dentin may be of any shade from the natural color to black. The progress of decay in dentin, as pointed out by Miller, fre- quently assumes the outline of a Florence flask and the over- lying undermined enamel often breaks under the pressure of mas- tication. In microscopic sections the enamel is seen separated i \\l;ii:s OF DKXTIX VXD CEMENTUM 343 from the underlying dentin. Caries in some cases proceeds rapidly at the dentoenamel line. In some eases the caries process advances in the shape of a narrow canal directly to- ward the pulp. These eases are designated as penetrating caries. The lateral spreading of caries in the dentin at the dentoenamel junction, or the progress toward the pulp, is governed by developmental conditions. In fully developed teeth, with many interglobular spaces at or near the dentoenamel Fig. 253. — Undermining caries; destruction of tooth substance from within. Miller.) (W. D. junction, the decay spreads rapidly on all sides under the enamel ; when teeth are dense the decay travels in the direction of the dentinal tubules toward the pulp. In some cases, in the molars and bicuspids, there will be externally a relatively slight indica- tion of caries while the crown of the tooth may be thoroughly un- dermined (Figs. 252. 253 and 254). As a rule, however, as the cavity in the dentin increases, the enamel at the opening becomes disintegrated and collapses upon the slightest pressure, inas- 344 DENTAL PATHOLOGY much as unsupported enamel easily breaks off. The progress of caries in the dentin is more rapid than in the enamel. The pu- trefaction of meats in a cavity through its alkaline end products may lead to the neutralization of the acids of fermentation, with the arrest of caries, but the caries may begin anew should starches or sugars replace the putrefactive material. The two phenomena which must be considered in connection Fig. 254. — Undermining caries of approximal surface; undecayed enamel cusp (a) about to break away. (W. D. Miller.) with dentin caries are (1) transparency, and (2) pigmentation, or discoloration of the decayed tissue. Transparent Zone or Zone of Tomes In carious dentin a transparent area between the pulp and the limiting line of the decayed portion is usually to be seen in mi- croscopic sections, but not always, the latter condition being probably due to the unfavorable plane in which some sec- tions are cut. When present, this phenomenon is designated CARIES OF DENTIN AND CEMENT! M 345 as the diaphanous halo, or the transparent zone of Tomes (Fig. 255). This area of transparency is present in the dentin which lias not as yet become involved in the carious process because of the preponderance of inorganic salt content, as compared with ordi- nary dentin thereby offering greater resistance to decalcifying agencies (Fig. 256). It has the form of a cone with the apex to- ward the pulp, the axis of the cone following the direction of the tnbuli. Miller found thai the cone is bounded on each side by an Fig. 255. — Caries of dentin. At b is shown the decayed area while at o is shown the transparent zone of Tomes. (W. D. Miller.) opaque baud. At least three hundred specimens of decayed teeth, which had been worn down, mounted on opposing plates were examined by him, and in no instance was any transparency found. Further, this phenomenon is not exclusively an accompaniment of caries. It is observed in sound teeth which have been worn off by abrasion or erosion, and in senile teeth where the roots in their entirety frequently become transparent. Miller observed the transparency in the teeth of old dogs which had undergone 34G DENTAL PATHOLOGY abrasion. The true cause of this transparency has not yet been definitely established, but several things have been definitely proved, namely, first, that it does not occur in devitalized teeth undergoing caries ; second, that decalcification has not taken place in the transparent area, as proved by differential quantitative chem- ical anatysis ; third, that microscopic examination of the transparent zone shows an increase in the thickness of the walls of the den- tinal tubules within the transparent zone, with a corresponding Fig. 256. — Transparent zone of Tomes in dentin; it offers greater resistance to de- calcifying agencies than normal dentin. (W. D. Miller.) decrease in the size of the dentinal fibrillar ; and fourth, that chemical analysis shows a greater proportion of lime salts in the transparent area. The area of transparency is in all probability due to an increase in lime salts, with a consequent thickening of the walls of the tubules and a corresponding decrease in their diameter which results in an equalization of the normally different indices of refraction of the tubules and of the calcified dentin matrix. The transparent zone is therefore the result of the stimula- CARTES OK DENTIN AND CEMENTUM 347 tion of the odontoblastic layer o£ tlie pulp, for the odontoblasts preside over the deposition of additional lime sails in the walls of the tubules. This increase in the amount of calcined tissue protects the pulp against the ravages of caries by rendering less rapid the decalcification process and by establishing a barrier to the thermal insults to the pulp which follow a loss of enamel structure, even in a small area. Pigmentation Every degree of discoloration of the dentin may be observed from the normal color of the tissue to a yellow, yellowish brown, dark brown, or black. The first appearance of decay is not characterized by any visible discoloration neither is it present in acute caries. But it is present in chronic, slow-developing caries, and hence it may be said that the intensity of discoloration is in inverse ratio to the length of time of the involvement. Dis- coloration of the dentin is not exclusively a phenomenon of decay but occurs also whenever dentin is laid bare. Discoloration in worn off teeth is frequently the case in both smokers and non- smokers. The same phenomenon is observed in the teeth of dogs. That the discoloration arises from without, and is not a phenom- enon of dentin caries, strictly speaking, is the prevailing opinion among investigators. It has been variously explained by the ac- tion of acids upon dentin; by the color-forming power of bacteria; and Black has explained it by the settling of coloring matter de- rived from the action of hydrogen sulphide upon such metallic elements as may be introduced into the mouth. Miller attributes discoloration to the action of microorganisms upon organic mat- ter. W. H. 0. McGehee 1 has found that practically all the color- ing agents or dyes which are used by manufacturers for coloring dentifrices, stain tooth structure. This investigator was able to stain enamel, dentin and cementum in the laboratory with a ma- jority of dentifrices on the market. Tooth structure was likewise stained in the course of his laboratory experiments by dentifrices which did not contain added coloring matter or dyes, the pig- mentation in these instances being due to the ingredients in the dentifrices which possess color. The stains were found to be pene- ^IcGehee, W. H. O.: Dental Cosmos, March, 1912. 348 DENTAL PATHOLOGY trating, and not to be affected by sunlight or continued washing. Clinically it was found by the same experimenter that vital teeth in the mouth are occasionally stained by the use of colored denti- frices. It was brought out that nonvital teeth stain much more readily than vital teeth, and that "vital and nonvital dentin and cementum, whenever exposed, readily take almost any stain with which they come in contact, as they are found discolored in practically every instance in which they have been exposed for Fig. 257. — Caries of enamel and dentin which beginning on the mesial surface has progressed beyond the enamel-cementum junction and involved the cementum and underlying dentin. Fig. 258. — Caries of cementum on la- bial surface of abraded upper left central incisor. any length of time;" and further that "crachs in the enamel, abraded and eroded surfaces, cavities of decay, and other similar conditions, offer excellent evidence of stains of every character." McGehee condemns the use of colored dentifrices, his experi- ments having shown that when constantly used they will stain the tooth structure. In connection with the study of dentin caries it should be noted that the average diameter of a dentinal tubule is greater than that of most of the bacteria found in the mouth, and conse- CARIES OF DENTIN AND CEMENT1 M 3-49 quently it must be inferred that bacteria find their way into normal tubules, regardless of any previous decalcification of their walls. The Decay of Cementum The inorganic portion of the cementum becomes decalcified by the action of the acid end product of fermentation, and this is followed by the Liquefaction of the remaining organic matrix (Figs. 257 and 258). It occurs when the peridental membrane has been detached from the cementum, food becoming lodged in the pockets so formed. The invasion occurs along Sharper's fibers. CHAPTER XXIII HYPERCEMENTOSIS General Considerations Hypercementosis, hypertrophy of the cementum (or dental ex- ostosis, as it is sometimes erroneously called) is an increase of cementum substance which serves no physiologic purpose. It is observed in the teeth of the young, as well as in those of the adult, and while it may not cause any reflex painful symptoms, it l'*ig. 259. — Hypercementosis of lower first bicuspid and deflection of its root. Fig. 2d0. — Hypercementosis in upper right second molar. may, on the other hand, be the etiologic factor of serious nervous manifestations. The cementum is not a self -reproducing tissue: it is built upon the dentin from the dentoenamel junction to the apex on all the aspects of the root by the follicular wall, which is also the source of the alveolar process which serves to retain the 350 HYPERCEMENTOSIS 351 tooth. The follicular sac persists throughout the life of the tooth as the peridental membrane, the latter retaining the function of building or tearing down cementum when normal or pathologic conditions demand it. Fig. 261. — Hypercemen- tosis in upper bicuspid. Fig. 262. — Hypercemen- tosis of root of lower mo- lar — the two roots are united by a band of ce- mentum. Fig. 263. — Hypercemen- tosis involving the three roots of an upper molar. Fig. 264. — Hyperce- mentosis involving the apical area of the three roots of an upper molar. Fig. 265. — Excessive hy- percementosis in a lower molar. Fig. 266. — Excessive hy- percementosis in a molar which rendered its removal difficult and entailed the fracture of the surrounding alveolar process. Hypercementosis may affect only the apical portion of a root or roots of a tooth (Figs. 259-264) ; it may affect practically the entire root area of the roots of a molar or bicuspid (Figs. 265- 352 DENTAL PATHOLOGY 268); or on]}' one root or two roots of a triple-rooted molar; and it may be localized upon some portion of the root in the form of a nodule (Fig. 269). Fig. 2o~. — Hypercementosis involving the three roots of an upper left fust molar. Fig. 26S. — Hypercementosis of the posterior Fig. 269. — Nodular form of hy- root of the lower first molar. percementosis. Etiology and Pathologic Anatomy A tooth root which is the seat of hypercementosis has a peri- dental membrane which for a prolonged period of time has been continuously subjected to a degree of irritation not strong enough to cause degeneration in the cells of the peridental membrane, HYPERCEMENTOSIS 353 and yel strong enough to cause a productive stimulation. An ir- ritation from any source which will cause unrecoverable degener- ations of the cells of the peridental membrane can not and will not result in hypertrophy and hyperplasia of the cementum. Therefore inasmuch as in hypercementosis there does occur an increase in the thickness as well as in the number of cementum lamellae, we are led to consider the process not merely as an hy- pertrophy, bul as a combination of both processes, viz.. hypertro- phy and hyperplasia. The cause of hypercementosis mav be Fig. 270. — Resorption of dentin and obliteration of the resorbed area by cementum. mechanical, as for instance the pressure against the root of an adjoining tooth caused by the efforts at eruption of an impacted tooth: tooth movement in orthodontia : the effect of pressure upon the roots of an impacted tooth by the unyielding character of the surrounding osseous structures: the presence of a particle of root filling beyond the apical foramen through continued stimulation of the peridental membrane; the pernicious thread- biting habit : the stimulation of the peridental membrane in- directly from the gingiva by the rough and protruding edges of fillings, or by salivary or subgingival calculi: or undue stress of occlusion upon one or several teeth when the result is several 354 DENTAL PATHOLOGY hypercementosed teeth in the same mouth. Hypercemen- tosis is also observed where a root whose peridental membrane has been the seat of a chronic inflammation caused by very mild infection which has spread from the pulp; and while the inflam- mation may have brought about the destruction of a limited area of peridental membrane, it has also stimulated the eementoblasts Fig. 271. — Ilypercementosis accompanied by dentin resorption and filling in of the resorbed area of dentin by cementum. a, normal dentin; b, c, outline of observed dentin area, cementum of repair containing vast numbers of lacuna with their respective canalic- uli radiating toward the peridental membrane. in the adjacent healthy peridental membrane. In those cases of hypercementosis in -which the hypercementosed area is involved in a chronic dentoalveolar abscess, the hypertrophy started at a time when the infection was of such a degree of mildness as to act as a regenerative factor — a stimulus. After the hypercementosed area was formed, the adjacent peridental membrane became the IIYl'KRCEMENTOSIS 355 seal of destructive changes upon the infection's acquiring greater virulence. It is thus thai we account for a hypercemen- tosed apical root area in juxtaposition to a chronic dentoalveolar abscess (dental granuloma). In chronic peridental inflammation in connection with pyorrhea alveolaris, hypercementosis may develop in root areas even beyond those from over which the peridental membrane has been destroyed. It may also develop consequent upon the removal of Hie pulp when it may be the result of frequent and often needless manipulations with root canal instruments beyond the apical foramen, or as the result of the action of concentrated chemical disinfectants, or again fol- lowing a mild infection of the periapical peridental membrane. Anatomically, hypercementosis manifests itself by an increase in the number and size of cementum lamellae and occasionally by areas of dentin absorption next to the cementum with the sub- sequent tilling thereof by cementum (Figs. 270 and 271). CHAPTER XXIV ABEASION AND EROSION The results of abrasion and erosion, which differ in etiology, are clinically identical. It may be possible to distinguish by im- plication between them, but not exclusively on the evidence afforded by an eroded tooth surface or by an abraded one. By carefully investigating the forces of occlusion, both normal and pathologic ; the character of the lateral contact of one tooth with another; the use of tough or coarse foods; the effect of extraneous forces upon the teeth, such as from pipe stems, the toothbrush, cigarette holders, thread-biting — a differential diagnosis between the two processes may be established. But not so on a clinical examination of the tissues themselves regardless of the influences of environment. Abrasion is a purely mechan- ical process; but erosion is either a purely chemical or a chemico- mechanical process. Etiology of Abrasion In abrasion of the crowns of teeth and, under certain circum- stances, of the roots, when these are exposed, portions are worn away producing surfaces with a high polish over which the end of an explorer will glide smoothly, resembling no other lesion of the enamel or dentin except erosion resulting from chemicome- chanical action. The teeth suffer from restricted degrees of abrasion from the time they assume their respective positions in the arch and begin to exercise their physiologic functions (Fig. 272). When this abrasion is the result of the forces of masti- cation and occurs in teeth in more or less normal alignment, and the diet does not habitually contain coarse or gritty foods in ex- cessive amounts, it can be considered as a physiologic process. It is a pathologic process when it results from the continued friction between the surfaces of opposing teeth in malocclusion, when the result of undue friction by the toothbrush, or when because of the use of gritty tooth powders, or masticatories such as chewing gum or tobacco, or of holding pipe or cigarette stems between the 356 ABRASION and erosion 357 teeth. The loss of the posterior teeth, throwing the bulk of the force of mastication upon the anterior teeth, will in time bring about marked abrasion or wearing away of the occlusal surfaces of the anterior teeth. Pathologic Anatomy of Abrasion The shape of the abraded surfaces will depend upon the posi- tion of the tooth in the arch and the direction and extent of the frictional forces. It may be nothing more than a decrease in the vertical diameter of an incisor with the formation of a square area as the result (Figs. 273, 274, and 275); or it may have pro- gressed to the extent of a complete wearing away of the crown of Fig. 272.— Abrasion— mechanical wearing away of the cusps of a lower molar. the tooth and a portion of the root (Figs. 276-279). Mechanical appliances, such as lingual bars, clasps, etc., are frequently the cause of abrasion. Such instances are seen in Figs. 280 and 281. Abrasions which resulted from abnormal stress of occlusion are seen in tin- scries from Fig. 282-289. Any tooth may suffer from abrasion of such severity as to result in the disappearance of all of its crown and even a portion of its root, The abraded surface presents a highly polished appearance, and, regardless of the ex- tent of tooth structure lost, the pulp does not become exposed, since a constructive and protective process takes place simul- 358 DENTAL TATIIOLOOY taneously with the loss of tooth structure. Tubular calcification and secondary dentin are going on constantly in teeth which are undergoing abrasion, and even in those extreme cases in which all of the crown and a portion of the root have been worn away the Fig. 273. — A series of incisors which have suffered from slight abrasion. At a and b the dentin has been exposed consequent upon the wasting away of the enamel. labially and lingually, and has assumed a brownish yellow color. Pig. 274. — Abrasion of the incisal edges of two upper central incisors; brownish dis- coloration of exposed dentin. remnant of pulp tissue will be protected by secondary dentin. The pulp may also become the seat of degenerative changes, the calcific form being the most frequently encountered. V.BH ^.SION AND I ROi [ON 359 Etiology of Erosion It had been assumed that erosion was a purely chemical proc- ess until the Late W. D. Miller, after years of painstaking in- vestigations and experiments in the laboratory, was v/iablc to produce the characteristic erosion facel by the action of acid sub- stances alone. He was able, however, to duplicate in the labo- ratory the typical erosion surface, with its high polish, by a com- Fig. 275. — Photomicrograph of ground section of one of the abraded teeth shown in Fig. 274. a, enamel; b, dentin; c, abraded enamel with a chip broken off in mounting, on right side of picture; d, abraded and discolored dentin. bination of acid and mechanical action (Fig. 290). He therefore reached the conclusion that at least the experimental form of erosion was not entirely the result of chemical action. Any acid which is capable of abstracting calcium salts from the enamel and dentin, or of dissolving the interprismatic substance, may be con- cerned in erosion ; any acid or acid substance which is sufficiently powerful to disintegrate the organic basic substance of the dentin 360 DKXTAL PATHOLOGY may cause wasting (erosion) with a minimum of mechanical action. 1 In a case of extensive erosion studied by Kirk 2 lactic acid ap- peared to be the cause of the wearing away of the surfaces of the teeth ; and in other cases studied by him he has attributed Fig. 276. — Upper right cuspid. Practically the en- tire crown has wasted away on account of abrasion. Fig. 277. — Upper cuspids which for many years had been the seat of abrasion. The entire crown in each case wasted away without exposing the pulp. the cause to the action of acid sodium phosphate and acid calcium phosphate, which are secreted by the gingival glands as the manifestation of a nutritional disorder. This nutritional dis- 'Miller, W. D.: Experiments and Observations on the Wasting of Food Tissue, Dental Cosmos, xlix, No. 2. 'Kirk, E). C: Items of Interest, xxiv, No. 7, July, 1902, p. 511. ABRASION \\1> EROSION 36] order is responsible for the presence in the blood of an excess of carbon dioxide which changes the basic sodium and calcium phosphates into their respective acid --alts. Fig. 278. Fig. 279. Fig. 280. Fig. 278. — Abrasion of lower third molar. Complete wasting away of the crown. Fig. 279. — Abrasion of lower third molar. Complete wasting away of the crown. Fig. 280. — Spiral-shaped abrasion in upper left cuspid caused by an ill-fitting clasp. The wearing down of the hard tissues advanced beyond the boundaries of the pulp cham- ber which was filled with secondary dentin. Fig. 281. — A series of abraded lower cuspids, upon their lingual aspects, the result of continuous friction by ill-fitting clasps and lingual bars. Kirk states that in those disorders which are classified as dis- eases of sulfoxidation, the blood is loaded with an excess of carbon 362 DENTAL PATHOLOGY Fig. 282. — Abrasion of upper right central incisor, the result of an abnormal frictional stress consequent upon malocclusion; exposed and discolored dentin. Fig. 283. — Abrasion of lingual surface of upper left cuspid reaching beyond the pu'P chamber; second- ary dentin was deposited in sufficient amount to keep the pulp protected from ex- ternal injury. Fig. 284. — Abrasion of the labial surface of the lower right first bicuspid. Fig. 285. -Cup-shaped abrasion in lower molars, the result of abnormal frictional stress consequent upon malocclusion. ABRASION AND EROSION 363 dioxide. "The excess of carbonic acid in the blood is to a certain extent taken care of in the excretory cells of the kidneys by the Fig. 286. — Cup-shaped abrasion in lower first molar, the result of abnormal frictional stress consequent upon malocclusion. Fig. 287.— Cup- shaped abrasion in a lower molar, the re- sult _ of abnormal frictional stress con- sequent upon maloc- clusion. Fig. 288. — Cup-shaped abrasion in lower molar, the result of ab- normal frictional stress conse- quent upon malocclusion. Fig. 289. — Abrasion in a deciduous molar, re- tained in the arch long af- ter the normal time for its exfoliation. mass action of carbonic acid upon the sodium phosphate of the blood, thus: H 2 C0 3 + Na 2 HP0 4 = NaHC0 3 + NaH 2 P0 4 364 DENTAL PATHOLOGY The acid sodium phosphate is separated by the kidneys and carried off in the urine, the sodium bicarbonate being returned to the blood plasma, which is thus made to retain its alkalinity. ' ' Fig. 290. — Action of acid calcium phosphate in conjunction with friction during two and one-third years. (W. D. Miller.) Fig. 291. — Tubular calcification in the dentin. This phenomenon is found in connection with caries, erosion or abrasion. (W. D. Miller.) In the event of the carbonic acid being produced in proportions greater than normal the conversion of the basic sodium phos- ABRASION AND EROSION 365 phate into the acid sodium phosphate also lakes place in the buccal glands, so that their acid exudate erodes the surfaces of the teeth. Pathologic Anatomy of Erosion The eroded surfaces may be shallow, irregular, saucer-shaped, or wedge-shaped. The eroded area lias a highly polished and dense surface, and 1 lie process may involve the enamel, the dentin, and in some instances also the eementum. The eroded surfaces are usually located upon the labial and buccal surfaces, rarely upon the lingual. They are, as a rule, markedly sensitive, al- though again a thorough tubular calcification (Fig. 291) under the eroded area may cut off the tubules from the pulp, rendering the area absolutely insensitive. ( lalcification of the dentinal tubules and secondary dentin are constant accompaniments of erosion to a greater or less extent, and there may also occur degenera- tive changes in the dental pulp leading to atrophy. CHAPTER XXV THE SALIVA Normal and Pathologic Considerations The saliva is the mixed secretion of the three paired salivary- glands — the parotid, sublingual and submaxillary — and of all the small alveolotubular glands of the mucous membrane of the floor of the mouth, the palate, cheeks and inner lining of the lips. Amount: Salivary Stimulants and Depressants. — The amount of saliva secreted in twenty-four hours is variable among in- dividuals and for each one under varying conditions of diet, ex- ercise, temperature, habits, etc.; it has been estimated at from 500 to 1200 cubic centimeters. The secretion is influenced by direct or indirect stimulation, which may be normal or pathologic. The smell of a meal in the course of its preparation and the noise incident thereto, the sight of a succulent dish, the mas- tication of an appetizing morsel, etc.. are common instances of indirect and direct stimulation. On the other hand, the salivary secretion is pathologically stimulated by inflamma- tions of the mucous membrane of the mouth (the several forms of stomatitis),* and by drugs such as pilocarpine, physostigniine, iodine and its compounds, mercury and its compounds, (which are specific sialogogues), acting by direct stimulation of the secreting cells of the glands. All acids, ethereal bodies, pungent substances, tobacco, nauseants, such as ipecacuanha, tartar emetic, are reflex sialogogues. The}* act by producing reflex dilatation of the glandular vessels through their action on the lining of the mouth. 1 In certain nervous disorders, as, for instance, during epileptic attacks, the salivary secretion is abundant. In the course of dental operations secretion of saliva is in some individ- uals markedly increased. It is the result of reflex stimulation. via the mucous membrane, by mechanical contrivances and be- cause of the pressure upon the parotid glands by the overlying tissues in the act of forcibly opening the mouth. The pres- *At the climax of an infectious inflammation of the mucous membrane of the mouth (stomatitis), the salivary secretion may be decreased rather than increased. 1 Preston, C. II.: In N. G. Bennett's Science and Practice of Dental Surgery. 366 THE SALIVA 367 ence in the mouth of ragged teeth and of carious cavities is also a source of reflex stimulation of the salivary secretion. In dis- eases of the hypoacid diathesis characterized by lymphatic en- largements, in chronic follicular tonsillitis and tuberculosis the flow of saliva is abundant. 2 Sialorrhea or an excessive flow of saliva, may be an accompani- ment of toxemias and febrile disturbances. 3 Dryness of the mouth (xerostomia), however, is not a rare occurrence in con- nection with febrile disturbances of some standing. Pain in the teeth produces an increased flow of saliva. The amount secreted by the parotid is less than one-third of the amount secreted by the submaxillary and sublingual together, and may be as low as one-twentieth or one-thirtieth. Acid substances produce greater secretion than sweet substances. 4 Color While saliva may be colorless, grayish or whitish, Michaels has observed that this may vary in certain pathologic states, while in others its normal color is not altered. The saliva of individuals of the hypoacid diathesis is colorless ; that of the gouty and of diabetics is grayish. On standing the "saliva assumes secondary colorations" which are caused by oxidations and ammoniacal fer- mentations of organic substances contained in the saliva, mainly biliary elements. The following table after Michaels is in itself sufficiently explanatory: Different Colors Assumed by Human Saliva Upon Standing, and the Sources Thereof Normal Pigments Pigments which produce it. Eiliverdin Color Greenish Yellowish Blackish green Bluish Brownish Dark brown Red Golden yellow Black Abnormal Pigments Biliflavin Biliprasin Bilieyanin Bilifuchsin Bilihumin Bilirubin Urobilin Melanin : Michaels, J. B.: Siaolo-Semeiology Transactions Fourth International Dental Con- gress, St. L,ouis. 1904. 3 Howe: Dental Cosmos, January, 1911. 4 Pickerill: Oral sepsis. 368 DENTAL PATHOLOGY The saliva, after it is poured on a watchglass, must be ex- amined with an oblique light, the rays striking the fluid from above downwards. The color assumed by the saliva on standing corresponds, in Michaels' opinion, to certain pathologic states. Thus, in gouty eczema the saliva assumes a greenish color; in indicanuria, a bluish color; in chorea, a brownish color; in rheumatism and oxaluria, a golden yellow color ; and in carcinoma, a blackish color. Normal saliva is a semitransparent, frothy fluid the aspect and consistence of which varies according to the proportion it con- tains of ptyaline, glycogen, mucin and inorganic salts. Michaels has stated that the saliva, if left in a bottle for some time, suffers a change in its consistence. In salivas containing cholesterin there is formed, after the specimen stands for some time, a thick, greasy, cream-white coating which floats on the surface. This characteristic is often found in the saliva of diabetics. ''In the normal state the sediments occur in small amounts and are whit- ish. In those suffering hepatic insufficiency, the sediment ap- pears brownish ; in cancer patients, it is blackish. The sediment is composed of epithelial cells and fibrinous substance, and in a few hours falls to the bottom of the vessel." ( Michaels.) Odor Regardless of the odor which results from fermentation proc- esses in the saliva, or lactic and butyric fermentation in indi- viduals of the hypoacid diathesis, certain peculiar odors are char- acteristic of certain diseases. And so it is that Michaels connects a garlic-like odor with phosphorous poisoning, an ethereal odor with diabetes, an acetonic odor with diabetes and alcoholism, etc. Taste The taste of the saliva, which is insipid in normal individuals, is, for instance, bitter in disorders of digestion with hepatic in- sufficiency, sweet in diabetes, salty when soluble chlorides are present in the blood in excess of the normal, and metallic in chronic poisoning with mercury, copper or lead. THE SALIVA Constituents of the Saliva Organic (a) Mucin. (b) Ptyalin. Proteins. (d) Potassium sodium and ammonium sulphocyanids. Inorganic 369 (a) Salts of Calcium (b) Salts of Potassium (c) Salts of Sodium Calcium phosphate. Calcium carl innate. I Calcium bicarbonate (in fresh saliva). | Potassium chloride. } Potassium phosphate. Sodium chloride. Sodium phosphate. Sodium carbonate. Sodium bicarbonate (in fresh saliva). ( Magnesium phosphate. I Magnesium carbonate. (d) Salts of Magnesium (e) Salts of Ammonium J Ammonium carbonate. S I'M MARY The composition of the saliva may be summarized as follows: Water 994.90 Organic matter 3.60 Inorganic matter 1.50 The secretion contains epithelial cells which have been thrown off by the epithelium of the mouth, and salivary corpuscles de- rived from the lymphoid tissue of the faucial, lingual, and pharyn- geal tonsils; but these have no relation to the salivary glands. On entering the mouth these corpuscles swell and their protoplasm be- comes granular. Mucin The source of mucin is from the submaxillary gland and the mucin secretions of the mucous membrane. It is precipitated by weak acid solutions, e.g., acetic and lactic acids and by acid salts. It is the probable material of which the so-called "plaques" are composed, but not as the result of chemical precipitation. It 370 DENTAL PATHOLOGY undergoes alkaline decomposition through the action of mouth organisms, and may be regarded under certain conditions only as an agent which protects the enamel, 5 for Gies has shown that the result of the fermentation of mucin has a dissolving power upon tricalcium phosphate. But, on the other hand, the mucin is not deposited by itself alone on the surfaces of teeth. Through its viscosity or stickiness it binds carbohydrate material to the teeth and soft tissues and the bacteria enmeshed in the mass bring about the fermentation of the carbohydrate material with the ul- timate production of lactic acid, the dissolving agent of enamel interprismatic substance and rods. Consequently, even should the mucin undergo putrefactive decomposition with the formation of alkaline end products, these are soon neutralized and rendered valueless as protective agents in the presence of acid substances when in amounts sufficient to counteract this alkalinity and also to dissolve the enamel structure; this, because the proportion of fermentable material exceeds by far the amount of the mucin in the slimy coatings or deposits. It may be precipitated not only by weak acids, but also by acid salts, such as acid potassium tartrate, and acid sodium phosphate (Kirk). Ropy saliva, in which this "ropiness" or "stickiness" is due to the relatively high mucin content, is associated with progressive caries in children and young persons. The source of mucin, to the extent of 80 per cent of its volume, is from the mucous membrane mucin-secreting glands, and the proportion of salivary mucin has been found by Vulpian to be as high in one healthy man as 0.32 per cent. Ptyalin Ptyalin is an anxiolytic enzyme, because it possesses the property of transforming complex carbohydrates, such as starch and dextrin, into simpler bodies. When the amount of ptyalin is inadequate, the digestion of starch in the mouth is slow and the intermediate products, the dextrins, help to bind the starchy mass to the teeth. The microorganisms contained in the mass cause the fermentation of the enmeshed carbohydrates, with the spickerill, II. 1'.: Prevention of Dental Caries, and Oral Sepsis, S. S. White Dental Mfg. Co., Philadelphia, 1914. THE SALIVA 371 production of lactic acid, which arrests the action of ptyalin and decalcifies the enamel. 6 The ptyalin index of normal resting saliva is increased more than tenfold by acid stimulation (Pickerill). The transforma- tion of starch into the end product maltose is by a process of hydrolysis, effected by ptyalin, the intervening products being erythro-dextrin, a-achroo-doxtrin, /?-achroo-dextrin, isomaltose and finally, maltose. The action of ptyalin (salivary amylase) is arrested in the presence of even a trace of free acid, as weak a solution as 0.003 per cent having that effect. It acts best in a neutral or slightly alkaline solution. The digestion of starch by ptyalin in the stomach continues for about forty minutes or longer after the ingestion of food, or until actual contact of the arresting free hydrochloric acid with the ptyalin. Albumin Albumin is of the nature of globulin ; it is precipitated by heat, and is found in very small amounts. The amount increases in Bright 's disease (Vnlpian, Pouchet, Michaels). In one patient suffering from albuminuria of cardiac origin the percentage of albumin in the saliva was 0.145, and in one suffering from par- enchymatous nephritis it Avas 0.182 (Vulpian, with affirmative control by Pouchet). 7 The Sulphocyanids (Potassium, Sodium and Ammonium) KCNS; NaCNS; NH t CNS Sulphocyanids are found in mixed saliva in proportions vary- ing from 0.0075 to 0.0100%.. The proportion seems to be greater in individuals of the hyperacid diathesis than in those of the hy- poacid. Rheumatic patients exhibit a greater amount than gouty patients, but in patients with phosphaturia the amount is less than in gouty patients. The complete absence of sulphocyanids has been associated with gastrointestinal disorders. Prof. Gies' 8 studies lead one to conclude that the amount of sulphocyanids in the saliva bear no relation ivhat soever to the incidence or prog- ress of caries. "Pickerill: Loc. cit. 7 Michaels, J. P.: Transactions of the Fourth International Dental Congress. 8 JournaI of the Allied Dental Societies, 1911, vi, pp. 289, 297, 323, and 334. 372 DENTAL PATHOLOGY Max Kahn likewise reports negative findings. 9 The sulphocy- anids in the saliva are products of protein metabolism and, Piekerill helieves. of the breaking down of such mouth proteins as mucin, epithelium, leucocytes, etc. He adds that the sul- phocyanids in the saliva, "may have a beneficial effect, if only present in sufficient amount." This investigator found that the sulphocyanids could exert a slight antiseptic action if present in the saliva in a one per cent solution or over. But as the percentage is practically always constant and does not vary by the application of such stimuli as cause an increase in the percentage of other salivary constituents, the role of the sulphocyanids as a preventive of dental caries is nil. The amount of sulphocyanids may. however, be rapidly in- creased in man by the administration by mouth of repeated doses of potassium sulphocyanid of from % to 1 grain in water. The percentage in the saliva was increased to 0.0200 from 0.0100 fa fair average of sulphocyanid content) in three hours follow- ing a dose of 0.1 gram in water. This increased percentage per- sisted for seven days. 10 Inorganic Constituents The inorganic salts are alkali and earthy phosphates, carbon- ates, bicarbonates and chlorides. The alkali group includes potassium and sodium phosphates; sodium carbonate and bicar- bonate (in fresh saliva); ammonium carbonate; potassium and sodium chloride. The earthy group includes calcium phosphate, carbonate, and bicarbonate, the latter in fresh specimens. Mag- nesium, because of its behavior toward analytic re-agents, is left in the so-called alkali group of metals (Simon). It is found in saliva as a phosphate and carbonate. The phosphates and car- bonates may exist in the saliva as acid or alkaline salts. In the gouty diathesis the proportion of chlorides is increased, and decreased in febrile affections. Ammonium carbonate is ac- cording to Michaels, a constant constituent of the saliva, being present in comparatively large proportions in the hyperacid diath- esis (rheumatism, gout). : 'Dental Cosmos, 1914, lvi, 175. 10 Pickerill: Loc. cit. THE SALIVA 373 In addition to all of the foregoing constanl constituents of the saliva, Michaels records the pathologic presence of fatty phos- phorous compounds (lecithin and tyrosin), glycogen, biliary pigments and biliary acids" urobilin, cholesterin, glucose, so- dium and ammonium urates, urea, propionic acid, acetone, suc- cinic acid, etc. The presence of these abnormal constituents is associated with certain pathologic slates. Thus, in the saliva of individuals of the hyperacid diathesis sodium and ammonium urates have been found; in salivas of diabetics, propionic acid, glucose, and acetone; and in that of cholemics and uremics, bil- iary elements. Reaction The old time custom of testing the reaction of the saliva by means of litmus is utterly unreliable. The saliva exhibits an amphoteric reaction and as pointed out by Kirk, in a specimen of saliva the acidity is not due to an uncombined acid, but to the presence of a salt which has resulted from only the partial re- placement of the hydrogen by the metal; the alkalinity in the same specimen is due to the presence of the alkaline salt of the acid by replacement of twice the number of hydrogen atoms. Thus, in a specimen of saliva the presence of the acid ion of the basic salt of phosphoric acid may cause blue litmus to turn red and the basic ion may cause red litmus to turn blue, if the salts do not neutralize each other. Phenolphthalein is the indicator most commonly employed. The Scientific Research Committee of the National Dental As- sociation has recommended that it be used as an indicator and titration be made against NaOH. Phenolphthalein is, however, sensitive to C0 2 , which may obscure the reaction for free and uncombined acids. Bunting 12 recommends the passing of C0 2 - free air through the sample to be tested, while heated to a tem- perature not over 50° C. All uncombined C0 2 will be discharged in from five to ten minutes. This method is less objectionable than that of boiling the saliva. Saliva, the mixed secretion of the parotid, submaxillary, sublingual, and buccal glands is alkaline to litmus although the same specimen may be amphoteric to litmus "Gorup-Besanez: (Quoted by Michaels, J. P., loc. cit.) "Bunting: Official Bulletin of the National Dental Assn., October, 1914, i, No. 4, p. 38. 374 DENTAL PATHOLOGY owing to the presence of acid and basic phosphates and carbon- ates. Saliva is as a rule acid to phenolphthalein because of the presence of C0 2 and acid phosphates and carbonates; it usually is alkaline to methyl orange, which is not affected by C0 2 . All salivas are hence alkaline to the latter indicator and to lacmoid and Congo red. The amphoteric behavior of the saliva is due to the presence in the fluid of free H and OH-ions and the reaction of the fluid is determined by the predominance of either of these groups of free ions. The saliva from a resting gland differs in reaction from that flowing under a stimulus. 13 and as shown by Piekerill the reaction varies according to the nature of the stimu- lus and the length of time it is applied. The result of this stimu- lation differs in different individuals. Thus it has been found by this investigator that the alkalinity is increased by acid stimuli which, from among all other substances, produce the greatest alkalinity per cubic centimeter, and that the alkalinity is depressed by such articles of daily food as white and brown bread, with or without butter, and cake, biscuit, meat and sweets. Pain causes a very alkaline reaction. The average alkalinity of the parotid saliva per cubic centimeter is greater than that from the other glands; but as the rate of flow from this gland is low. the total alkalinity per minute is very much less (Piekerill). The character and the amount of normal or abnormal constit- uents of the saliva reflect to quite an extent the nature of the biochemical reactions in the body. It varies in composition not only in different individuals, but at different times in the same individual, because of the temporary or constant results of nutritional phenomena and of bacterial or chemical intoxications. The investigations of Michaels, Gies, Kirk. Piekerill, Howe, Bunt- ing, Ferris and others have made it possible to enlarge our knowl- edge of saliva and of its possibilities in semeiology. Howe, for instance, has shown that an excessive carbohydrate diet is mani- fested in the saliva by the presence of imperfectly oxidized bodies ; that in artificially induced glycosuria the saliva contains traces of glucose or an aldehyde, and, in intestinal disturbances, traces of indiean. Howe's investigations have led to conclusions confirmatory of the work of Michaels and Kirk: that the saliva is a fair barometer of normal and abnormal body reactions. "Howe, Percy R. : Dental Cosmos, lv, 1913. CHAPTER XXVI THE GUMS AND GINGIVAE Normal and Pathologic Considerations The gums are the soft tissues which cover the alveolar process of the maxilla and mandible and extend from the crest of the alveolar process to the commissure of the lips and cheeks exter- nally; and internally arc continued, in the maxilla with the pala- tal mucous membrane, and in the mandible with the mucous mem- brane of the floor of the mouth. The gums consist of an underlying fibrous connective-tissue mat containing a few elastic fibers, and of an external covering of stratified squamous epithelium (Figs. 292, 293, and 294). The underlying fibrous connective-tissue mat, designated as the tunica propria or the stroma of the mucous membrane, presents a number of elevations, or papilla, which penetrate into the epithelial layer, giving to the oral mucous membrane an appearance under the mi- croscope sui generis. Connective-tissue cells, round, stellate and spindle-shaped, are supported by the fibrous tissue of the tunica propria. The mucous membrane is connected with the underlying structure by means of a layer of areolar tissue, i.e., the submucous layer. The attachment of the mucous membrane may, under normal conditions, be very firm as in the case of the gums and the mucous membrane covering the hard palate, or very loose, as in the case of the buccal and labial mucous membrane and that form- ing the lining of the floor of the mouth. The blood supply of the gums is very rich, being distributed to the connective-tissue under- structure (stroma) the epithelial covering obtaining its nutrition by osmosis from the capillary loops at the apices of the papilhe. The arteries after penetrating and passing through the submucous areolar tissue, break up into arterioles, which in turn break up into capillary loops in the substance of the papillae in close rela- tion with the epithelial layer. The veins follow the arteries in their general course. The nerve supply is good, but the gums are not, when normal, as sensitive to pain as other mucous mem- branes, and particularly is the sensitiveness reduced in the pos- 375 376 DENTAL PATHOLOGY terior, or lingual, portion of the gum due, undoubtedly, to the con- stant traumatism it is subjected to in the process of mastication. GINGIVA Normal and Pathologic Considerations By the term gingivce is meant that extension of the gum tissue proper which, starting at the crest of the alveolar process, reaches Fig. 292. — Normal gingiva of sheep. The relation of its cellular elements is similar to that in the human structures. The cells being larger, the tissue can be studied more satisfactorily than in the human specimen. In man, the horny layer, (stratum corneum) is not nearly as prominent as it appears in this specimen, a, area in which individual epithelial cells with their respective nuclei can be clearly seen; b, stratum germinativum or stratum Malpighii; c, connective tissue stroma; d, capillaries in connective-tissue papilla. (Section by Dr. A. C. La Touche.) to the free unattached margin of the gingiva?, called the gingival border. It is composed of (1) the body of the gingivae, or that portion which is attached, 1 at one end, to the crest of the alveolar process by means of the fibers of the alveolar periosteum, and 1 G. V. Black's classification. THE GUMS AND GINGIWE 377 at llic oilier to thai portion of the root between the alveolar crest and the cementoenamel junction by means of the filters of the peridental membrane; of (2) the \'n'v gingivae, or thai un- attached portion of tissue which extends on the labial, buccal and Lingua] surfaces for a distance of from one to live millimeters; and of (3) the septal gingivae, or that portion of tissue which Fig. 293. — Gingiv.-e of sheep. The arrangement of the epithelial and connective tis- sue structures is identical to that found in man. At the gingival cul-de-sac (subgingival fold) in man the epithelial layer becomes thinner, affording little protection against in- fectious agents which upon breaking through the epithelium involve the underlying con- nective tissue mat from whence the possibility of metastasis is self-evident, a, stratum corneum, or horny layer; b.b, stratum germinativum or stratum Malpighii; c, c, capil- lary network in papilla from underlying connective-tissue stroma (mat) ; d, d, connec- tive-tissue stroma; c, blood vessel in stroma; /, epithelium lining internal surface of gingi- val cul-de-sac, g. almost entirely fills up the interproximal space to a short dis- tance from the contact point, and which springs from the ap- proximal portions of the body of the gingivae. To the gingiva? are attached sets of fillers from the peridental membrane as follows : 378 DENTAL TATHOLOGY A group of fibers which springs from the peridental membrane and is attached to the body of the gingivae; a group of fibers which runs a little below the alveolar crest and connect the peri- dental membrane of one tooth with that of another. This group of fibers passes through the septal gingivae. A group of fibers runs from the peridental membrane, curving at first in an oc- clusal direction and then becomes attached to the crest of the al- veolar process. Fig. 294. — Unman gingiva. The dark border, a, a, is the stratified squamous epithelial lining. Between the epithelial prolongations and within the connective-tissue papillae are found the capillary loops at b; the connective tissue stroma at c, is composed of connective tissue fibers and of round, stellate, and spindle-shaped cells. The epithelial layer being devoid of blood vessels its nourishment is derived by osmosis from the capillary loops in the connective tissue papilla. Functions The functions of the gingivae are protective so far as the peri- dental membrane is concerned. They encircle the tooth in its entirety from the alveolar crest to the external or free gingival border over a distance of several millimeters. The consistence and contour of the gingivae favor the gliding of food over their surfaces in the course of mastication, with the minimum of lodg- ment of debris against the free border, and this protection is further augmented by the crown contour commonly described THE GUMS A\n cixciv.i; 379 as bell-shaped. 1 This arrangement exists when the tissue is qo1 subjected to abnormal degrees of mechanical, chemical, or other forms of irritation. The septal tissues depend to a large extent upon the character of the contact point for the mainte- nance of their physiologic function. Lack of contact or broad contact, between two approximal surfaces leads in time to dis- ease of the gingivae, and ultimately to involvement of the periden- tal membrane and alveolar process. Black and Xoyes attach considerable importance to the gin- givae in maintaining the correct relationship of the teeth to each other and to the arches. They argue that following the extrac- tion of a tooth a mass of cicatricial tissue is formed at the point where the transseptal fibers are attached, (i. e., the peridental fibers which cross from the peridental membrane of one tooth to that of another), and that the contraction of this tissue moves the adjacent teeth bodily toward one another. It is unquestionable that disease and destruction of the gingivae bring about mal- position of the teeth, as frequently seen in pyorrhea alveolaris, where a tooth will move in a direction away from the so-called pus pocket. This is due to the fact that the peridental fibers on the affected side have been lost or destroyed, the pull of the group of fibers on the opposite tooth surface carries the tooth away from the area of peridental and gingival involvement. Destruc- tion of the group of fibers which attaches to the crest of the alveolar process results in the extrusion of the tooth, a phenomenon observ- able in pyorrhea alveolaris. The epithelium which covers the gingivae exercises under nor- mal conditions, a protective function similar to that which per- tains to the epithelium of the covering of the body. In the ease of the free and septal gingiva? the epithelium covers its ex- ternal surface as well as the subgingival space (i. e., that sur- face in contact with the enamel at the neck of the tooth), al- though upon the internal aspect the stratum corneum (horny layer) is attenuated or absent. In people who are careless in the hygiene of the mouth, food debris and mucin become lodged against the free border of the gingiva? and there undergo de- composition, with the formation of acid or alkaline end products. The gingivae are thus at first merely irritated ; but by undergo- iFriesell, H. E- : Jour. National Dental Assn., vi, 579. 380 DENTAL PATHOLOGY ing- a decrease in their power of resistance by reason of this con- stant irritation, they soon become the seat of bacterial activity. Degeneration and death of the epithelial cells lining the gingivae, particularly of those lining the subgingival space, follow, and these tissues and the underlying connective-tissue stroma become not only the seat of bacterial activity, but also an active source of absorption for bacteria and their toxins. It is well to remem- ber that the papilla? of the tunica propria contain capillary loops and that perivascular lymph spaces are also present. Absorption of these noxious substances occurs by the hematogenic or lympho- genic routes, or by both. Clinically the writer has observed and studied a large number of patients exhibiting symptoms of gen- eral toxemia and of infection in the digestive and respiratory organs. which improved markedly by proper treatment being directed at these tissues; viz.. the subgingival spaces. While the life and usefulness of the peridental membrane depend to such a large extent upon the health and integrity of the gingival tissues, again the latter depend for their own health and physiologic ef- ficiency upon the topography of the teeth and the character of the contact between the approximal surfaces.* *Hartzell in his investigation of gingival infections and subsequent systemic involve- ments has thrown considerable light on the absence of protectiveness in the subgingival cul-de-sac. The reader is referred to his writings in the files of the Journal of the National Dental Association. CHAPTEB XXVI I CALCAKEOUS DEPOSITS Calcareous deposits upon the surfaces of teeth are divided, from the standpoint of their origin, into salivary and subgingival (se- rnmal and sanguinary). The former originate entirely from the saliva, the latter probably partly from the saliva and partly from sources other than the saliva, viz.. blood, lymph, and pus. Cal- careous deposits throughout the body, including, of course, de- posits upon the crowns and roots of teeth, are invariably composed of an organic matrix which becomes impregnated with inorganic suits. The organic nucleus, or matrix, is the binding substance. In the month the organic matrix is a mixture of mucin, epithelial a Us, food debris, and bacteria. In the ducts of the salivary glands the calcareous deposit, when present, is composed of an organic matrix made up of a thickened secretion of the epithelial lining of the duct. 1 Calcareous masses in the intestines are formed by the deposition of calcium phosphate, calcium carbonate and ammonio-magnesium phosphate, in varying proportions: arterioliths (calcareous depos- its in the arteries), and pkleboliths (calcareous masses in the veins), are due to the calcification of thrombi. It will therefore he seen that the general arrangement of the calculus is fundamentally identical, no matter where found. Two theories have been advanced in explanation of the phenom- enon of salivary calculi (tartar) formation. One of these worked out by the late H. H. Burchard is based upon the theory that the solubility of water for certain salts of calcium is increased when the water holds carbon dioxide in solution, so that, upon the escape of any carbon dioxide from solution, any amount of soluble cal- cium salts previously held in solution above the normal amount which the water can hold, will be precipitated. He argues that the saliva, after it is poured into the month, loses its carbon dioxide contents, and that calcium salts, particularly calcium phosphate, are precipitated upon and into a mass of organic debris compos.',! 1 Ziegler: General Pathology, New York. Win. Wood & Co. 381 382 DENTAL PATHOLOGY of mucin shreds, epithelial cells, food debris and bacteria. That the end product of carbohydrate fermentation constantly going on in the mouth, especially in locations in which food debris is re- tained because of inaccessibility to the toothbrush or to muscle and tongue action, furnishes a sufficient amount of acid to pre- cipitate the mucin; and that this precipitate, together with bacteria and desquamated cells, forms the organic nucleus which becomes impregnated with calcareous salts. Clinical examinations show that those deposits are found upon surfaces in proximity to the openings of the ducts of the salivary glands, namely, the buccal surfaces of the upper molars and the lingual surfaces of the lower central and lateral incisors. These deposits occur upon surfaces which are rough. Congenital or ac- quired enamel defects are to be constantly borne in mind in con- nection with the slmly of the prophylaxis of calcareous deposits. A tooth surface that is smooth and polished does not favor deposits of tartar. Also, surfaces which are constantly subjected to friction in the course of mastication by the tongue, cheeks or lips are, as a general rule, free from deposits. Concerning the nature of tar- tar composition Kirk 2 analyzes the studies of Rainey, Hartin?-. and of Ord, explaining that when certain earthy salts are pre- cipitated in a medium containing a colloidal substance in solu- tion the resulting precipitate, instead of being crystalline, is in the form of minute spheroidal masses; and further, that as the precipitation progresses, these spheroidal masses increase in diameter so that adjoining masses grow into contact, and by accretion of new material these spheroidal masses coalesce, giv- ing rise to mulberry-like bodies. Professor Harting 3 extended his experiments and showed that when the precipitates are formed in egg albumen, blood serum, or a solution of gelatin, a variety of forms may be produced which resemble concretions found in the animal body. The basic substance or matrix which results after deposition, if treated with an acid, dissolves out the inorganic constituents of the con- cretion, and he named the residue calco-globulin. The spheroidal bodies he named calco-globulin. As has already been shown, the mixed saliva contains a propor- -Kirk: American Textbook of Operative Dentistry, Philadelphia, Lea & Febiger. 3 Ibid. CALCAKI'.OI S M.I'MSITS 383 tiou of calcium salts in solution, mos'1 of which is calcium phos- phate; and consequently the main inorganic ingredienl of salivary deposits is calcium phosphate. Unmixed parotid saliva deposits calcium carbonate on standing. Kirk is of the opinion thai as a result of putrefactive decomposition in the mouth, ammonia is formed, and thai the ammonia will precipitate calcium phosphate Erom its acid solution as calcium ammonium phosphate, or, when magnesium phosphate is present in addition to calcium phos- phate, also as ammonium magnesium phosphate, a salt which is found to lie one of the constituents of certain forms of tartar. A form of deposit eaused by the chewing of the betel nut is of rapid formation and extremely destructive to the investing t issues. Fig. 295. — Salivary calculi on the lingual surfaces of the roots of lower cuspids. The proximity of these surfaces to the mouths of the ducts of the submaxillary and sub- lingual glands is the reason for their vulnerability to these deposits. In essence, the theory just outlined is one which assumes that the organic nucleus of the salivary deposits is furnished by precipitated mucin, desquamated epithelial cells, food debris, bacteria, etc., as found in the mouth; and that the inorganic ma- terial is furnished by the saliva which, as it pours into the mouth, loses to a certain extent its holding power for a number of inor- ganic salts, particularly tricalcium phosphate (Ca 3 (P0 4 ) 2 ). G. V. Black, on the other hand, believed that calcareous deposits upon the surfaces of teeth, either salivary or subgingival, are formed by the deposition upon slightly roughened surfaces of teeth, of a combination of an organic material (possibly a globulin 384 DEXTAL PATHOLOGY which he named agglutinin of salivary calculus) with inorganic salts. In this theory it is assumed that the organic and inorganic Fig. 296. — Voluminous salivary calcu- lus with shelf-like formation which rested upon the mucous membrane of the floor of the mouth. Fig. 297. — Salivary calculus with shelf iike formation. Fig. 298. — Salivary calculus in lower right incisor which had accumulated to within one-eighth of an inch of the apex. ( (bserve the saddle-like arrangement of tin deposit Oil the lingual aspect, resting upon the soft tissues. Fig. 299. — Salivary calculus which had attained considerable size and had caused the exfoliation of the tooth. The apical area was entirely covered by the deposit. elements of salivary calculi are brought together into the mouth in the saliva and deposited upon the surfaces most accessible to c UjCAREOUS deposits :;>:. Fig. 300. — Salivary cal- culus in lower incisor which had caused the ex- foliation of the tooth. Fig. 301. — Salivary cal- culus covering all of the crown and most of the root of the tooth. Fig. 302. — Salivary cal- i nl us which covered a large area of crown surface and all of one-half the root sur- face, the latter upon all as- pects. Fig. 303. — Salivary calculus on lower right cuspid involving approximately two-thirds of the root. Fig. calculus I lit of 304. — Salivary on lingual as- the root of a lower central incisor. Fig. 305. — Salivary calculus covering a por- tion of the labial surface of a lower right central incisor and reaching on the disto-lingual aspect over one-half the length of the root. The invest- ing tissue had been de- stroyed to a level slightly beyond the lowest edge uf the calculus. 386 DENTAL PATHOLOGY the ducts of the salivary glands. He found that the deposit will form in preference upon surfaces of teeth which have lost their natural smoothness or polish, and also that while the quality of the ingested food played a small part in the production of calculi the same could not be said of the quantity. Salivary deposits vary from the minutest possible particle to such a size as to cover the roots of several teeth from the gin- gival margins to the apex (Figs. 295-309). They do not occur in every mouth. Some individuals are practically free from them, while with others they form rapidly in spite of careful brushing of the teeth. They vary in color from a very light chalky color Fig. 306. — Salivary calculus entirely covering the buccal surface of the crown and one-half the length of the roots of an upper left first molar. Fig. 307. — Voluminous salivary .deposits upon buccal and part of the occlusal sur- faces of an upper molar. to a deep yellow. The yellowish variety is usually the harder. There is a gradual increase in density from the time of the first deposi- tion until the calculus assumes a decidedly hard texture. During the beginning of their formation, varying in different individuals from a few days to a few weeks, they are soft and may be re- moved by a thorough brushing of the teeth. In contact with the gingivae as they invariably are, they produce degrees of irritation Avhich lessen the power of the tissues to ward off infection, at the same time rendering the field a favorable one for bacterial activity. CALCAKKOl'S DEPOSITS 387 Lesions in the Investing Tissues Caused by Salivary Calculi The deposition begins a1 the gingival margin, and, following a decrease in the resistance of the soft tissues by virtue of the me- chanical irritation induced by the deposit, bacteria invade the area. An inflammation follows which results eventually in a Fig. 308. — Large masses of salivary calculi removed from the teeth to which they were attached. Fig. 309. — Large masses of salivary calculi. destruction of those peridental fibers which are attached to the gingiva, with a loss of structure in the alveolar process and over- lying gum tissues. The disappearance of the alveolar process, as well as of the gingival tissue, is the result of an absorption of these structures consequent upon nutritional interference, but may also be the result of the liquefaction of tissue cells incident 388 DENTAL PATHOLOGY to bacterial activity in the part ; or it may be the result of both. The deposit is at first located upon the enamel at the gingival margin, but as destruction of the peridental fibers occurs and the alveolar process and the gum tissue gradually disappear, if the deposit be not removed it will increase in size and again impinge upon the peridental fibers, so that the now receded alveolar process and gingival tissue will again suffer another series of pathologic phenomena similar to that just described. In this way the process goes on unless the deposit is removed by instrumental means. The type of inflammation which these salivary deposits induce in the investing tissues should be clearly differentiated from the disturbances induced by other forms of calcareous deposits. In the case of the salivary variety, the destruction of the investing tissue reaches but a short distance beyond the deposit, and when the teeth are thoroughly scaled and polished, and the gum tissue properly stimulated by suitable medication, a return to a healthy condition is invariably the case. The gum tissue can not. however, be brought back to its original relation with the gingival margin. The denuding of the ce- mentuni will be permanently established. Attempts have been made in the past to remedy gum recession by surgical means, but the results have not so far justified the means. P. Rosenthal 4 recommends the following technic to remedy recession of the gums — the result of deposition of tartar, trau- matism, erosion, or caries. He calls attention to the necessity of first restoring the surface contour of the tooth, if necessary, by gold fillings. "The gum above the tooth to be operated on is carefully ster- ilized with tincture of iodin. and a horizontal incision is made the width of the tooth, at right angles with the long axis and sufficiently high up on the gum to furnish a good-sized flap. This incision should involve the periosteum. The flap is then stripped off the bone by inserting a fine instrument under it, starting at the neck of the tooth, and should be large enough to allow of easy mobility. A silk ligature is then passed under the central por- tion of the flap parallel with the incision and taking in almost the entire breadth of the flap. Another ligature is tied tightly around the free portion of the tooth, and to this ligature the first ligature is secured, the flap being drawn up a little higher than 4 Le Laboratoire, Paris, November 26, 1911, Dental Cosmos. CALCAREOUS DEPOSITS 389 the normal gum line of the tooth to allow For a recession from cicatrization. The wound and the ligature are painted with tincture of iodin, this antiseptic treatmenl to be repeated daily. Prom the second day on the gum is massaged in the direction of the long axis and toward the Five portion of the tooth. On the fifth or sixth day the ligatures are removed. As a rule, cicatriza- tion is then sufficiently advanced to prevent recession of the flap. The primary incision would fill up completely without leaving a scar. Rosenthal claims that in eases kept under observation for several years the results are still perfect. In summarizing the effects of salivary deposits upon the in- vesting tissues, it must be stated that salivary deposits exercise a detrimental influence by reason of 1. Mechanical irritation of the gingiva and peridental mem- brane. 2. By favoring the deposition and decomposition of food par- ticles, either fermentation or putrefaction, or both. 3. By rendering the field of their location a suitable one for bacterial invasion — lowered vital resistance. The products of these processes of molecular simplification — fermentation or putrefaction of food particles — produce a degree of irritation in the investing tissues which invites bacterial in- vasion. Bacteria play a leading part in the process. The form of disturbance caused by salivary deposits — salivary calculi gingivitis — may be localized or generalized throughout the mouth. In the former case the investing tissues over one or a few teeth only are affected ; in the latter case the investing tis- sues throughout the mouth are affected. The clinical symptoms of salivary calculi gingivitis are: 1. Disappearance of the gingiva and gums as the result of pathologic absorption (atrophy), bacterial activity, or both. 2. Congestion and tumefaction of the gingiva and gums. 3. Bleeding at the slightest provocation. 4. A change in the color of the tissues from a healthy pink to a deep red, purple, or bluish black. 5. Putrefactive and fermentative changes. 6. Tenderness or pain upon mastication, or upon the intro- duction of irritating articles of food. 7. Fetor of breath. 8. Svstemic involvement. CHAPTER XXVIII SUBGINGIVAL DEPOSITS Etiology Subgingival deposits are those which are in the first place formed under the free gingiva. They are of a darker color than the salivary deposits and are also harder. The darker the de- posit, the more adherent it is to the root. They are evidently Fig. 310. — An upper lat- Fig. 311. — Subgingival Fig. 312. — Subgingival eral incisor with its root deposits in upper right lat- deposits in upper right dis- covered with subgingival eral incisor, distal view. pid. deposits over half of its length. the result of an abnormal degree of irritation of the gingival tissues (Figs. 310-316). The irritation is afforded by the de- composition of food debris and mucin at the necks of the teeth, by ragged or rough edges of fillings, poorly adapted gold crowns, or from any other form of prosthetic appliance or defective res- toration leaving a rough edge at the neck of the tooth which continually irritates the gingiva. Any form of injury to the gin- giva may become the etiologic factor in the deposition of subgin- 390 SUBGINGIVAL DEPOSITS 391 gival deposits. Gingival irritation is not, however, by any means entirely due to defective crowns or fillings, but may be broughl about by defective or insufficient contact points leading to food impactions in the interproximal spaces, with concomitant irri- Fig 313.— Subgingival deposits in Fig. 314.— Subgingival deposits in unper right second molar. u PP. er rl S ht second molar These de- posits were greenish in color and sur- rounded the tooth at the enamel-ce- mentum junction upon all of its sur- faces except the lingual. Fig. 315. — Roots of a molar cov- Fig. 316. — Subgingival deposits on ered with subgingival deposits. the anterior and posterior roots of a lower molar. tation of the gingiva? ; they likewise may be induced by the pres- ence of salivary calculi. Salivary and subgingival deposits may be found upon the same tooth, the supposition being that the 392 DENTAL PATHOLOGY salivary deposit was formed first and the other occurred fol- lowing the gingival irritation induced by the former. It is not infrequent that patients have their teeth sealed and polished and consequently have the salivary deposits entirely removed, while the subgingival deposits remain untouched. In this way Ave may in part account for the fact that in a number of in- stances the subgingival deposit is found while the salivary is not to be seen. The subgingival deposit, once formed, irritates the gingiva, thereby inviting bacterial activity. As the result of the infection, the peridental fibers are destroyed so that additional deposils of calculi will form and encroach upon the still attached border of the peridental membrane. Infection will become active again and more peridental fibers will be destroyed, the process ad- vancing in this way until a so-called "pocket" results. This proc- ess of pocket formation is decidedly chronic in the sense that it is of slow formation, years elapsing in most cases before a well-formed pocket is present. It is not to be assumed, how- ever, that in the presence of any one or several of these etiologic factors, subgingival deposits will be invariably present. The inorganic salts in suitable amount must be present in the gin- gival exudate and the conditions leading to the formation of the organic matrix must be present, and then this takes place only when the body metabolism is disturbed, even though only slightly. LESIONS PRODUCED BY SUBGINGIVAL DEPOSITS: CHRONIC GINGIVITIS Pathologic Anatomy The student should bear in mind the striking difference in the character of the effect upon the investing tissues of salivary de- posits and of subgingival deposits as originally pointed out by G. V. Black. In the former, well-defined pus pockets are rare, while in the latter form pockets almost invariably follow. The early deposition of subgingival calculi can be detected by the color of the gingivae, which are of a deep red, in some instances running to a blue, purple, or even black. The tissues are flabby and present an appearance typical of a chronic inflammation. The stratified squamous epithelium dips into the connective tis- SI BGINGIVAL DEPOSH - :;:»:; sue to a greater Length than is the case with normal epithelium, and the connective-tissue mat of the mucous membrane is almost everywhere infiltrated with Large masses of round cells, most of which are mononuclear Leucocytes, large and small, plasma cells, lymphocytes and polymorphonuclear leucocytes in small numbers (Figs. 317, 318 and 319). Mast cells so often found in mucous membranes which are the seat of chronic inflammation Fig. 317.— Section of human gingiva. The stratified squamous epithelium has lost its characteristic appearance; the projections of epithelial cells between the papillae of connective tissue have become elongated. The gingiva was the seat of a chronic inflam- mation which by continuity involves the peridental membrane and the alveolar process. It marks the beginning of pocket formation. a, a, elongated epithelial projections; b, connective-tissue stroma. are also to be seen. The infection spreads slowly as a general rule, and. involving the fibers of the peridental membrane and the alveolar process, initiates the progressive process of destruction in the supporting tissues of the tooth (Figs. 320-325). The pus 594 DENTAL PATHOLOGY pocket is the result of the destruction of the peridental fibers and of the alveolar process. The proteolytic toxins formed in the course of the inflammatory process liquefy the peridental fibers. The pathologic phenomena which develop in the bone of the alveolar process in pocket formation are characteristic of an // Fig. 318. — Chronic inflammation of gingiva. The epithelial prolongations in the sub- jacent connective tissue elongate as the result of the continued low degree of irritation. The connective-tissue stroma has lost its characteristic appearance and the cells and fibers which were present under normal conditions have been replaced by inflammatory cells; i. e., mononuclear wandering cells comprising mononuclear leucocytes, lymphocytes, and plasma cells and polymorphonuclear leucocytes in small numbers, a, a, elongated epithelial projections; b, b, round cell infiltration. Mast cells are also to be located under the higher magnifications. infectious osteomyelitis. The medullary substance contained in the cancellated spaces becomes the seat of a chronic inflamma- tion in which osteoclasts play an active part. The hard sub- stance of the bone disappears through osteoclastic action, the SUBGINGIVAL DEPOSITS 395 cancellated spaces are eaten through, and the Haversian canals widened. The contents of the spaces become filled with large masses of inflammatory cells, viz., mononuclear and polymorpho- nuclear leucocytes, lymphocytes, plasma cells, and giant cells. Suc- cessively the bone lamellae are destroyed or carried away by osteo- clasis and the inflamed medullary contents of the canal breaks down. Fig. 319. — Chronic inflammation of the free gingiva. The tissue has lost all its histologic characteristics and is gradually disappearing as the result of interference with its nutrition, and cell liquefaction. Kirk 1 believes that "the principles governing- the precipitation of earthy phosphates and carbonates directly from the saliva in the production of true salivary tartar govern also the pro- duction of the girdle-like concretions that are found encircling the teeth at and below the anatomic neck and beneath the gum IKirk: American Text-book of Operative Dentistry, Philadelphia, Lea & Febiger. 396 DENTAL PATHOLOGY margin." The preliminary step in the formation of subgingival deposit this investigator attributes to the retention under the gingival tissues of an inflammatory exudate rich in colloid ma- terial, the latter being the binding material of the deposit, giv- ing to it its characteristic hardness. The difference in color be- Fig. 320. — Gingivitis, chronic, advanced stage, the infection is progressing toward the peridental membrane, a. dentin; b, cementum; c, c, stratified squamous epithelium lining subgingival space; d, d, fillers of peridental membrane in the gingiva; e, e, round cell in- filtration. tween salivary and subgingival deposits is believed to be due to the formation of sulphomethemoglobin; the source of the hemoglobin is from the disintegration of erythrocytes, and the sulphur from the putrefactive changes in nitrogenous food re- tained at the gingival margin. KUP.UINUIVAL DKI'OSITS 397 Tu sections of the gingivae the Layer of stratified squamous epi- thelium and 1 lie epithelial prolongations into 1 he underlying connec- tive tissue assume unusual Conns by reason of a pronounced pro- liferation of epithelial cells and also on account of the level at which the section is cut. In the interpretation of sections of a gingiva which has been the seat of a chronic infectious process, these facts should be borne in mind. Fig. 321. — Gingivitis, chronic, advanced stage, induced by subgingival deposits, a, subgingival cul-de-sac; b, b, portions of stratified squamous epithelium from the internal lining of the gingival cul-de-sac; c, break in the epithelial layer marking one of the portals of the infection (the bit of tissue projecting out was torn in mounting the section) ; d, d, round-cell infiltration; e, fibers in the connective-tissue stroma. rjOS DENTAL PATHOLOGY f- k * ** ■*.. \ Fig. 322. — Progressive chronic gingivitis. Decalcified longitudinal section. The in- fection which originated at the gingival margin has advanced to where the peridental membrane begins. It is only a matter of time before the peridental fibers which are attached to the crest of the alveolar process will become involved, a, alveolar septum; b, crest of alveolar process; c, peridental fibers which are attached to the crest of the alveolar -process; d, dentin; e and /, areas of round-cell infiltration marking the progress of the infection. SUBGINGIVAL DEPOSITS 399 Fig. 323. — Chronic inflammation of gingiva. The light area at the lower section of the picture is the subgingival cul-de-sac. To the left of the picture a portion of cementum and dentin is to be seen, while to the right of the picture is the gingiva and gum. a, subgingival space; b, dentin; c, cementum; d, epithelium of subgingival space; e, point at which infection has brought about liquefaction of epithelial lining; f,f,f, areas of round-cell infiltration. (Chronic inflammation.) 400 DENTAL PATHOLOGY b /•-...- Fig. 324. — Chronic inflammation in the gingiva which has spread to the peridental membrane. An area of marked chronic involvement (round-cell infiltration i is seen in the horizontal peridental fibers, a, a, alveolar process; b, b, cementum; d, d, horizon- tal fibers of the peridental membrane; e, an area of involvement which includes some of the horizontal fibers of the peridental membrane. Sl'l!(il\(il\ \l, DKI'OSITS 401 Fig. 325. — Progressive chronic gingivitis, a, cementum; b, space produced by detach- ment of cementum from dentin in process of decalcification and sectioning; d, fibers running from peridental membrane into gingiva; c, f, and g, stratified squamous epithe- lium lining internal surface of gingival cul-de-sac; h and i, round-cell infiltration in gingiva (chronic inflammation) progressing in the direction of the fibers of the peri- dental membrane at / and d. CHAPTER XXIX DISEASES OF THE PERIDENTAL MEMBRANE The peridental membrane, 1 or pericementum (alveole-dental peri- osteum, or root membrane) is a fibrous structure with a rich vas- cular and nerve supply, devoid of elastic fibers, encircling- the root of the tooth in its entirety, and attached to the cementnm by means of fibers which bear the same relation to the cementnm as the periosteal fibers of Sharpey do to bone (Figs. 326, 327 and 328). The functions of the peridental membrane are: 1. To act as the means of attachment of the tooth to the al- veolus. 2. To exercise a cushion-like function, thereby protecting the more sensitive internal organ of the tooth, i.e., the pulp, from traumatism such as would result from mastication, blows, etc. 3. To act as a nourishing periosteum to the cementnm and as the source of collateral circulation to the alveolus. 4. To maintain the gingival contour by virtue of the arrange- ment of its fibers at the neck of the tooth. 5. To absorb and build alveolar bone and cementum during the life of the tooth in response to degrees of stimulation, and until such time as occlusion has been permanently established. 6. Tactile function. It is thicker near the neck of the tooth and in the apical re- gion, but becomes thinner throughout with age. This fact ac- counts for the greater susceptibility of the peridental membrane to infectious processes in the middle-aged and the old. With a thinning of the membrane there occurs a decrease in the num- ber and in the caliber of arteries and capillaries, and the less- ened circulation in the membrane renders more difficult or im- possible the warding off of infectious processes. The blood supply of the pulp and that of the peridental mem- brane are intimately associated. This consists of a variable num- nVe are indebted to the late Dr. G. V. Black ami to Dr. F. B. Noyes for their valuable investigations of the histologic elements of the peridental membrane. 402 MSKASKS OF Till: PERIDENTAL MEMBRANE 4<>:J ber of arteries and veins (as a rule one main artery and its vein, but occasionally more than one), passing through the apical foramen into the pulp where it undergoes ramifications; the other two or more arteries and their respective veins are distributed to the peridental membrane. They follow in the peridental mem- brane a direction parallel to the long axis of the tooth, break- ing up into arterioles and capillaries which encircle the mem- Fig. 326. — Normal peridental membrane, prepared by carefully detaching the peri- dental membrane from a freshly extracted tooth in which no pathologic processes had taken place. Notwithstanding the care in dissecting the peridental membrane some layers of cementum were removed unsuspectingly and are shown in the section. That scaling of root surfaces without removing some of the cementum is an impossibility is confirmed by this section, a, a, cementum lamelhe; b, b, normal fibers of the peridental membrane. brane in its entirety. The peridental membrane is brought into close relationship with the gingiva from the crest of the alveolar process to the cementoenamel junction, by means of the alveolar crest fibers. These fibers run from the peridental membrane into the body of the gingiva and are attached to the fibers of the al- veolar periosteum as they turn over the crest of the alveolar process. In addition, the peridental membrane sends into the gingiva the free gingiva groups of fibers, and across the septal 404 DENTAL PATHOLOGY gingiva the transseptal fibers which run from the peridental membrane of one tooth to that of the next. The fibers of the peridental membrane are wavy or un- dulated in order to enable the tooth to have a certain amount of play in its alveolus without traumatizatiou of the fibers. They may for convenience of description be divided into the intraal- c d e d ___. C fi Fig. 327. — Normal peridental membrane in situ, a, dentin; b, b, cementum; c,c, peri- dental membrane; d, d, d, cancellated spaces in alveolar process; c, c, c, compact or Haversian bone. veolar and the extraalveolar fibers. The intraalveolar fibers pass into the substance of the cementum and of the alveolus for pur- poses of firm attachment, and are the prototypes of Sharpey's fibers in periosteum. They comprise the horizontal fibers, the oblique fibers, and the apical fibers. DISEASES OF TIIK PERIDENTAL MFIVIBRANE 405 Horizontal Fibers. -Horizontal fibers are a narrow group of fibers attached to the eementum at one end and to the alveolar process al the other, occupying a space immediately beyond the alveolar crest. Their function is to support the tooth againsl lateral displacements, and to assist in preventing rotary move- ments of the tooth. Fig. 328. — Normal peridental membrane and its relation to eementum and alveolar process, a, a, peridental membrane; b, b, eementum; d, d, lamellae of alveolar process (compact or Haversian bone). Oblique Fibers. — Oblique fibers run obliquely from the ee- mentum to the alveolar bone and constitute the bulk of the mem- brane. The attachment of the fibers at the eementum is at a higher level than in the alveolar process in the case of the upper teeth and at a lower level in the case of the lower teeth. Their function is to support the tooth against occlusal impactions. Some of these fibers run direct to the alveolar process without split- 406 DENTAL PATHOLOGY ting into smaller fibrillse; others split into fibrillae which are joined together for attachment at the alveolar process. Apical Fibers. — Apical fibers are a continuation of the oblique fibers which, by altering their course for a more direct approach to the alveolar process, assume a fan-like distribution. Around the apical area of the tooth these fibers, together with the con- nective-tissue cells between them and blood vessels and nerves, constitute the periapical tissues. The extraalveolar fibers comprise the alveolar crest fibers, the free gingiva fibers (unattached at the gingival extremities), and the transseptal fibers. Alveolar Crest. — Alveolar crest fibers follow for a short distance in a direction at right angles to the long axis of the tooth curv- ing in an apical direction for attachment at the crest of the alveolar process. Free Gingiva. — Free gingiva fibers are unattached at their terminations in the free gingiva and septal tissues. The group which penetrates the septal tissues is known as the septal fibers. Transseptal Fibers. — Transseptal fibers take a course immedi- ately under the alveolar crest fibers on the approximal aspects of the tooth, and are attached to the peridental membrane of the ad- jacent tooth. This classification of the fibers of the peridental membrane into groups is not to be discerned in every specimen studied microscopi- cally. It should indeed be accepted pretty much as a theory which satisfactorily explains the forces which tend to maintain the tooth in its alveolus and enable it to have a limited movement in certain di- rections. In the average sectioned specimen of peridental mem- brane in situ this arrangement of its fibers can not be discerned at all, or only with considerable difficulty. That some such ar- rangement as above described actually occurs and is micro- scopically visible, there is no doubt; but the variations therefrom in arrangement and disposition are also numerous. The Structural Constituents of the peridental membrane are: 1. White fibers, i.e., apical, oblique, horizontal, alveolar crest, transseptal and free gingivae, the latter including the septal fibers. 2. Fibroblasts, i.e., spindle-shaped connective-tissue cells occu- pying positions parallel to the long axis of the tooth or almost any other direction. DISEASES OF THE PERIDENTAL MEMBRANE 407 3. Cementoblasts — cementum-building cells located on the ce- mentum side of the membrane. 4. Osteoblasts — alveolar tissue building cells — located on the alveolar side of the peridental membrane. 5. Osteoclasts — alveolar tissue resorbing cells, large multi- nucleated cells lying at points along the alveolar side of the peridental membrane. 6. Cementoclasts — cementum resorbing cells presenting the same characteristics as the osteoclasts, but located on the cemen- tum side of the membrane and concerned in the process of ce- mentum resorption. 7. Epithelial debris — remnants of the enamel organ. 8. Blood vessels and nerves. An arterial trunk branches out into a number of arteries before it penetrates the tooth. One or more of these enters the root canal and the others run up on each side of the peridental membrane and branch out into a veritable network of capillaries which at the crest anastomose with the blood vessels of the gingiva and gums. The nerves fol- low an analogous course. Blood vessels also enter the peridental membrane from the alveolar process and pass out from the peri- dental membrane into the alveolar process, thus affording to the peridental membrane a collateral circulation from the alveolar bone, rendering it possible for the peridental membrane to live after the apical circulation and the anastomoses with the blood of the gingiva) and gums have been destroyed by infective proc- esses or by surgical intervention. The fibroblasts are the cells which form the white fibers of the peridental membrane. These cells are spindle-shaped and their number decreases with age. The cells occupy places be- tween the fibers. The cementoblasts are the cementum-building cells and are to be found between the white fibers of the peridental membrane. They are irregular in outline. The osteoblasts are the bone-building cells, and those which are to be found in the peridental membrane represent the remains of a group of cells that were concerned in the building up of the alveolar structure. CHAPTER XXX NONSEPTIC PERICEMENTITIS By nonseptic pericemental inflammation is to be understood that the peridental membrane or pericementum has become the seat of vascular changes following abnormal degrees of irrita- tion from which bacterial influences are excluded. It may begin at the gingival margin and spread to the entire membrane, or at the apex and likewise involve the organ throughout its entire extent. The causes of nonseptic pericemental inflammation may be enumerated as follows: Root fillings protruding through the apical foramen, broaches, etc.; the introduction of medicaments into the root canal which upon evaporation bring about a degree of irritation from which the pericemental fibers are unable to quickly recover; the mal- lethig of gold fillings; the artificial separation of teeth for op- erative purposes; the use of clasps, etc.; the construction of fillings which interfere with the normal articulation of the tooth with its opponent; the impingement upon the gum and peridental membrane by crowns, clasps, clamps, and other appliances; rapid movement of teeth for orthodontic purposes. The use of any irritating drug which under ordinary circum- stances will cause marked irritation of soft tissues in other parts of the body, should be avoided in root canal medication, or so modified in its degree of concentration as to produce the least degree of tissue injury compatible with germicidal efficiency. For instance, the irritating effect of an otherwise so efficient a germicide as formaldehyde, or such of its preparations as trioxy- methylene, is pronounced; formaldehyde in any form disorgan- izes protein matter readily, and therefore its employment in solutions of strong concentration defeats the purpose for which formaldehyde is generally employed in root canal therapeutics. Verily it destroys microorganic life, but it does this simultane- ously with a partial or complete disorganization, not only of the periapical tissues, but also of the surrounding alveolar structures. 408 NONSEPTIC PERICEMENTITIS 409 From the standpoint of practical efficiency, it is not alone neces- sary that a chemical substance should invariably kill bacteria, but it is likewise of importance that it should do Ibis with the least possible impairment of the functions of the healthy cells with which the antiseptic must come in contact. We surmise that the tendency to overlook this point is just the echo of the practitioner's bacteriologic conception of inflammatory disorders, to the exclusion of the factors that render possible bacterial in- vasion with its attendant reactions. In the seat of an inflammatory process, whether acute or chronic, it is of the utmost importance that the cellular elements be maintained at their maximum degree of functional activity in order that the defensiveness of the area and the opportunities for recovery be at their highest. If the functional efficiency of the cells of the periapical tissues is lessened by virtue of hav- ing been exposed for some time to substances which coagulate their protein contents, or which deoxidize or dehydrate their protoplasm, or in some other way alter their physical or chemical characteristics, the outcome is bound to be detrimental to the future efficiency of the tooth. The effect of strong germicidal concentrations upon the delicate periapical tissues, made up of the fan-like arrangement of the peridental fibers which begin at a point where the surfaces of the root begin to converge to- ward the apex, plus blood and nerve supply, and interfibrillar connective-tissue cells, is manifested in a series of degenerative changes eventually ending in their death. Furthermore, the partial or complete interference with the chemical mutations in protoplasm results in the presence, in the osseous tissue im- mediately surrounding the periapical tissues, of areas of partly or completely devitalized bony structure which act as a source of continuous irritation to the as yet healthy adjacent tissue, so that eventually the resistance to bacterial invasion becomes subnormal. There is little doubt that areas which have been subjected to the action of strong germicides become at some future time, bacteria being available, foci of chronic in- fection. As all steps in root canal operations are, in only a small number of instances, performed with due regard to strict asepsis ; and furthermore, as foci of infection may develop in the jaws as the result of bacterial invasion via the circulation and 410 DENTAL PATHOLOGY arising from other focal points in the body, it can not be rea- sonably argued that even in the presence of partial disorganiza- tion of periapical and osseous tissue the bacteria necessary to bring about an acute, subacute or chronic inflammatory process are not almost always available in sufficient numbers. As a pos- sible means of lessening postoperative complications in root canal work, the use of milder concentrations of germicidal agents is suggested, so graded as to employ in the neighborhood of the peri- apical tissues the weakest possible solution compatible with germicidal efficiency. Any form of irritation or any abnormal degree of pressure at the gingival margin or apex of the root, may give rise to non- septic pericementitis. It also results frequently upon extirpa- tion of the pulp and is due in such an instance to the tearing of the pulp from its connection, with the formation of thrombi, and to extravasation of blood into the apical peridental mem- brane. The nonseptic inflammation which thus develops, trans- lated clinically as pain or tenderness, will persist until such time as the coagula will have been taken care of by mononuclear leucocytes. "When anesthetizing the pulp by the cocain pressure method the blood content of the pulp is partly driven into the vessels of the peridental membrane and this together with the formation of thrombi resulting from the extirpation of the pulp brings about not infrequently a painful complication in the shape of a nonseptic pericementitis. This is assuming, of course, that bac- teria have not invaded the periapical tissues, but that they do is, however, the case more frequently than the former. In the case of teeth devitalized by means of arsenic, if the arsenical applica- tion be not correctly gauged, its absorption into the pericemental tissues will give rise to a severe nonseptic pericementitis which soon thereafter, however, becomes septic in character. Another source of apical traumatic nonseptic pericementitis is to be found in frequent and unnecessary manipulations with root canal in- struments in the neighborhood of the apical foramen, and the forcing of root fillings beyond the apical foramen. If the cause or causes of a nonseptic inflammation of the peri- dental membrane should persist, in time the result will be the development of the septic form of pericementitis. In the case of the apical form of nonseptic pericementitis a dentigerous cyst NONSEPTIC PERICEMENTITIS 411 may be the ultimate result. It is no1 an infrequenl occur- rence for the area of nonseptic inflammation in the peridental membrane to become infected by microorganisms which gain ac- cess to ii via the circulation. The accidental perforation of a root with a drill may give rise to a uonseptic pericementitis even though the instrumenl was a sterile one. This is, however, rarely the case, and instead a septic pericementitis results, accompanied by the absorption of an area of cementum and of dentin im- mediately surrounding the perforation, and of the gum tissue which proceeds until the area of absorption is completely ex- posed at the gingiva. The passage, accidental or intentional, of root canal instruments and filling materials through the apical foramen, only rarely results in a nonbacterial inflammation. The lowering of the vital resistance of the periapical tissues conse- quent upon a continued irritation, chemical or mechanical, soon results in their invasion by bacterial forms. CHAPTER XXXI SEPTIC PERICEMENTAL INFLAMMATION AND ACUTE AND CHRONIC DENTOALVEOLAR ABSCESS Septic pericemental inflammation may be acute or chronic and is caused by the presence in 1 lie periapical tissues of microor- ganisms which, in the vast majority of instances, have gained access to that territory via the root canal. If the bacteria are in sufficient numbers and their virulence is relatively high, and if, on the other hand, the resistance of the individual and particu- larly of the invaded tissue cells is unequal to the task of success- fully combating the invasion, an acute dentoalveolar abscess will in all probability result. If the reverse should obtain, the dis- turbance in the peridental membrane will be slight, and the in- fection will be overcome with no permanent injury to the peri- dental membrane. In such a case the bacteria will be destroyed by the polymorphonuclear leucocytes with horseshoe-shaped or partite nuclei. The small destruction of peridental fibers will be replaced by cells which proliferate from the preexisting fixed fibers of the membrane, while the unaffected leucocytes will enter the lymph stream in the perivascular lymph spaces, and the dead leucocytes and fixed tissue cells will be carried away in a similar manner. In other words, the bacteria having been disposed of and their toxins neutralized, a repair of the limited destruction of cells takes place and conditions return to normal. If the invading bacteria are of low virulence from the begin- ning, or following the subsidence of an acute dentoalveolar ab- scess, a chronic dentoalveolar abscess will result, provided, of course, that the defensive forces of the body are unable to cope with the situation. As explained later in this chapter, all in- fections of the peridental membrane via the root canal do not result in the formation of abscesses, acute or chronic. It is for this reason that the title of this chapter specifies pericemental in- fection and acute and chronic dentoalveolar abscess. The pres- ence of pyogenic bacteria in the apical region, while leading in most cases to the formation of a dentoalveolar abscess, never- 412 SEPTIC PERICEMENTAL INFLAMMATION 413 theless, in some few eases, cither because of an optimum of de- fensive forces, or of timely preventive measures (so-called abor- tive measures measures intended to reestablish a normal cir- culation in the area), the infection in the periapical tissues does not advance to the stage of visible pus formation with involve- ment of the adjacent cancellated bone of the jaw. A pulp may be the sent of suppuration, of putrefaction, or of suppuration followed by putrefaction. It is well to remember, therefore, thai a "decomposed" or so-called "putrescent pulp" is the result of a suppurative process, followed in a large num- ber of instances by putrefactive changes; or it may be the re- sult of purely putrefactive changes. Suppuration is, of course. the result of the infection of a tissue — in this instance the dental pulp, by pyogenic and other organisms, whose toxins are capa- ble of causing degenerative changes and liquefaction of tissue cells. The remains of the dead cells and the extravasated serum offer excellent pabulum for that kind of bacteria (saprophytic) which thrive upon dead or disorganized tissue. Saprophytic bac- teria gain access to the tissue previously disorganized and de- vitalized by the activity of the pyogenic bacteria; or else it is possible that the pyogenic cocci, and others among the original bacterial exciters, have in themselves the power of further split- ting the dead nitrogenous matter; viz., the dead cells of the pulp and the dead wandering cells. The end products of the suppura- tive process are in this way further broken down. The simplifi- cation of dead nitrogenous matter by the activity of saprophytic microorganisms is termed putrefaction. Basic cadaveric alkaloids, or ptomaines, are produced by the decomposition of this dead nitrogenous matter, through the agency of saprophytic organisms. Cadaverin, putrescin, neuridin, neurin, and methyl guanidin are some of the most important. 1 In the study of pericemental infections, we should constantly bear in mind that the products of nitrogenous decomposition are in themselves capable of inciting an inflammatory process. When particles of a pulp which has been the seat of suppuration and subsequent putrefaction, or of putrefaction alone, are forced through the apical foramen accidentally or in the course of de- fective root canal technic, an acute infection may develop in the 1 Ziegler: General Pathology, New York, Win. Wood & Co. 414 DENTAL PATHOLOGY periapical tissues within twenty-four hours thereafter. It is probable that the activity of the process is due not only to the forcing of pyogenic organisms through the apical foramen, and to a change in the oxygen tension in the root canal and peri- apical tissues, which confers increased virulence to the faculta- tive anaerobic bacteria in the periapical tissues, but also to the presence therein of some of the cadaveric alkaloids above men- tioned although this latter is not the most important contin- gency. The organic contents of the dentinal tubules, viz., den- tinal fibrillar and their ramifications, are, of course also subject to putrefactive changes. According to Vaughan and Xovy, ca- daverin and putrescin are capable of producing strong inflam- mation and necrosis. In large doses they are poisonous to mice, rabbits, and guinea pigs. Cadaverin lias been found to produce suppuration in the absence of bacteria; neuridin is one of the most common products of putrefaction, and while it is not poi- sonous in itself, it develops a toxic action when in association with other products of putrefaction. 2 Neurin, however, which occurs in the putrefaction of human flesh is in itself a highly poisonous alkaloid. In by far the larger percentage of cases the apical section of the peridental membrane is the one first to be attacked by in- fection via the root canal. These involvements of the pulp are the immediate consequence of neglected dental caries and in the absence of the latter disease it is safe to assume that, ex- cepting a negligible percentage of cases, septic apical perice- mentitis would, of course, not develop. The importance of pre- venting the onset and progress of dental caries is the key to the prevention of septic infections of the apical peridental mem- brane, and of dentoalveolar abscess, either acute or chronic. Prophylaxis of Pulp Involvements Dental caries is, to a large extent, a preventable disease, and the secret of its prevention lies in the thoroughness and per- sistence with which the prevailing methods of prophylaxis are carried out. While the constitutional factor in dental caries un- doubtedly influences the extensiveness and rapidity of the proc- ess, it does so, however, only in a small proportion of cases. 2 Vaughan and Xovy: SEPTIC PERICEMENTAL INFLAMMATION 415 What these constitutional predisposing causes are we arc un- able to state with any degree of definiteness. Theories have been promulgated here and there in the effort to blaze the way to- ward a reasonable solution of the problem, but as yet nothing bearing the stamp of scientific conviction has been adduced. The influence of the mineral constituents of drinking water, the na- ture of the food used, climate, soil, the influence of the internal secretions, the elaboration within the body and the secretion within the oral cavity of substances capable of being split into compounds having solving properties on the enamel of the teeth, are some of the factors which have been discussed as having a possible bearing upon the prevalence of dental caries. But after all, about the only phases of the problem of caries prevention about which accurate data are available are the actual steps of its production beginning with the dissolution of the conti- nuity of the enamel prisms by lactic acid. In other words, while we know the steps in the process of caries, we are in ob- scurity regarding the underlying factors or conditions which bring about caries, rapid or slow r progressing, or which determine an immunity or nonsuseeptibility to this disease. Therefore, in the work of caries prophylaxis all measures are generally aimed at the ultimate causes responsible for its onset — causes of a purely local character and preventable in most cases. The continuous supervision of patients from the time of the erup- tion of the deciduous teeth, with the view of maintaining the surfaces of the teeth in a condition of strict cleanliness, and to insure correct occlusion of their permanent successors; the oc- casional treatment of the fissures of the molars with silver nitrate, if supplemented by the thorough brushing of the teeth upon ris- ing, after each meal, and upon retiring, will greatly reduce the prevalence of caries. And ipso facto the involvement of the pulp, its death by suppuration or putrefaction or both, and the spread- ing of the infectious process to the peridental tissues, will like- wise be circumvented. Etiology of Septic Apical Pericementitis The causes of septic apical pericementitis may be enumerated as bacteria and bacterial products which have invaded the peri- apical tissues proceeding from the root canal inwardly (Figs. 416 DENTAL PATHOLOGY 329-334). They are a combination of the pyogenic organisms ■which have been instrumental in destroying the pulp, and the saprophytic organisms which may follow in their wake; and to these must be added the products of nitrogenous decomposition. The peridental membrane is infected by continuity from the in- Fig. 329. — Chronic dentoalveolar abscess of an upper lateral incisor with a large area of rarefaction. The infectious proc- ess involved an adjacent tooth on each side. An incompletely tilled root canal was evidently the cause of the continued infection. Fig. 330. — Chronic dentoalveolar ab- scess, in a lower right first molar involving both roots. The source of the infection was the incompletely treated and filled root canals. Fig. 331. — Chronic dentoalveolar ab- scess involving the upper first and second left bicuspids. The apical portion of the root of the second bicuspid has undergone absorption. Fig. 332. — Three chronic dentoalveolar abscesses in connection with upper right first and second bicuspids and first molar. The root canals were the source of the in- fection. fection in the root canal. It may also become the seat of an in- flammation following the passage through the apical foramen of the saprophytic bacteria with the products of their activity, ■which were concerned in the decomposition of a pulp which has SEPTIC I'KKICKMKNTAL INFLAMMATION 417 succumbed following the infliction of a traumatism, such as a blow or the sudden impact upon a hard substance in 1 lie course of mastication, or the continued action of thermal irritation in the absence of external opening in the crown. Occasionally even in the absence of dental caries, saprophytic infection of the pulp occurs either via the blood stream (i. e., blood vessels of the apical peridental membrane), or through imperfections in the enamel. In the latter instance, the process has been compared by Inglis 3 to the putrefactive decomposition of eggs in the presence of apparently unbroken shells. The putrefactive process spread- ing from the pulp into the periapical tissues doubtless plays an Pig. 333. — Chronic dentoalveolar ab- scess in upper first and second bicuspid. The root canals were the source of the in- fection. Fig. 334. — Chronic dentoalveolar ab- scesses in upper first bicuspid and second molar. The path of the periapical infec- tion in the molar has joined with an in- fection also chronic which originated at the gum margin. indirect role in the development of an acute suppuration. There follows a decrease in the vital resistance of the periapical tis- sues, and a subsequent infection by pyogenic organisms which reach the area by way of the blood stream; or, the bacteria re- sponsible for the putrefactive decomposition consist of varieties among which some assume parasitic powers by a change of en- vironment from a disorganized to a living medium. At any rate, the passage of the bacteria concerned in the decomposition of a dead pulp, and of the animal alkaloids to which they give rise, is soon followed in the periapical tissues by suppuration and dentoalveolar abscess formation. 3 Inglis-Burchard: Dental Pathology. 418 DENTAL PATHOLOGY The etiology of periapical infection is not, however, limited to preexisting infections in the root canal resulting from suppura- tion or putrefaction of the pulp, or of a combination of both proc- esses. In a number of cases after extirpation of a noninfected pulp the periapical tissues become the seat of an infectious in- flammation. The infection in these instances has been carried beyond the apical foramen by unsterile instruments or dressing cotton, or by failure to properly protect the root canal by means of the rubber dam against contamination from the saliva. F" *• d Fig. 335. — Chronic dentoalveolar ab- scess involving the roots of the upper left second bicuspid and upper left first molar. The roots did not penetrate the maxillary sinus as might be surmised from the pic- ture and the maxillary sinus was not af- fected. The infectious process involved the osseous tissue of the maxilla anterior to the external wall of the maxillary sinus. Fig. 336. — Chronic dentoalveolar abscess involving the upper right central and lateral incisors. The chronic osteomyelitis resulted in caries of bone over a relatively large area. Fully two-thirds of the lateral incisor projected into this cavity. Again, the periapical tissues may become the seat of an infec- tion by continuity from an infection in an adjoining tooth (Figs. 335, 33G and 337). It is not at all rare to find that one or two adjoining teeth on either side of the primarily infected periapical peridental membrane have become involved. The infectious proc- ess spreads through the cancellated spaces to an adjoining tooth and from there it may involve one or two teeth more. Infec- tion of the peridental membrane, with acute dentoalveolar ab- scess formation as the consequence, may also occur from an in- fection which, beginning at the gum margin, advances toward the apical region. Here the infection involves the pulp which, how- ever, does not succumb at once in all instances. One of this type SEPTIC PERICEMENTAL [NFLAMMATION 410 of cases showed n wel L-ma rke.l area of ra re l';iet inn in the apical region, and when examined clinically by percussion, gave every indication of being the seal of a chronic dentoalveolar abscess. The tooth was opened into, bu1 ool before having to resort to novocaine anesthesia, much to the intense surprise of the operator and the discomforl of the patient. The pulp was removed and this was followed by a discharge of pus. The pulp had main- tained its vitality in spite of the suppurative process in the peri- apical region, probably through an attenuated connection with its source of blood and nerve supply. Septic pericementitis, acute or chronic, is also caused by per- forations of the walls of root canals by drills, burs, etc., (Figs. 338-339), or by the passage through the apical foramen of in- fected broaches or drills (Fig. 340). A chronic infection is usu- Kig. 337. — Chronic dentoalveolar abscess (so-called dental granuloma) in connection with an upper left first and second bicuspid. By a process of continuity the infection spread to the mesio-buccal root of the adjoining first molar. ally the result, located on the lateral aspect of the single-rooted teeth and in the bifurcation of bicuspids and the trifurcation of molars. In some instances the alveolar process and the gum tis- sue from the gingival margin to the perforation disappear (fol- lowing the infection of the perforated area of the peridental membrane) to the level of the perforation, exposing that much of the root surface. Several such eases have come under our ob- servation. Another interesting cause of alveolar abscess is intraalveolar root fractures, caused by external severe traumatisms (Fig. 341). We have recently observed two such cases. One of them was in a young acrobat, who presented upon the gum between the upper left central and lateral incisors a sinus one inch in length parallel 420 DENTAL PATHOLOGY to the long axis of the face. The alveolar infection was of long duration and had been brought about by the intraalveolar frac- ture of the root of the lateral incisor, following presumably an effort to lift with his teeth some extraordinary weight. The in- fection became apparent years after the accident. At times con- Fig. 338. — Chronic dentoalveolar abscess in the Fig. 339. — Chronic dentoalveolar bifurcation of the roots of the lower right first abscess caused by the perforation of molar brought about by the perforation of the the distolingual aspect of an upper mesial wall of the posterior root. second bicuspid. Fig. 340. — Chronic dentoalveolar ab- scess caused by a fragment of a broach broken in the root canal. Fig. 341. — Intraalveolar root fracture of an upper right cuspid, which caused a chronic infection of long standing. The destructive inflammation had produced a sinus whose course was through the labial alveolar plate. ditions would be quiet, at others a discharge would take place from the sinus. When examined by the writer the fragment of root was found at the mouth of the sinus, and was removed with a pair of dressing pliers. The other case was that of a woman giving no history of traumatism, but having suffered in- tensely from "an abscess in one of her upper teeth." Two or SEPTIC PERICEMENTAL INFLAMMATION- 421 three teeth posterior to the upper left cuspid had been extracted to remedy ;i condition brought about by the intraalveolar frac- ture of the upper left cuspid. The extraction of the fractured tooth, as expected, resulted in the disappearance of all symptoms of infection. The foregoing causes may he summarized as follows: 1. Through the root canal or canals, by a process of continuity. following suppuration or putrefaction or both as the result of deep-seated dental caries. 2. Following death of the pulp by traumatisms or thermal irri- tation, in the absence of caries or any break in the continuity of the hard tissues of the crown but with the development of pu- trefactive processes in the dead pulp. 3. Following the extirpation of a healthy pulp (preliminary ab- sence of infection in canal contents), the infection being carried to the periapical peridental membrane in the course of canal in- strumentation, or because of insufficient protection against con- tamination from the saliva. 4. By continuity from an infection in an adjoining tooth or teeth. 5. By continuity from an infection of the gingivae the peri- apical tissues become infected and a dentoalveolar abscess fol- lows. This source of infection may also give rise to pathologic reactions in the peridental membrane of the pyorrhea alveolaris type. A paroxysmal intensification of the infection which orig- inates in the gingival margin results in a form of abscess of the investing tissues known as "pyorrhea abscess" or "lateral ab- scess." 6. Through accidental perforation of the floor of the pulp chamber or wall of a root canal. 7. As the result of intraalveolar root fracture. Periapical Infection by the Hematogenic Route Bacteria may reach the periapical tissues by way of the circu- lation and become active in some area of the periapical tissues or some other section of the peridental membrane previously weakened by mechanical or chemical irritation. This mode of in- fection of the peridental membrane, while not of frecpaent oc- currence, is nevertheless not to be overlooked. 122 DENTAL PATHOLOGY There is as much Logic in assuming that foci of chronic infec- tion upon areas of the body at remote distances from the teeth and jaws may bring about infections of the peridental memhrane, as there is in accepting the possibilities of metastatic infections from foci of infection around or upon the roots of teeth. The --'•ailed pericemental abscess, first discussed by D. D. Smith, and subsequently minutely investigated by Kirk and Darby, is a possible instance of infection of the peridental membrane via the blood stream. It is of course admitted that the infection in these pericemental abscesses in teeth having live pulps may also originate at the gum margin, but the clinical evidence in the cases described by Kirk points with more definiteness toward the hematogenic mode of invasion. The lateral or pyorrheal abscess is a pathologic reaction different from the pericemental abscess, and is the result of either an exacerbation of an infection in the soft tissue of the gum. the bacteria having penetrated through the subgingival space, or else of the infection through the epi- thelium of the gum tissue overlying the pyorrhea pocket when the gingiva has been previously destroyed by the infection. Recovery from Periapical Infections. Acute and Chronic Processes Septic apical pericementitis does not lead in every case, as pre- viously stated, to the formation of an acute or chronic dento- alveolar abscess. In those instances in which the invading or- ganisms are of low virulence and are present in relatively small numbers, and when the vital resistance of the invaded tissue cells is high, the symptoms of the inflammatory process subside be- fore reaching the stage of abscess formation. Again, it should be noted that the periapical tissues may be invaded by bacteria which from the start give rise to chronic symptoms. For in- stance, following the extirpation of a normal pulp, if every step of the operation has not been performed with regard to complete asepsis there will develop in twenty-four to forty-eight hours symptoms of periapical pericementitis. This inflammation is in many cases due to the introduction of bacteria into the peri- apical tissues in the course of instrumentation. These forms of septic apical pericementitis do not always pro- gress to abscess formation. One or two conditions account for SEPTIC PERICEMENTAL INFLAMMATION 123 the subsidence of the symptoms. The infection is either entirely overcome by the natural defenses of the body, or else all of the bacteria are qo1 overcome; and then, being of Low virulence, re- main in the periapical tissues and se1 up a low grade inflamma- tion, thus establishing a chronic periapical abscess a so-called blind abscess or, erroneously a dental granuloma, encapsulated by a Avail of fibrous tissue. In the former ease (viz., when the infection is overcome following- active phagocytosis) it is to be assumed thai the bacteria have caused recoverable cell degeneration or. at most, the death of so few cells thai their re- placement by new cells through the agency of fibroblasts is readily accomplished. CHAPTER XXXII ACUTE APICAL DENTOALVEOLAR ABSCESS The infection, if it progresses to the point of acute clento- alveolar abscess formation in the periapical tissues, because of the high virulence of the bacteria and their presence in large num- bers, together with the low resistance of the invaded tissue cells, advances through the alveolar bone to discharge at some point in the mouth, or on the face, or neck, and in rare instances in areas of the body even more remote from the original seat of the infection. An acute apical dentoalveolar abscess may be defined as an area of infection localized in the apical region of the peridental mem- brane, originating in the vast majority of cases in a preexisting- infection in a root canal or canals of the corresponding tooth, and in a few instances from a previously infected apical area of a neighboring peridental membrane. It is at first but poorly circumscribed. It develops as readily upon deciduous as upon permanent teeth and is in the majority of cases the sequela of neglected dental caries. In multirooted teeth the pulp in one, and even in two root canals may be alive, while in the remain- ing root canal it may have undergone suppuration or putrefac- tive decomposition, or both, involving the apical peridental mem- brane and resulting in an acute dentoalveolar abscess. Such an abscess shows at first evidences of being slightly cir- cumscribed. The virulence of the infection — the rapidity with which the bacterial toxins destroy the cells with which they come into contact, either directly or indirectly — prevents to some ex- tent that form of tissue proliferation which eventually results in the encapsulation of a focus of infection. Tissue proliferations are in inverse ratio to the virulence of the infection, the less virulent the infection, the more abundant the tissue prolifera- tions ; and vice versa. From a pathologic standpoint the chronicity or acuteness of an inflammation is not determined exclusively by the relative de- gree of virulence of the bacteria, or the severity of the symp- 424 ACTTTE APICAL DENTOALVEOLAR ABSCESS 425 toms, or the time consumed by the infectious process up to the establishment of a sinus. An inflammation is chronic when the amount of connective tissue of repair (fibroblasts) predominates, and "when among the leucocytes which have been called to the seat of the infection the mononuclear variety predominates; it is acute when the fibroblasts and the fibers to which they give origin are in the minority and the polymorphonuclear leucocytes are in the majority. In chronic inflammations the mononuclear leucocytes and plasma cells are in the majority, while in the acute inflammations the polymorphonuclear leucocytes are in the ma- jority. Clinical Symptoms The symptoms accompanying the development and progress of an acute apical alveolar abscess are: 1. Tenderness of the tooth to percussion and upon mastication. 2. Pain. 3. Swelling. 4. Increased redness of the gum overlying the affected tooth and adjacent areas. 5. Tenderness on pressure on the gums over the apical region of the tooth. 6. Looseness and protrusion of the tooth. 7. Rise in temperature. 8. Constipation. 9. Fetor of breath. 10. General malaise. 11. Headache. The pain, slight at first, increases gradually in severity; it is throbbing in character and is intensified upon assuming a re- clining position and does not begin to subside until the im- prisoned inflammatory exudates, liquid and solid, reach the soft tissues overlying or underlying the affected tooth. Tenderness to pressure is in all instances indicative of inflammation of the peridental membrane and the greater the area of peridental mem- brane involved the more pronounced the tenderness. In severe inflammations of the pulp, it might be remarked in passing, either septic or nonseptic, the periapical tissues become likewise in- volved in the inflammatory process and thus, even in the pres- 426 DENTAL PATHOLOGY enee of a vital pulp, a painful response to percussion may occur. This tenderness is in response to stress of occlusion or to per- cussion of the tooth for diagnostic purposes. Pain is also due to an exaggerated intraosseous pressure, the inflammatory ex- udates, liquid and solid, being enclosed in the cancellated spaces, freely supplied with blood vessels and nerves. Practically all acute dentoalveolar abscesses, if proper measures are not in- stituted to remove all sources of infection in the root-canal, be- come in time chronic. The protrusion of a tooth is caused by infiltration of the peri- dental membrane by inflammatory liquid and solid exudates (leu- cocytes), and by the swelling of the cells of the peridental mem- brane — the cloudy or hydropic degeneration which accompanies inflammation in connective tissue.* In the acute form of dento- alveolar abscess there is, as a general rule, comparatively little destruction of peridental fibers, and consequently these teeth frequently recover following correct instrumental and therapeutic technic and the filling of the root canals, previously rendered aseptic, to the apex. With the increase of intraosseous pressure there is an increase of pain, increased blood pressure, and a rise in temperature of from one to four degrees F. The tongue is thickly furred, the breath offensive, and the patient shows evidences of toxemia. From twelve to thirty-six hours, but in some cases longer, after the pain becomes well marked, the infectious process has pro- gressed through the cancellated and cortical bone and estab- lished an opening through the latter. The inflammatory exudate (serum, lymph, degenerated and dead leucocytes and fixed-tissue cells) is now under the periosteum, and after the infection has brought about a destruction of a small area of the periosteum the adjacent soft tissues become involved, and the face swells. The gum tissues overlying the root of the affected tooth appear red, flabby, and swollen from the beginning of the infection, slightly at first, but increasingly so as the infection progresses. The extensive swelling of the tissues of the mouth, face and neck is not due entirely to diffusion of pus through the tissues, be- cause edema enters largely into the process. The cellulitis is accompanied by difficulty in opening the mouth, which persists for days after the establishment of the sinus. But the difficulty in *Adami and McCrae: Texl Book of Pathology, Philadelphia, Lea and Febiger. SlCUTE APICAL DENTOALVEOLAR ABSCESS 1*2 i opening the mouth is due qoI only to the distention of the tis- sues by swelling, bu1 also to involvemenl of muscular tissue, par- ticularly of the masseter and buccinator muscles, which for the time being supplied with an excess of stimulus are maintained in ,i semicontracted state. Sinus Formation The course of a sinus from a dentoalveolar abscess is governed by the location of the affected tooth, upper or lower, in the arch, the density of the tissues overlying the seat of the abscess, the virulence of the infection, gravity, and the injudicious applica- tion of hot poultices (Fig. 342). Acute dentoalveolar absc< in connection with the upper central and lateral incisors and cuspids may discharge upon the labial or palatal aspects of the maxilla, but, as a general rule, the sinus will open upon the ex- ternal, or labial, aspect. Dentoalveolar abscesses in connection with the lateral incisor and palatal root of the first molar have occasionally been observed to discharge upon the palatal as- pect of the jaw. 1 Sinuses from dentoalveolar abscesses in upper single-rooted teeth and in the buccal roots of multirooted teeth discharge, as a rule, upon the labial and buccal aspects, respectively; discharge upon the palatal side is the exception. Dentoalveolar abscesses in connection with the central and lateral incisors, cuspids, or first and second bicuspids, may dis- charge into the nasal cavity, the sinus opening in the floor of that cavity. An abscess upon a cuspid, bicuspid, first, second or third molar, may discharge into the maxillary sinus. The shape, size and location of the maxillary sinus vary with practically each individual; consequently, the relationship of the upper teeth to that cavity varies with equal frequency. The upper cuspid, and even the lateral incisor, have been known to produce infection of the maxillary sinus. 2 It is of importance to note that bone changes are not always visible in cases in which the maxillary sinus has become involved by continuity from an infection on the root of the tooth. It has been shown by Hunsberg and Hyjek that it is possible to have an 1 Turner, J. G. : In Science and Practice of Dental Surgery, by N. G. P.ennett. -Seydell, E. M : International Journal of Orthodontia, ii, Xo. 6, 344. 428 DENTAL PATHOLOGY extension of an infection through the Avails of the frontal and sphenoidal sinus to the neighboring parts without macroscopic changes in the bone. 3 Fig. 342. — Result of poulticing the face in connection with acute dentoalveolar abscesses (Oakman). It is rare that teeth abutting against the floor of the antrum have not a thin lamina of bone between the apices of the roots 3 ibid. ACUTE APICAL DENTOALVEOLAR ABSCESS 429 and the mucoperiosteuni of the sinus. If a tooth suspected of being the cause of an involvement of the sinus should be extracted and no opening should be found leading into the sinus, it is no evidence thai such a toot li was not at fault. The infectious proc- ess may have established a microscopic opening undiagnosable by instrumentation. Teeth rarely discharge upon the lingual aspect of the mandible, because of the greater thickness of bone between the apical areas of the teeth and the lingual aspect of the mandible, than toward the labial side. A dentoalveolar abscess in connection with any one of the lower teeth may " point" externally, gravity being to some extent a factor in deciding upon that course of discharge. If the infection has followed a course above the origin of tbe deep cervical fascia, the point of discharge will be above the lower border of the mandible ; but if, on the other hand, the course of the infection has been under the deep cervical fascia, the point of discharge may be somewhere upon the neck, one or more inches under the border of the mandible. In some exceptional cases the infectious process has spread under the deep cervical fascia to discharge at some point on the chest, and in one case the opening of a sinus from a lower tooth was upon the upper third of the thigh. Dentoalveolar abscesses in connection with the lower teeth, more frequently than any others, discharge externally un- der the mandible, establishing submental fistulae (Fig. 343). In the case of the upper or lower teeth, particularly if the roots are long, the buccinator may act as a barrier against evacuation into the mouth, the infection in that event spreading subperios- teally and, after causing a rupture of the periosteum at a higher or lower point beyond the attachment of the buccinator (accord- ing as to whether it is an upper or a lower tooth, respectively), involves the overlying soft tissues, causes an interstitial abscess among the fascial layers, and discharges at some point on the face or jaws. 4 The symptoms accompanying the involvement of the soft tis- sues of the face or neck, in the case of an acute dentoalveolar abscess, which will discharge upon the external aspect, are unmis- takable. At some area in the swelling in the face or neck the 4 Turner, J. G.: In "Practice of Dental Surgery," by N. G. Bennett. 430 DENTAL PATHOLOGY inflammatory symptoms are exaggerated: there is increased red- ness, a marked degree of heat to the touch, exquisite tenderness to palpation, and toward the last unmistakable fluctuation. Following the rupture of the skin the discharge will continue until the cause is removed — or else will heal over temporarily, to again discharge when exacerbations of the infection occur (sub- acute abscess. In the event that the cause is not removed, or is only Fig. 343. — Submental sinus. Opening of a sinus from a subacute dentoalveolar abscess in a lower incisor. partially so, the condition becomes chronic. It may be timely to add that a sinus leading from a focus of infection to the ex- terior is nature's way of eliminating the infection so far as it may be possible without mechanical or surgical interference, and a more logical way than that which attempts to drain it through the pinhole opening at the apex of the root. In some cases the drainage of a dentoalveolar abscess takes place through a channel between the alveolar wall and its perios- A i i Ti: APICAL DENTOALVEOLAR ABSCESS I'M triiin. and this occurs as well in the case of abscesses upon the upper teeth as upon the lower. Abscesses in connection with lower molars, apparently disobeying the laws of gravity, will discharge ;it the neck of the tooth, owing to the fact thai the density of the mandible in the region of its border offers a decided resistance to the infectious process. That stage of ;i dentoalveolar alisc^s immediately preceding the perforation of the alveolar bone and its periosteum and the in- flammatory infiltration of the soft tissues is the one accompanied by the most severe pain. The piercing of the periosteum and the invasion of the gum tissues and those of the face is marked by a subsidence of the pain and an increase in the size of the swelling. The invasion of the overlying soft tissues may give rise to a small and limited swelling', or to one involving large areas of the face and neck. Those abscesses in which streptococci are pres- ent in small numbers and staphylococci in large numbers cause limited swelling of the soft tissues, while those in which the streptococci are present in large numbers give rise to extensive involvement of the soft tissues of the face and sometimes of the neck. Following this stage, the inflammatory discharge pene- trates the soft tissues of the gums and of the mucous membrane lining the cheeks and spreads into the soft tissues, causing a cel- lulitis, viz., a diffused or phlegmonous involvement of soft tissues. Phlegmonous inflammation of the face, or facial cellulitis of dental origin is, therefore, the result of the involvement by infec- tion of the soft tissues of the face and neck, and of the mucous membrane of the mouth and marks the last stage of an acute dentoalveolar abscess. In some instances the periosteum is not perforated at once, but the pus remains under it to find an exit at some point remote from the seat of the infection. These sub- periosteal abscesses or paridcs, are the ones usually causing acute or chronic periostitis and osteomyelitis accompanied by limited or extensive necrosis. The products of the inflammatory process, by reason of a strong resistance of the outer fibrous layer of the periosteum, do not find a ready exit into the overlying soft tis- sues. The pus remains confined for some time under the perios- teum and the infectious process continues subperiosteal^ causing its detachment from the bone and the death of the latter over, in 432 DENTAL PATHOLOGY some cases, large areas. Eventually it will discharge at some point distant from the original focus, and in addition to the sinus thus formed, other sinuses will lead from the sequestrum or sequestra to various points on the face or within the mouth. In the absence of early surgical intervention several sequestra will be formed and the case may assume alarming proportions. CHAPTER XXXIII PATHOLOGIC ANATOMY OF ACUTE DENTOALVEOLAR. ABSCESS A typical dentoalveolar abscess presupposes the death of the pulp. The infection of the peridental membrane is caused by pyogenic and other organisms previously engaged in the de- struction of the pulp with suppuration as the result, and the in- fection of the peridental membrane takes place by a process of continuity. Once more we are constrained to emphasize that saprophytic organisms and the by- and end-products of their activity doubtless play some part in the process as previously noted. A septic apical pericementitis, in the sense that the in- fection is at first not at all circumscribed, precedes the formation of a dentoalveolar abscess. One of the first symptoms of pericementitis, whether acute septic, or acute nonseptic. is tenderness of the tooth to percussion, or to any force, no matter how slight, when applied against the tooth. This symptom is due to the congestion of the vessels of the peridental membrane, the increased amount of blood having reached that area in response to the increased stimulus (the ir- ritant) whether bacterial, chemical or mechanical. The conse- quence is an undue pressure against the sensitive filaments of the membrane. The congestion of the blood vessels is the hyperemia of the inflammatory cycle. As the infection progresses, the tooth protrudes in its socket, consequent upon the presence among the fibers of the peridental membrane of liquid and solid inflamma- tory exudates, and of fibroblasts of repair; this protrusion is also the result of the hydropic degeneration of the fibers of the peridental membrane. Following a momentary acceleration of the blood stream, in the presence of an irritant, slowing takes place simultaneously with the rearrangement of the blood cor- puscles — the red cells taking a position in the axial stream, the leucocytes accumulating in the parietal stream. It is the passage into the meshes of the peridental membrane of a serous exudate and multitudes of leucocytes, which marks the beginning of the 433 434 DENTAL PATHOLOGY subconscious struggle on the part of the individual to successfully combat the bacteria] invasion. If the bacteria are in numbers or virulence unequal to the power of the body defenses, the symptoms will quickly subside, and there having occurred but slight structural derangement, conditions will return to normal. Investigations by the author have shown him conclusively that such is the termination in some cases of mild infection of the peridental membrane. True, a comparatively small number of cells may have died, and some may have become the seat of degenerative changes. Those in which the degenerative changes are slight may recover; those in which they are not, succumb, and these few, as well as those that had at first died, are carried away, probably in the lymph of the perivascular lymph spaces and lymph clefts, and by the lymphatics of the cancellated spaces. In the event of an acute dentoalveolar abscess developing, all the phenomena typical of an acute inflammation in any other region of the body will fol- low in sequence with such modifications as the topography of the part induces. The destructive infectious process affects first the tissues of the peridental membrane, then those of the surrounding bony struc- ture, then those of the overlying mucous membrane, and finally the products of the septic inflammation find an outlet into the mouth; or externally onto the face, as under the mandible (sub- mental fistula I ; or into the maxillary sinus, in the cases of bi- cuspids and molars, and of cuspids, and even of lateral incisors. Dentoalveolar abscesses in relation with the central and lateral in- cisors and cuspids may discharge into the nasal cavity, and in ex- ceptional cases, especially following the use of hot poultices, the in- fection may spread between the deep cervical fascia and underlying muscular structures to discharge at some point in the body removed from the head. In acute dentoalveolar abscess the progress of the infection is clinically observable in all of its stages, and its symptomatology is definite and unmistakable. Beginning with the tenderness of the tooth, the redness of the overlying gum tissues, the throbbing character of the pain increasing in in- tensity as long as the inflammatory exudates remain imprisoned within the unyielding osseous tissue of the jaw, the decrease of the pain concomitantly with the perforation and phlegmonous PATHOLOGIC AWTOMV OF ACUTE DENTOALVEOLAB ABSCESS 435 involvemenl of the soft tissues of the mouth and face — every stage c;iii be easily identified. As the tissues of the periapical peridental membrane are destroyed following degeneration, death, ;)n•"> instances they found diphtheroid bacillus which grew both an- aerobically and aerobically. Additional facts of interest concerning the bacteriology of al- veolar abscess and infected rool canals are quoted from Gilmer and Moody *s reporl : "Anaerobically, in old cultures, we have seen in material from three different abscesses a black-pigment-producing organism. This organism is slow-growing and does not usually appear for about five days. We do not believe that it is of any importance in these infections. "In three of 1 lie chronic eases from which material was ex- amined the patients were treated with autogenous vaccines with striking beneficial results. The vaccines were made from the cul- tures of both the aerobic and anaerobic organisms, and were given in graded doses at five-day intervals. "These were chronic suppurations, following that class of acute infections of the mandible characterized by much brawny swell- ing, persisting over a week or more with little or no indications of pointing. The pus discharge continued with no seeming diminution for several weeks after the acute symptoms had sub- sided. In each instance the pus flow stopped promptly on the use of the vaccine treatment. "Those who have made extensive observations of the tendency of acute attacks of alveolar abscess recognize that they occur epidemically. Whether the epidemics of streptococcus nose and throat infections follow or occur simultaneously with epidemics of alveolar abscess is a question both of interest and importance. We have not sufficient data to warrant a definite statement rela- tive to the subject, however, since we have found in both infec- tions the same bacteria, and as both occur epidemically, it may be discovered that there is a \ery definite relationship between the two infections. "It seems reasonable to suppose that the presence of the strep- tococcus of nose and throat infections may easily cause simul- taneous or secondary infections in the jaws, the organisms reach- ing the apices of the roots through cavities of decay in the teeth, or through the circulatory channels." Eos enow"' has made cultures from the pus withdrawn from a 5 Rosenow, E. C. : The Pathogenesis of Focal Infection, Jour. National Dental Assn. 454 DENTAL PATHOLOGY chronic dentoalveolar abscess with sinus and has obtained al- most pure culture of Streptococci viridans in association with a few colonies of Streptococcus hemolyticus. He has also obtained from a chronic dentoalveolar abscess a short chained streptococ- cus. The cultures from the pulp of the same tooth after extrac- tion yielded two days later the same organisms that were isolated from the pus of the abscess. CHAPTER XXXV BONE Normal and Pathologic Considerations Bone is a form of connective tissue impregnated with lime salts. There are two varieties of bone, spongy or cancellated, and compact. The spongy bone is the fundamental form, yet only in the compact form are all the structural peculiarities of bone present. A cross section of compact bone shows a number of round openings, the Haversian canals. The central opening of a Haversian canal is surrounded by layers of bone concentrically arranged — the concentrically disposed lamellce — this canal and the surrounding lamellae forming a Haversian system. In the longitudinal section the course of these canals seems to corre- spond to the long axis of the bone, although some run obliquely and establish communication between adjacent canals. All the Haversian canals communicate with the central marrow cavity and may be viewed in the light of continuations from it. Each Haversian canal contains bone marrow — myelitic substance — a tissue richly supplied with blood vessels, lymphatics and nerves. The spaces between the Haversian systems are filled by short lamellae, which are not arranged in any definite way — the inter- stitial or ground lamellce. The circumferential lamellae are those which surround the bone on its outer and inner circumference; i.e., they are located immediately under the periosteum and around the central marrow cavity. In the ground matrix are located the lacuna-, from which minute channels radiate — the canaliculi. Each lacuna contains connective tissue elements, the bone corpuscles. These bone cells exhibit processes which ex- tend into the canaliculi. The lacunas of a Haversian system com- municate with one another by means of their canaliculi, but not with the canaliculi of adjoining systems. The channels through the circumferential lamellae which carry blood vessels, lymphatic vessels, and nerves from the periosteum to the Haversian canals, and those which run across the inner circumferential lamellae to the central marrow cavity, are known as Volkmann's canals. 455 456 DENTAL PATHOLOGY Bone is surrounded by a nitrous membrane, the periosteum. It consists of two layers — the outer fibrous, dense protective layer; and an inner, less dense layer very rich in blood vessels and com- posed of delicate white and elastic fibers. The inner layer is con- cerned with the formation of bone and is known as the osteoge- netic layer. The outer layer contains the larger blood vessels, the inner layer the smaller though more numerous blood vessels. The osteoblasts are located in the osteogenetic layer. The fibers of Sharpey are fibers from the periosteum which have remained in the lamellae without undergoing calcification. The central cavity and all cancellated spaces are filled with marrow of which two va- rieties are recognized, the red and the yellow, the red being the younger variety and the yellow the older. Bone marrow is a bb.od-forming organ and consequently contains all varieties of blood cells as well as myelocytes, nucleated red blood cells, giant cells, fat cells, mast cells, etc. Bone marrow consists of a delicate connective-tissue framework supporting a rich supply of capil- laries. The connective tissue cells in marrow are the marrow cells which are concerned in bone formation. In yellow marrow, the mar- row cells have been replaced by fat cells. In addition there an- to be found in marrow some lame connective-tissue cells — the giant cil's — which are concerned in the absorption of calcified tissue and which are known under the term of osteoelasts. With the ex- ception of the bones of the vault of the cranium, of the face, and part of the lower jaw. the skeleton is mapped out in its fetal con- dition by solid cartilage of the hyaline type. \Yhen bone de- velops from centers of ossification in cartilage it is known as endochondral bone. When formed directly under the perios- teum it is known as periosteal bone. The changes evident in en- dochondral bone formation consist in an increase in the size of the cartilage cells, their rearrangement in rows, and an increase in the size of intercellular substance and the deposition of lime salts. In endochondral bone formation the process is one of sub- stitution: namely, the cartilage cells are absorbed and replaced by new bone. In periosteal bone formation the process is car- ried out through the agency of the osteoirenetic layer. 2 -This histological description of bone lias been compiled from the writings of G. A. Piersol (Textbook of Normal Histology). BONE 457 Bone Involvement in Dentoalveolar Abscess If a section of the mandible be examined it will be found that it is composed of thick layers of compact bone externally and in- ternally and thai within the layers of compact bone the cancellated or spongy bone is found (Figs. 357, 358, 359,360,361,362 and 363). The latter is made up of the thin bony walls of the cells which contain the medullary or myelitic substance, the so-called cancellated spaces. In life these cells are not exactly spaces, be- ing almost entirely filled up by the myelitic substances. The char- acter of the bone in the walls is identical with that of the compact layer which surrounds the mandible in all of its aspects except at the upper aspect through which retention is afforded to the teeth. The walls of the alveoli, internally, appear more or less smooth and are made up of a layer of compact bone, although everywhere as seen in ground sections examined microscopically, cancellated spaces open through it. Not infrequently some such cancellated space will be located on a line with a root canal, and consequently when a root canal instrument is forced past the apical foramen it will penetrate for a distance without finding any obstruction in its way. The alveoli are supported by layers of compact bone which are the w alls of the cancellated spaces and are so arranged as to afford the greatest possible support against direct and lateral stress upon the teeth. In the maxilla there is likewise a cortical layer made of com- pact bone buccally and lingually, the alveoli of the teeth being embedded, so to speak, in the spongy bone between the cortical layers. The alveoli here, as in the mandible, are lined internally by a semi-compact bone into which open many of the cancellated spaces. Infections of the periapical tissues invariably lead to varied degrees of involvement of the surrounding bony structure. The pathologic process which originates within the alveoli, spreads to the cancellated substance of the jaw, exhibiting the character- istics of an osteomyelitis, but with no tendency, except rarely, to spread (Figs. 357, 358 and 359). Ostcom yel it is is a destructive process affecting the periosteum, the cortex and the marrow? The cortical bone lining the alveoli soon breaks clown as the result of the spreading of an infectious process in the peridental 3 McCallum: A Textbook of Pathology, New York, Wm. Wood &• Co. 458 DENTAL PATHOLOGY membrane, and upon the establishment of a passage through the cortical layer at any particular point, the infection reaches the cancellated substance of the alveolar walls which is, of course, continuous with the cancellated substance of the jaw proper. The absorption of the cortical bone of the alveoli in the course of an infectious inflammation is probably due to the combined ac- tion of osteoclasts and of leucocytes, it having been satisfactorily shown by a number of investigators that the presence of osteo- clasts is not essential to the absorption of bone (Ribbert). 4 Fig. 357. — Alveolar bone in the periapical region. The section was obtained from the alveolar bone around the apex of the root. The lamellae of bone (calcification install- ments) are easily observed, also the lacunas or bone cell spaces. The medullary or myelitic substance in the cancellated spaces becomes the seat of an inflammation. Through osteoclastic and leucocytic action, as previously noted, the hard substance of the bone, viz., the walls of the cancellated spaces, disappear; they are, so to speak, eaten through, and the Haversian canals are made wider. The contents of the spaces, viz., the myelitic sub- stance, become the seat of an acute inflammation in which the cellular elements typical of this form of inflammation are present. In time the inflamed medullary substance, as the result of the *Adami and McCrae: Textbook of Pathology, Philadelphia, l.ea & Febiger. BONE 459 big. 358. — Transverse section of tooth showing the arrangement of bone in the alveoli The peridental membrane, it will be seen, joins with the medullary substance in the can- cellated spaces; a, a, dentin; b, b, cementum; c, c, peridental membrane; d, d, d, d section ot compact bone lining alveolus; c, junction of peridental membrane with myeloid sub- stance. 460 DENTAL PATHOLOGY K ,.- N# i ■ ' •< •. *. • "{"■'*? /fc 3r^^~ r 'iS^ < -■ alii Fig. 359. — Arrangement of cancellated bone in region of central incisors. Fig. 360. — Bone of alveolar process and two cancellated spaces. a, a, a, areas of compact bone in the cortical layer of an alveolus; b, cancellated spaces; c, c, peri- dental membrane. BOXE 461 action of the Liquefying bacterial toxins, breaks down. In some places the cortical layer of the alveoli is less than one-third of a Fig. 361. — Arrangement of bone in incisal region, showing at a, bone of alveolar septum between upper central incisors. Fig. 362. — Arrangement of bone in bi- cuspid region showing at b, bone of alveo- lar septum between the upper bicuspids. Fig. 263. — Arrangement of bone in mo- lar region, showing at c, bone of alveolar septum between upper molars. millimeter in thickness. Its involvement and disappearance in the direction of thickness is therefore quickly brought about, thus 402 DENTAL PATHOLOGY opening' an abundance of pathways for the absorption of bacteria and bacterial toxins. Acute or chronic apical infections can not therefore be regarded from the viewpoint of localized infections. If all acute or chronic infections of the periapical tissues do not give rise to systemic manifestations, it is not because the products of such infections are not in all cases at the portals of absorption, hut because the individual is able to combat successfully the bacterial invasion. It is purely a question of individual resistance or immunity to infection. Various chains of streptococcus and staphylococcus seem to be the predominating bacteria in these lesions, although other or- ganisms may bring about the same results in association with the staphylococcus and streptococcus, viz.. the pneumococcus, ty- phoid bacillus, and the fusiform bacillus. The bacteria invading the cancellated spaces produce an inflammation of the medullary substance, — a myelitis. The cells of the medullary substance around the focus of infection are destroyed and their places taken by leucocytes which liquefy the necrotic tissues and attack the bony lamellae which they reduce to fragments. 5 Necrosis, Caries and Rarefying Osteitis of the Alveoli and of the Jaws. Necrosis of the Apical Areas of Roots Necrosis is a term applied to the death of an area of bone tissue which is immediately surrounded by living cells. It is death of bone en masse. It implies the contemporaneous death of a large number of cells and their subsequent separation from the sur- rounding healthy bone following an inflammatory process in- augurated in the surrounding healthy bone. It is distinguished from the process designated as rarefying osteitis, osteoporosis, or caries, in that in the case of the latter the individual cells die successively. Caries is a term applied to the molecular de- struction of bone "corresponding to the ulceration of soft parts." In caries both the calcified structure and the organic matrix disappear, the former through osteoclastic activity, the latter through the action of peptonizing bacterial toxins or by the discharge of peptonizing enzymes from the leucocytes, or by both. B McCallum: A Textbook of Pathology. r, Stengel and Fox: A Textbook of Pathology. Philadelphia, \\*. B. Saunders Co. i5o.ni: 4(>:5 The causes of necrosis are all those which directly or indirectly interfere with the blood circulation in bone. They may be grouped as follows : 1. Mechanical Blows, accidental traumatism. 2. Physical — Extreme degrees of temperature. 3. Chemical — (a) Burns by acids, strong alkalies, ar- senic trioxide phenol, formaldehyde, etc. (b) The administration beyond the individual's tol- erance of mercury, phosphorus, and bismuth. 4. Bacteria] causes — Infections; viz., action of bacteria and bacterial toxins and formation of bacterial em- boli and infarcts. Necrosis follows the obstruction of the blood supply, the re- sult of the occlusion of a main artery by an embolus, thrombic or infectious. The part dies without its cells undergoing a progres- sive degeneration. The infectious emboli play a leading part in necrosis of the jaws caused by peridental infections — dentoalveo- lar abscess, acute and chronic. Masses of bacteria occlude a series of capillaries and result in the formation of infarcts in a territory adjacent to or slightly removed from the infected tooth root. Mechanical Causes. — In this group are included causes which in- terfere with the blood supply and which result from degrees of vio- lence to the jaws. It is well to bear in mind that necrosis in the case of bone, and gangrene in the case of soft tissue, results from disturbance of circulation whereby the cells do not re- ceive the necessary amount of blood or are not properly drained, or from disturbances in the cells which prevent them from as- similating the required amount of food even though available in normal quantity and quality. A blow in the mouth may result in such an impact upon the vessel supplying the peridental mem- branes of several teeth as to result in the cutting off of the blood supply by emboli, with death of the teeth and eventually their exfoliation, and in the death of portions of the surrounding bony areas following the formation of occluding thrombi in the injured vessels. In the group of mechanical causes are also included the necro- sis and exfoliation of sections of the alveolar plate following such accidents as falls, blows, fractures during an extraction, etc. 464 DENTAL PATHOLOGY Chemical Causes. — Necrosis of the alveolar bone is occasionally the result of destruction of masses of cells by the action of chemi- cal agents. The soft tissues of the mouth are likewise liable to destruction by this means, particularly following the use of ar- senic in the devitalization of teeth. In the event that arsenic leaks out from a cavity the soft tissues are first affected, and then the underlying bone. Necrosis of the deeper osseous structure of the jaws, following the injudicious use of arsenic trioxide, also occurs. Unnecessarily large amounts of arsenic in contact with the pulp will lead to that result. Too much care can not be ex- ercised in the use of this chemical for purposes of devitalizing the pulp, particularly so in the case of teeth whose roots are not completely developed so that the apical foramina are large. The injudicious use of phenol, trichloracetic acid, chromic acid, sul- phuric acid, phenolsulphonic acid or formalin (the last three in root canal therapeutics) may cause necrosis in the periapical region. The careless forcing of acid compounds and strong alkalies through the apical foramen is a relatively common source of de- struction of periapical alveolar bony tissue immediately surround- ing the apex of the root. Necrosis of the maxillary bones occurs in those under a mer- curial regime and in persons engaged in the manufacture of phosphorus matches. Those with carious teeth and diseased gums are particularly liable to the form of necrosis caused by phos- phorus fumes. It was of frequent occurrence in the early days of the manufacture of phosphorus matches. At the present time, owing to the care which is given to the teeth and gums of the men employed in this industry, the occurrence of phosphorus necrosis has been greatly reduced. Bacterial Causes. — In this group is included the most frequent source of tissue destruction in the roots of teeth and the support- ing alveolar structures. An apical abscess, acute or chronic, may cause a destruction of peridental fibers which is followed by nec- rosis of that portion of the root which is denuded of peridental membrane, or in which the peridental membrane has undergone retrograde metamorphosis. The process which takes place in the root following destruction of the peridental membrane is not exactly typical of necrosis, i.e., death en masse, for the reason that BONE 465 the cementum being devoid of a blood supply of its own is no1 sub- ject to sequestrum formation, [nstead it undergoes a molecular disintegration equivalent to bone caries, and manifests itself by the condition so frequently diagnosed as pathologic root resorp- tion (Pigs. 364 to 367). The process which occurs in the alveolar Fig. 364. — Resorption of the apical areas of the root of a lower molar consequent upon chronic dentoalveolar abscesses (den- tal granulomata) of long standing. Fig. 365. — Resorption of the roots of a lower right first molar consequent upon a chronic infection of the periapical peri- dental membrane, the sequela of a septic pulpitis. Fig. 3t'6. — Beginning of resorption of the apical third of a root of an upper cen- tral following necrosis of the apical area of the root consequent upon a chronic dentoalveolar abscess. Fig. 3f>7. — A chronic alveolar abscess (dental granuloma) in the lower right cuspid, right central incisor, left central incisor and left cuspid. The apices of the roots of the central incisors have un- dergone marked resorption. osseous tissue in chronic dentoalveolar abscess typifies tissue death by consecutive disintegration of cellular elements through rarefying osteitis, osteoporosis or caries, practically synony- mous terms; or in other words, gradual cell death, as already 4GG DENTAL PATHOLOGY described in the case of osteomyelitis leading to rarefying ostei- tis, or to the more complete process of hard-tissue resorption with liquefaction of the organic hone matrix — caries of bone (Fig. 368). Necrosis of areas of alveolar process and jaw bone proper is occasionally observed in connection with ulcerative stomatitis. The periosteum at the crest, or alveolar border, becomes involved, Fig. 368. — Chronic dentoalveolar abscess (dental granuloma) of very long standing in which the chronic osteomyelitis which developed in the alveolar process resulted in caries of hone in a relatively large area. The apex of the tooth was found to penetrate into a cavity in the cancellated substance of the maxilla. the infection brings about its detachment, and the involvement of the myeloid substance in the cancellated spaces follows. The blood supply is cut off from the periosteal side and infectious emboli obstruct any number of capillaries in the cancellated substance, with necrosis as the result. CHAPTER XXXVI PERIOSTITIS OF THE JAW Inflammation of the periosteum of the jaw may be acute or chronic, depending on the vital resistance of the patient and the virulence of the infecting organism. The mosl frequent causes of periostitis of the jaws are: 1. Acute or chronic dentoalveolar abscess. 2. Traumatic injuries with or without a communicating ex- ternal wound. 3. Chemical irritation such as may be induced by the continued use of mercury or the inhalation of vapors of phosphorus. 4. As a sequence or in the course of acute or chronic systemic infections. 5. As a sequence to the eruptive fevers and anemia in children. G. As the result of tuberculosis or syphilis. The acute form of periostitis may be traumatic or infectious, although the traumatic form, by establishing areas of decreased vital resistance in the periosteum, soon becomes infectious, through bacteria gaining access by the hematogenic route in the case of traumatism without external communicating injuries, or from the outside in the case of traumatisms accompanied by ex- tensive breaks in the continuity of the soft tissues. In the chronic infectious periostitis in which the bacteria are of low virulence, thickening of the periosteum with new bone formation in the form of osteophytes and nodular formations, oc- curs wherever the osteogenetic layer is stimulated, but, of course not where the cells are undergoing degeneration. The infectious or suppurative form of acute periostitis may or may not lead to necrosis of the underlying bone. If the infected area is speedily drained by a sinus, or following surgical interference, necrosis will not occur: but if the reverse should be the case, necrosis will result. The infectious inflammation is intraperiosteal or sub- periosteal, or both. In the event that no drainage through the periosteum is established, the inflammation proceeds between the periosteum and the bone, strips the latter of its overlying peri- 468 DENTAL PATHOLOGY osteum, and necrosis of the superficial layers of bone follows. The infection may then penetrate back into the cancellated spaces wherein, as the result of multiple infectious emboli (occlusion of arterioles and capillaries), interference of the circulation takes place, resulting in more extensive areas of necrosis than where the periosteum alone is affected. Dentoalveolar abscess is a frequent source of periostitis of the jaws accompanied by necro- sis and the formation of sequestra (Fig. 369). Acute periostitis may be localized or diffused, according to the degree of resistance of the tissues immediately over the path of the Fig. 369. — Sequestrum wliicli came away attached to a tooth following a chronic dento- alveolar abscess of long standing. infection, and the type of microorganism concerned in the infec- tion. A small area of bone may die ; and again, the process may be of a progressive character — a diffuse acute periostitis — caus- ing the formation of a number of sequestra over a relatively extensive area of the jaw. An acute dentoalveolar abscess re- sults usually in a localized acute periostitis, which subsides upon the removal of the infectious source in the root canal. The perios- tiiis may, however, be of the diffuse type, accompanied by exten- sive necrosis. Acute periostitis, if diffused, results in secondary osteomyelitis, causing a greater depth of necrosis of the jaws or PERIOSTITIS OF THE .1 \\\ 409 caries of bone. It occurs with greater frequency in the lower than in the upper jaw, by reason of the Ead thai in the upper the blood supply is more abundant and anastomosis of blood vessels is greater than in the lower. Periostitis is more frequenl in chil- dren and young persons, inasmuch as it is during childhood and early maturity that there is greater susceptibility to dental caries (a prolific source of periostitis) by reason of involvement of the pulp, and later of the peridental membrane. The infection may spread from a root canal into the can- cellated substance of the jaws and then into the periosteum where it sets up an acute, though limited infection. The symp- toms of such a periostitis are as a general rule attributed to the infectious process in the peridental membrane and periapical structures — the acute dentoalveolar abscess. The symptoms are masked by the pain incident to the inflammation of the peridental membrane and the osteomyelitis in the alveolar bone. If the periosteum, at the point through which the infection passes, were to be examined, it would be found red and swollen and the area around the opening to be the seat of an infiltration by polymor- phonuclear leucocytes, some lymphocytes, and by serum and Lymph. Sometimes the area of periosteum is infiltrated with blood. A periapical infection leading to a dentoalveolar abscess with involvement of the cortical and cancellated substance of the jaw and the soft tissues of the face, induces a periostitis in all cases. The opening through the external cortical plate of the alveolus into the soft tissues marks the location of the area of periostitis. The infection persisting even in a mild de- gree, regeneration of the periosteum is prevented and the chan- nel leading from the focus of infection to an external opening- persists until such time as the source of the infection is completely removed, and, in abscesses of long standing, until the rarefied area as the result of rarefying osteitis and bone caries is curetted and mildly stimulated to fill up the loss of osseous tissue. The reten- tion of pus subperiosteal^ is responsible for the death (necrosis) and exfoliation of one or more sequestra. Periostitis of the jaws may be preceded by osteomyelitis, or vice versa. In the case of a spreading pericemental infection resulting in a periostitis, acute and of short duration, or in chronic periostitis when the inflamma- tory exudates become incarcerated under the periosteum, the peri- 470 DENTAL PATHOLOGY ostitis has been preceded by infectious processes in the substance of the bone involving the osseous and medullary substances, viz., an osteomyelitis. Again if the pus finds no outlet, owing to the resistance of the periosteum, the infection may penetrate back again into the bone through the cortical layer, causing a more ex- tended osteomyelitis leading to more extensive rarefying osteitis, bone caries, or necrosis. The commonest form of chronic periostitis is that of syphilitic origin. Growth of bone through stimulation of the osteogenetic layer occurs. The inflammation must be mild and continuous in character in order to result in new bone formation. It can not, of course, occur where the cells of the osteogenetic layer have undergone degeneration, but. on the other hand, it does take place in areas beyond those of degeneration in which the effect of the infection does not overbalance stimulation. In chronic phosphorus poisoning, periostitis of the noninfec- tious type develops at first, but remains as such only a short time. The irritation caused by the phosphorus fumes lowers the re- sistance of the periosteum and this becomes the seat of bacterial proliferation with its sequelae. Fever; general indisposition: swelling of the gums and face on the affected side ; looseness and exfoliation of the teeth; pus discharges from around the necks of the teeth: trismus; sinus or sinuses, intra-oral or extra-oral — are some of the most salient symptomatic manifestations of perios- titis of the jaws. OsU itis is an inflammation of the bone leading to either rare- faction or condensation involving the cancellated and compact substance of bone. Osteomyelitis affects both the calcified tissue and the medullary substance. Osteitis and myelitis invariably go together. In the rarefying form the inflammation of the medul- lary substance brings about osteoclastic activity, and disappear- ance of particles of calcified tissue follows, giving the bone a honeycomb appearance. Karefying osteitis is a chronic process. The erosions on an area of bone undergoing rarefying osteitis are called Howship's lacuna, in which osteoblasts and giant-cells (osteoclasts) are to be seen together. CHAPTER XXXVI] PYORRHEA ALVEOLARIS Historical Sketch An examination of ancienl skulls leads to the belief that the earlier races were subject "to diseases of the investing tissues of the teeth which are very closely allied in pathologic characteris- tics to the pyorrhea alveolaris of modern limes. The lesions of the alveolar process to he seen in many specimens seem to confirm the opinion held by most writers on the subject that pyorrhea al- veolaris. or some other disease leading to the exfoliation of the teeth, dates almost as far back as the human race. Under the term "scurvy of the gums" Pierre Fauchard, in 1746, described a lesion of the gums beyond the power of therapeutic means to eradicate and which invariably terminated in the loss of the teeth. 1 In 1778 Jourdain, in his treatise on diseases of the mouth, de- scribes pyorrhea alveolaris under the name of "suppuration con- jointe des alveoles et des gencives," namely, a simultaneous sup- puration of the alveoli and gums. Toriac, in 1823, seems to have been the first writer to suggest the word "pyorrhea," he having named the disease "pyorrhee inter-alveolo-dentaire." The term was first used by him on the occasion of an oral communication to a medical society of Paris. 2 Oudet, in 1835, recognized the peridental membrane as the seat of the disease, and Marechal de Calvi, in 1861, described pyorrhea alveolaris with perhaps more clearness than any one of his pred- ecessors in the field, and named it "expulsive gingivitis." Thos. Pell', in 1829, recognized two forms of the disease: one of local origin with deposits as the exciting cause; the other of constitu- tional origin. Chapin A. Harris, in 18,53, in his work, "Principles and Practice of Dental Surgery," describes the disease under consideration under the heading of "Chronic Inflammation and 'Fauchard, Tierre: Chirurgien dentiste, 1746, i. 2 Frey, Leon: Pathologic des-Dentes et de la Bouche. 'Marshall, J. S.: Operative Dentistry, Philadelphia, J. B. Uppincott Co. 471 472 DENTAL PATHOLOGY Tumefaction of the Gums Attended by Recession of Their Mar- gins from the Teeth." Harris recognizes a lo, epithelial proliferations, the result of the chronic inflammation involved in the tissue; c, c, areas of round-cell infiltration in which the mononuclear wandering cells predominate (leucocytes, plasma cells and some mast cells). Pyorrhea Alveolaris Caused by Subgingival Deposits In the form caused by subgingival deposits (Fig. 370), the de- structive inflammation affects the peridental membrane, alveolar bone, and gingiva?; but the gum tissue proper, while the seat of ;i chronic inflammation, does not disappear or break down simul- taneously with the peridental membrane and alveolar process, as is the case in the form caused by salivary calculi. Following octrees of irritation to the gingiva' by food impactions which PYORRHEA ALVEOLARIS 477 Fig. 377.— Gum tissue overlying a pyorrhea pocket, decalcified section. Little remains to identify the character of the tissue, the major portion of which is now substituted bj inflammatory wandering cells. Areas of chronic inflammation are seen throughout the t.s- ~ a a, gum tissue; b,b, decalcified area of tooth; c, c pyorrhea pocket; d d Gratified squamous epithelium from gingival cul-de-sac; e c c, large areas of round-cell infiltration (predominance of mononuclear wandering cells). 478 DKNTAL PATHOLOGY Fig. 378. — Chronic gingivitis in the gingiva which by process of continuity will spri ad to tin d peridental membrane, a, a cementum; b, b, dentin; c,c,c, stratified ous epithelium lining gingival cul-de-sac; d, large area of round cell infiltra (predominance of mononuclear wandering cells). \'\ ORRHEA \1.\ EOLARIS 479 find lodgmenl between the teeth in the presence of either defec tive approximal contacts (Figs. 371, 372, 373, 374, and 375^, or in t lio absence of contacts; by tiegled of the teeth through in- sufficienl brushing, etc.; by the rough edges of fillings or crown bands; by salivary calculi; by severe manipulations of ligatures and rubber dam clamps; or by improper handling of the tooth- brush, producing injuries of the gingival margins, an inflamma- tory process is inaugurated in these tissues (the Eree gingiva?) ac- companied by the depositions of calcareous masses thereunder. Fig. 379. Decalcified transverse section of upper central incisor. In the gum tissue ;i chronic inflammatorj process is going on which has resulted in ana- of tissue liquefac- tion. In this instance the chronic gingivitis had not as yet involved the alveolar process, although eventually it will il" so. a.ti. alveolar process; b, b, areas of tissue liquefaction in stroma of mucous mfembrane of gum tissue; c, cementum; d, dentin; e, pulp. The subgingival deposits thus produced irritate and subsequently bring about an infectious inflammation of the gingivae, gums, and later of the peridental membrane immediately adjacent to them (Figs. 376-382). Through the action of Liquefying bacterial tox- ines the peridental libers disappear and the infectious inflamma- tion, as soon as the cresl of the alveolar process is reached, enters the bone and there sets up an osteomyelitis with the absorption of the bony Lamella (Fig. 383). The inflammation extends again, 480 DENTAL PATHOLOGY Fig. 380. — An area of peridental membrane the seat of chronic inflammation in pyor- rhea alveolaris. a, decalcified section of tooth; b,b,h. fibers of peridental membrane cut at different angles; c,c,c, areas of round-cell infiltration (predominance of mononu- clear wandering cells). PYORRHEA \l.\ EOLARIS 181 Fig. 3M. — Chronic inflammation of peridental membrane. Areas of tissue liquefaction a, a. dentin; b, b, cementum; c, c, c, fibers of peridental membrane; :; Fie 383— An infection from the peridental membrane has involved the medullary substance in the cancellated space, an osteomyelitis being the result a. decalohed sect.on StoSE £ 6? peridental membrane; c, c, c, alveolar bone; d, chrome inflammation in llary substance of a cancellated space. 484 DENTAL PATHOLOGY bringing' about the deposition of further subgingival deposits higher up on the root surface, so that the processes of irritation, in- fectious inflammation, and bone resorption consequent upon osteo- myelitis, is repeated; and so on until the entire peridental mem- Fig. 384. — Destruction of alveolar proc- ess and peridental membrane caused by food impactions due to absence of normal contact between the upper left cuspid and upper left first bicuspid and between the latter tpoth and the upper left second bi- cuspid and between this tooth and the upper left first molar. Fig. 385. — Destruction of the alveolar process and peridental membrane in py- orrhea alveolaris, between the upper right cuspid and upper right first molar caused by a defective bridge restoration. Fig. 386. — Absorption of the apical areas of the roots of the upper central incisors caused by an infection which had originated at the gingival margin and which had caused a large pyorrhea pocket. brane and alveolar process are destroyed, and the tooth is exfo- liated (Figs. 384-401). In any one of the two forms of pyorrhea alveolaris so far described the presence of any systemic disorder in the digestive, respiratory or urinary tract, or any chronic l'YOKKIIKA ALVEOLARIS 4S.1 nervous disorder, or any systemic intoxication of whatever origin it mighl lie. acts as the means of "perpetuating" the disease in A B Fig. 3S7. — Two radiograms loaned to the author by Dr. T. A. Lynch of Los Angeles. These pictures were taken a few hours apart and on account of faulty radiographic technic, B shows a marked improvement over the pyorrhea! condition shown in A. The "regeneration" of the alveolar process which is shown in the picture on the right side is a fictitious result. Fig. 388. — Destruction of the alveolar process and peridental membrane caused by a defective crown impinging upon the gingiva. By continuity the infection spread to the alveolar septum bringing about its partial destruction. In time a deep pyor- rhea pocket would result. Fig. 389. — Destruction of the alveolar process and peridental membrane resulting in the formation of a pocket caused by the perforation of the distal wall of the root of an upper right cuspid. the investing tissues. The causes of the pyorrhea alveolaris may be of a local character, but the presence of systemic disorders 486 DENTAL PATHOLOGY f£-: it jM Fig. 390. — Destruction of alveolar process and peridental membrane in pyorrhea alveolaris con- sequent upon chronic osteomyelitis in alveolar bone. ft. Fig. 391. — Destruction of the al- veolar process and peridental mem- brane in pyorrhea alveolaris conse- quent upon chronic osteomyelitis in alveolar bone. Fig. 392. — Destruction of alveolar process and peridental membrane in py- orrhea alveolaris. A deep pocket existed between the central incisors and between these teeth and the lateral incisors. Fig. 393. — Destruction of alveolar proc- ess and peridental membrane establishing a pocket distal to t he Inst molar. Fig. 394. — Extensive pockets involving all the roots of lower first and second mo- lars. Fig. 395. — Extensive destruction of al- veolar process in pyorrhea alveolaris. Deep pockets in molar region; subgingival deposits are to be seen on mesial surface of upper first molar. PYORRHEA \l.\ I OLARIS 1-7 makes it possible for the disease to gain a foothold upon the in- vesting tissues such as t<> render its eradication a problem beyond the power of available surgical and therapeutic means. Pyorrhea Alveolaris of Systemic Origin Any systemic disorder which produces alterations in the quan- tity or quality of the blood, such as. for instance, Bright's disease, diabetes, or the uric acid diathesis, tuberculosis, syphilis, etc., may ad as the systemic predisposing causes of pyorrhea alveo- Fig. 396. — Pyorrhea alveolaris. Destruction of the alveolar process and peridental membrane to a depth of from 5 to 7 millimeters. Distal movement of the affected teeth on account of the destruction of the peridental membrane fibers which run from the peridental membrane of one tooth to that of the other (transverse fillers i. Malocclusion had been the predisposing cause of the disease in this case. Observe the absence of the greater portion of the gingiva around the affected teeth. Subgingival deposits were present upon the mesial, labial, and distal root surfaces. laris. These disorders are reponsible for the lowering of the de- fensive forces of the body, and this decrease in vital resistance is perhaps nowhere more pronounced than in the investing tissues of the teeth ; for, as pointed out by Talbot, the peridental mem- brane, alveolar bone, gingiva? and gums are in the nature of end- organs — devoid, or practically so, of collateral circulation, and consequently are markedly sensitive to circulatory changes. These systemic derangements are to be viewed in the light of predisposing causes. They render possible the infection of the investing tissues by reason of their having established in those structures areas of decreased vital resistance. The bacterial ex- 488 DENTAL PATHOLOGY J' 1 "- •> ''■ — Pyorrhea alveolaris in the lower teeth in the same case as shown at Fig. 395. Distal movement of the affected teeth. Considerable loss of alveolar bone and peri- dental membrane between the lower central incisors. Fig. 39S. — Pyorrhea alveolaris in the upper right cuspid, first bicuspid and first molar. ' omplete destruction of gingiva and destruction of alveolar process and peridental membrane for a distance of several millimeters. l'YORKIIKA \l.\ EOLARIS IS! I eiters are of course presenl a1 all times in the mouth, and there- fore, following the slightesl break in the continuity of the tissues consequent upon an injury to the gingival structures, bacteria gain entrance; and the causes which made this possible persist- Fig. 399.— Pyorrhea alveolaris. Subgingival deposits were present on the surface of the roots in relation with the so-called "pyorrhea pockets. - ' Fig. 400. — A typical case of pyorrhea alveolaris. Xote absence of the septal gingivae and of the body of the gingiva. The alveolar process for a short distance beyond the crest was also absent. ing, the peridental membrane and alveolar bone eventually be- come involved. The foregoing description applies to a group of cases in which treatment by instrumentation is of only temporary value unless it is carried out at frequent enough intervals to 490 DENTAL PATHOLOGY prevent the recurring infection from acquiring an impregnable foothold on the tissues. The systemic factor is frequently associated, in etiology, with a series of local conditions, the same as are responsible for the development of the purely local forms of gingivitis and pyorrhea — which leads to equivocal conclusions. Under those circum- stances frequently the local causes alone are incriminated, when as a matter of fact the systemic disorder is frequently just as much at fault. The former set of causes incite the disease, the latter perpetuate it. 1 i ■-, -V.V ■ • -JF !*c '. : % ' JUL.* J^i ' ji I # V p;~ V c >' ' « Fig. 401. — Destruction of alveolar process in an extensive case of pyorrhea alveolaris. Specimen was secured from Anatomical Laboratories of the College of Dentistry, L ni- versity of Southern California, and photographed by Dr. A. C. La Touche. In another group of cases local causes are apparently absent, or if present are not possible of determination unless the operator carry out a very minute examination of the gingival tissues. The infection in these apparently obscure cases frequently originates in the subgingival cul-de-sac (subgingival trough), and the initial irritation is traceable to the decomposition by putrefaction, fer- mentation, or both, of the slimy deposits in proximity to the gingival structures. These slimy deposits are particularly evi- dent in badly neglected mouths and in those of people who neg- PYORRHEA \l-\ I OLARIS t!M lecl the toilel of their teeth immediately after meals. These de- bris c(msist of a mixture of saliva and food particles. The end products of this decomposition, whether alkaline or acid, irritate the tissues in the subgingival trough, and infection by the com- mon bacterial inhabitants of the mouth soon follows. The in- fection, once becoming established, generally persists, notwith- standing the mosl careful and thorough operative and therapeu- tic measures. This form of pyorrhea alveolaris originates and persists independent of calcareous deposits. Some investigators —the late G. V. Black in particular — incline strongly toward the elimination of the systemic factor, attributing to purely local causes all the phases and characteristics of the disease. That a considerable proportion of cases is of local causation is admitted by practically all investigators, hut that all cases are of that origin has not received, happily, that unanimous acceptance. The evidence of clinical observation strongly points to many systemic disturbances as etiologic factors in pyorrhea alveolaris. Certain forms manifest themselves as. complications of digestive, renal, or pulmonary disturbances; and again, a form of loosening of the teeth is the result of a gradual and progressive atrophy of the investing' structures of the tooth, occurring in connection with arteriosclerosis, atheroma, anemia, etc. In the case of the latter group of diseases the loss of the teeth is the result of true atrophy of the peridental membrane and alveolar process, due to the fact that the gingiva, peridental membrane and alveolar proc- ess, being end-organs as previously stated, have their nutrition greatly impaired by abnormal changes in the circulatory appara- tus. These dental manifestations become evident even before they induce manifestations of a more serious nature in any of the vital organs. Miller, as far back as 1885, submitted a series of investigations concerning the bacteriology of pyorrhea alveolaris, and came to the conclusion, which holds true today, that pyorrhea alveolaris is not caused by any specific bacterium, but is highly polymicro- bic in character. Various bacteria are concerned in the process, just as is the case with suppurations, in which not only one, but various species of bacteria are active. The following is an ex- cerpt of Miller's investigations: 492 DENTAL PATHOLOGY "When the disease is so far advanced as to necessitate the ex- traction of teeth, Ave first cleanse the crown and neck of the tooth, as well as the adjacent gums, with 5 per cent carbolic acid ; and then, after removing the antiseptic with sterilized cotton carefully extract the tooth so as not to graze the gums, cheek or lips with the apex of the root. A small quantity of pure, fresh pus will be found on the root at the border between the dead and the living pericementum. I used this matter, as well as part of the periosteum of the apex of the root, in my culture experiments. In order to obtain in pure culture the bacteria pos- sibly contained in the cement-corpuscles or dentinal tubules, I placed the tooth for a short time in a sublimate solution of 1 :;")000 (so as to destroy the £>'erms on the surface). Thereupon it was rinsed in a large quantity of sterilized water, dried with steri- lized blotting-paper, and the outer layers removed with a steri- lized knife. Small particles from the deeper layers were then scattered on a culture plate. If extraction is not desirable, we may proceed in the following manner: The neck of the tooth is carefully cleansed and a slight pressure exerted on the gums; by this means the desired pus is pressed out between the sums and the neck of the tooth. "I made dilution and line-cultures on beef -water peptone gelatin of twenty-seven teeth afflicted with pyorrhea alveolaris. The gelatin was liquefied in five cases only. Staphylococcus pyogenes aureus developed but once; likewise Staphylococcus pyo- genes albus. "Two formed yellow, one green coloring-matter: the latter is of interest from the fact that it forms no pigment when the access of air is prevented; if. however, the liquefied colorless gelatin is shaken with air, a beautiful deep green color almost imme- diately forms. In most cases I obtained but one kind, or one kind so predominated that the rest could be left out of account. In Cases 8 and 13 the bacteria cultivated were found to be identical; also in Cases lfi and 17. In all the rest they were different; that is to say, twenty-seven cases yielded twenty-two different kinds of bacteria. "From these experiments Ave might conclude that if there is a specific bacterium of pyorrhea alveolaris, it does not readily sjroAv on gelatin, a result which is of value in so far as it indicates PYORRHEA ALVEOLARIS 193 that in further experiments on this subjed media should be em- ployed which admit of being kept at the temperature of the mouth. At the same time the thoughl suggests itself that possi- bly tlic bacterium of pyorrhea alveolaris, like so many mouth bac- teria, is cultivated on mine of the artificial nutrient media, which would of course render all experimenting useless. "The few experiments which were made on animals resulted negatively. The gums of healthy dogs (these animals often suf- fer from pyorrhea alveolaris) were slightly detached from the neck of the tooth and inoculated with pus, as well as with the deposits on teeth attacked by the disease. Slight inflammation invariably ensued, in one ease also a little suppuration, hut in- side of a week all eases were completely healed. Further experi- ments are necessary to determine whether positive results may be gained in the ease of old or emaciated and sick dogs. "I next made a series of culture experiments on agar-agar, at blood temperature. Twelve eases of pyorrhea in human beings and six in dogs wi^v examined. I isolated twenty different bac- teria from human beings and nine from dogs. Among the twenty kinds. Staphylococcus pyogenes aureus Avas found twice. Staphy- lococcus pyogenes albus once. Streptococcus pyogenes once. Of the other sixteen, nine subcutaneously injected produced no particu- lar reaction, four a slight, and three a severe suppuration in the subcutaneous connective tissue. "Among the nine species in dogs, Staphylococcus pyogenes al- bus occurred once. Of the other eight, two subcutaneously in- jected caused no reaction, five but a slight, and one very profuse suppuration, by which large portions of skin were thrown off. "I succeeded, consequently, in cultivating a large number of bacteria of pyorrhea alveolaris which possessed pyogenic proper- ties, but was not able to determine the constant occurrence of any particular one which might be defined as the specific microorgan- ism of pyorrhea alveolaris. "The microscopical examination of stained sections revealed masses cf different bacteria, cocci and bacilli, and more seldom leptothrix. on the surface of the cementum. and where there were microscopic cavities in the cementum. or the dentinal tubules were exposed in consequence of resorption, the microorganisms Avere found to have penetrated for a short distance." 494 DENTAL PATHOLOGY M. T. Barrett in collaboration with Dr. Allen J. Smith 5 , in an examination of forty-six patients, found endameba buecalis in the contents of pyorrhea pockets, and the absence of endameba in seven patients with no recognizable lesion of the peridental mem- brane. These findings were taken up by a large number of men in the medical and dental professions as satisfactory evidence of the pathogenic importance of this parasite in pyorrhea alveola ris. That such a conclusion was unwarranted by the findings of Bar- rett, Allen J. Smith, Bass, and Johns is now a generally admitted fact. Chiavaro 6 , among others has concluded that the endameba buecalis, while it is found in the pus of pyorrhea alveolaris, has not a pathogenic action: but to the contrary, as it feeds on bac- teria, "it is most probably an aid to the auto disinfection of the mouth. ' ' A study of cultures from pyorrhea pockets of forty-seven pa- tients by J. Marion Read gives the results shown in the accom- panying table : ORGANISM 1. Staphylococcus pyogenes albus 2. Streptococcus pyogenes 3. Pneumocoeeus 4. Micrococcus eatarrhalis 5. Diplococcus mucosus 6. streptococcus viridans 7. Staphylococcus aureus S. Bacillus mucosus 9. Friedlander 's bacillus 10. Streptococcus mucosus 11. Bacillus proteus 12. Streptococcus (in short chains) 13. Bacillus coli 11. Bacillus prodigiosus 15. Diphtheroid bacillus 16. Bacillus pyocyaueus ALONE ONE TWO TOTA OTHER OTHERS 1 10 18 29 1 G 11 18 2 12 14 3 6 9 1 4 8 3 3 1 7 4 o 6 2 4 6 2 2 4 1 2 3 2 2 2 2 1 1 1 1 1 1 1 1 E Barrett and Smith: Dental Cosmos, 1914. c Chiavaro: Dental Review. CHAPTEE XXXVIII PYORRHEA ALVEOLARIS AND PERICEMENTAL ABSCESS OF GOUTY ORIGIN* With diseases of suboxiclation characterized by the presence of given amounts of urates of sodium, calcium, magnesium and am- monium in the blood, the presence of inflammatory disturbances in the investing tissues of the teeth has been associated. The "gouty diathesis," or as it is better described by French writers, the diathesis of arthritism, is a condition characterized by the presence in the blood and tissues of an excess of the prod- ucts of the incomplete oxidation of protein bodies in the shape of xanthin bases, amido acid compounds, and uric acids. The dep- osition of uratic salts upon the roots of teeth seems to occur in that diathetic state. Urates are held in solution in the blood by virtue of the alkalinity of that fluid, so that when the blood passes over an area of decreased alkalinity or of actual acidity, the urates are precipitated. These uratic deposits are the source of a. degree of irritation to the peridental membrane which re- suits in the establishment of areas of decreased resistance — a 'locus minoris rcsistcntux — in which bacteria thrive successfully. The area of decreased resistance becomes infected by bacteria, and suppuration follows. Pus is of a degree of alkalinity greater than that of the blood, which fact accounts, according to Kirk, for the precipitation of calcium salts upon and around a nucleus of uratic deposits. The discharge from this area of infection may take place along the gingival margin, this, of course, occurring af- ter the infection has destroyed an area of tissue extending from the primary seat of the infection to the gum margin. The etiology of pericemental abscess — an abscess upon an area of the peridental membrane of a tooth containing a live pulp and supported by investing tissue whose continuity at the neck of the tooth is unbroken — is fundamentally alike to that of pyorrhea alveolaris of systemic origin, associated with the uric acid diathe- sis. This difference, however, exists: that in pericemental abscess the pus discharges into the mouth from an opening in the gum *Kirk, E. C. : Abscesses upon Teeth with Living Pulps, Dental Cosmos, 1898. Peri- cemental Abscesses, Dental Cosmos, 1900. 493 496 DENTAL PATHOLOGY tissues opposite the area of infection; whereas, in pyorrhea al- veolaris the discharge is at tlie margin of the gum. Any abscess which originates from an infection of the peridental membrane secondary to suppuration and putrefaction of the pulp, and which discharges into the mouth through a sinus, is not a pericemental abscess. \'>y pericemental abscess is definitely understood that it is ;i condition in which an abscess develops upon -ome aspect of the peridental membrane of a tooth having a live pulp. Peri- cemental abscesses may be subpericemental or intrapericemental. according to whether the destruction of tissue by bacteria has taken place under the pericemental membrane, bulging it out, and eventually rupturing it. or within the fibrous substance of the peridental membrane 1 . Etiology and Pathologic Anatomy of Pyorrhea Alveolaris and Pericemental Abscess of Gouty Origin It is a well known fact thai the salts of uric acid arc maintained in solution in the blood by virtue of the alkalinity of that fluid and that they are precipitated by acids, or at leasl by substances of a lower degree of alkalinity than thai of the solvenl in which tiny are present. Scheele, as early as 177*1. had discovered the fact that urinary concretions are dissolved by alkalies, and pre- cipitated by acids. The application of these known facts to the conditions present in the peridental membrane can be made to explain the phenomenon of the formation of uratic deposits upon the roots of teeth. If, as has been previously pointed out, and as does occur, uratic salts are precipitated by preference ;) t -ome point in tin- apical region of the tooth root, it necessarily follows that there the fluids and structures musl be of a degree of alkalinity less than that of the blood. Several years ago, in the course of a de- tailed study of pyorrhea alveolaris of gouty origin, this phase of etiology was forcefully brought to the author's attention by reason of a conspicuous lack of reference in our literature to this initial phenomenon in the evolution of thai form of pyorrhea. Ordinarily, that is to say. under conditions of rest or slight activity, all articulations, their ligaments, synovial membranes, articulating cartilages, and the fluids in which they are bathed, 'Kirk, E. C: Pericemental Aliscess, Dental Cosmos, PYORRHEA \l.\ lol.AUIs 4!»< are of an alkaline reaction; on the other hand, under conditions of activity the reaction a1 once changes to one of less alkalinity (relative acidity), or, in extreme cases, to one of actual acidity. These reactions of the tissues in question constitute a physiologic fact which is frequently demonstrated to students in medical and dental schools in the course of their studies of general physi- ology, and requires no argument to substantiate its trustworthi- ness. A comparatively simple experiment will convince one that the reactions are as here stated. After preparing a frog for ex- perimentation by first severing the spinal cord at its .junction with the encephalon, expose the middle articulation of either of the hind le^s and test the reaction with litmus paper. It will he found decidedly alkaline. Xow suhject the exposed tissues to a series of active contractions through electrical stimulation, and again test their reaction. It will be found to be markedly acid. These changes in reaction, no doubt, also occur in the ease of the alveolodental articulation. The peridental membrane is com- posed of bundles of fibrous connective tissues which, upon being subjected to abnormal degrees of irritation, undergo a chemical disintegration ending, it is believed, in the production of acid compounds. Collagen, the principal element in fibrous tissue. when hydrated is converted into gelatin which, upon further dis- integration, is found to be composed of proteins; these may be detected by any one of the known proteic reactions. Proteins. upon breaking down during activity, may give rise to sarcolac- tic or the plain lactic acid, among other compounds. It is submit- ted that the above facts satisfactorily explain the conditions which take place in the apical region of the root, and which, in the presence of pus-producing organisms, lead to the development of a tophus abscess. As an additional argument of the theory under consideration, it may be stated that the frequency of gouty deposits upon the metatarso-phalangeal articulation of the greal toe is, in the writer's opinion, due to the fact that in tin 1 act of walk- ing a great proportion of the body's weight is thrown upon that part of the foot. The consequence of this strain results in the formation of acid substances, and so renders that particular re- gion a suitable field for the precipitation of uratic salts. It will he seen, therefore, that the initial phenomenon re- sponsible for the deposition of uratic salts in any articulation is 498 DENTAL PATHOL' the result of a change in the reaction of the tissues brought at by the breaking down of protein bodies in the course of physical activity, and the consequent formation of acid sub- stances. In the case of the alveolodental articulation, -whenever - ibjected to a . ■ of activity greater than normal. the eatabolism of the cellular elements of the peridental mem- brane results in the production of acid substances which les the alkalinity of the membrane, particularly at the point at which the greatest degree of stress is felt. In single-rooted teeth the uratic deposits are found as a rule in or near the apical re- gion of the root, and in multirooted teeth either upon one of ts in a location c .ding to that upon which the uratic salts are deposited in incisors, canines, and bicuspids, or else upon the bifurcation area. These areas of uratic precipitation are ac- counted for by the fact that in the pri E the slightest degree of overactivity the loea*: - -rred to are the ones which sus- tain the greatest degree of stress, for reas a slusively physical and based upon laws of mechanics. Teeth re very often, in fact more often than is generally believed, subjected to degrees of sfa ss greater than normal. A slight deviation from the position which a given tooth should occupy in the arch is sufficient to cause that tooth to perform an amount of - greater than its normal share should be. This leads I .eraetivity. e delation, decrease of al- kalinity, and probably to the formation of lactic acid through the breaking down of the complex protein molecules of the peridental membrane, and finally to the precipitation upon the areas under greater stress of the uratic salts held in solution in the blood by virtue of its alkalinity. In a large number of instances of pyorrhea alveolaris. or peri- cemental al >s _ igin, the main et: _ causative factor is the relative or actual acidity of some portion of the peri- dental membrane. This is then followed by the precipitation of uric acid salts which, acting as an irritant, convert that peridental area into a suitable field for the development of pyogenic organ- isms. The deposited urates create a locus minoris resistentia?. and the pyogenic organisms which find there a suitable field for devel- opment are responsible for the formation of pus, which, beinsr of an alkalinity greater than that of the blood, causes a precipi- PYORRHEA A.LVEOLARIS 499 tation of the calcium phosphates thai are frequently found to be componenl of the gouty deposit (Kirk). As the result of the infectious process which spreads by continuity to the alveolar process and gum tissue, a sinus is established. If the sinus should lead directly to and through the gum, a pericemental abscess will be established; if the infection and consequent tissue destruction should involve the peridental membrane and alveolar process along the side of the root to the neck of the tooth a so-called pyorrhea pocket will result. CHAPTER XXXIX THE DENTAL PULP AXD ITS DISEASES The dental pulp is the soft tissue contents of the pulp chamber and root canals of teeth (Figs. 402 and 403). It is in close relation with the peridental membrane at the apical foramen (Fig. 404). It is the remains of the dental papilla — the aggregation of connec- tive-tissue cells — supported by a framework of minute fihrilhe. It presides over the formation of dentin during the developmental period of the tooth and throughout the life of the tooth in response to physiologic and pathologic stimuli. It occupies the pulp chamber in the crown of the tooth and the root canal or canals in the root of the tooth. Its outline is in a general way thai of the tooth in which it is contained. It resembles embryonic tissue in its delicate fibrillar basis, and in its cells which are round, oval or stellate. The dental pulp is proportionately larger the younger the individual, and becomes smaller with aye as the hulk of dentin increases. It is the sensory organ of the tooth and the source of the blood and nerve supply of the dentin. After the dentin at- tains its full development, the pulp deposits new dentin, through the agency of its odontoblasts, under conditions of abnormal stimulation and as a physiologic manifestation of increasing age. Histologic Constituents The histologic constituents of the dental pulp are six, to wit: 1. Odontoblasts. 2. Layer of Weil. 3. Connective-tissue cells. 4. Intercellular substance. 5. Blood vessels. 6. Nerves. Odontoblasts. — Odontoblasts are tall, columnar cells lining the pulp on the dentin side (Fig. 405). They are about twenty-five microns in length and five in width. The nucleus is located to- ward the pulpal side, viz., away from the dentin wall. They form a protecting layer around the pulp, and from the fact that 500 THE DENTAL PULP A.ND [TS DIS1 v-i S 501 Vie 40'— A longitudinal section of a normal pulp of man. a. a. a. a odontoblastic layer- & nerve trunk; c, c, plexus of nerves under odontoblastic layer. The connective ?«ue cells distributed everywhere in the matrix of the pulp are of three kinds, round, spfndleshape and stellate. The latter are fewer in number and more difficult to locate. 502 DENTAL PATHOLOGY they adhere to the walls of the root canals they have been collectively named the menibrana eboris. The odontoblastic layer of the pulp is the only connective tissue in the body having cells of columnar form. This columnar form does not, however, persist throughout the life of the pulp. It is particu- larly evident prior to and during' the formation of dentin; but in old pulps, i. e., after dentin has been formed, the odontoblasts are round or oval. They are the specific dentin-produeing cells — a function which they retain throughout the life of the pulp. They send processes into the tubules of the dentin — the Fig. 403. — Longitudinal section of normal pulp. The same structural elements are to be found as are indicated in the previous section. dentinal fibrillar or fibers of Tomes, and probably are connected among themselves by delicate fibrous processes. Layer of Weil. — The layer of "Weil is supposed to be that por- tion of the pulp lying between the odontoblastic layer on the outside, and the portion of the pulp which is thickly studded with connective-tissue cells distributed throughout the gelati- nous matrix of the pulp on the inside. It itself is described as being very sparingly embedded with connective-tissue cells. In numerous specimens this layer does not exist, but whether pres- THE DENTAL ITU' AND ITS DISEASES 503 ciil or not, is of qo physiologic import. Von Ebner has attributed the layer of Weil to shrinkage of the body of the pulp, while WahlkoflE considers thai the phenomenon is caused by a shrink- age of the odontoblasts. 11 is best studied in transverse sections. Connective-tissue Cells. — The connective-tissue cells of the pulp are of three shapes — round, spindle-shaped and stellate. In Fig. Apical foramen [i ntal membrane . . I it -mm . V Dentin . . Bone of alveolar process . Peridental membrane . Dentin . Dentin Pulp Fig. 404. — Section of a tooth showing relation of the pulp at the apical foramen to the peridental membrane. Some of the blood-vessels are shown partly filled with blood cells. The fibrillar character of the pulp matrix is seen. 402 the round and spindle-shaped cells are readily distinguished, but the stellate cell is very rare and exceedingly difficult to find, being best shown by focusing for depth. Intercellular Substance. — The intercellular substance is a gelat- inous mass resembling the tissue found in the umbilical cord, and known as Wharton's jelly. It is an immature form of con- 504 DENTAL PATHOLOGY nective-tissue consisting of very fine fibrillae. Besides these ex- tremely slender fibrous elements, connective-tissue fibers of or- dinary size are also found supporting the blood vessels and nerves. Blood Vessels. — The pulp has. relatively speaking, a very rich blood supply. During the formative period of the tooth the blood is carried to it by means of several arteries. "When the development of the tooth is completed the blood supply consists as a rule of one small artery and a correspondingly small vein, or again the arrangement may consist of three or more arteries with their corresponding thin-walled veins entering the tooth through one or several foramina. Weil has found that from three to ten blood vessels may enter the tooth through the apical foramen. The difficulties attending the treatment of roots pos- sessed of more than one apical foramen are obvious. This artery, or arteries, breaks up into numerous branches which are distrib- uted throughout the substance of the pulp, and as these branches reach the odontoblastic layer they split into capillary plexuses, which lie in close proximity to the odontoblastic cells, from where veins carry off the venous blood. The walls of the vessels of the pulp are very thin and easily affected by changes in blood pres- sure. 1 There is no collateral circulation in the pulp, so that any in- jury to the blood vessels at the apex affects the vitality of the entire pulp. As shown by A. Hopewell-Smith its veins are valve- less and noncollapsible. 2 Noyes has recently demonstrated that lymphatics exist in the pulp. Nerves of the Pulp. — One or more nerve filaments enter the pulp through the apical foramen, each filament being composed of from ten to thirty medullated nerve fibers. These nerves enter with the blood vessels. After entering the pulp tissues they spread out into plexuses and eventually become nonmedul- lated. forming rich networks close to the odontoblasts. The protoplasmic prolongations of the odontoblasts are the only structures which have thus far been demonstrated to enter the dentinal tubuli, and until such time as nerve fibrillse can be dem- •Black, G. V.: Dental Pathology. 2 Hor>e\vell-Smith, A.: The Histology and Patho-Histology of the Teeth and Asso- ciated Parts, Philadelphia, P. Blakiston's Son & Co. Fig. 405.- -Section of a pulp of sheep, showing histologic characteristics of odontoblastic layer. Section prepared by Dr. A. C. La Touche. THE DENTAL PULP AM) lis DISEASES -'^-> onstrated within the tubules, the odontoblastic prolongations or fibers of 'Pomes, in usi continue to be looked upon as the only means by which impulses are carried from the dentin to the pulp. Fibers of Tomes The transmission of sensations from the dentin to the pulp lakes place through the medium of the fibers contained in the dentinal tubuli. These fibers are prolongations of the odonto- blasts and while physiologically Ihey play the role of nerves, his- tologically they in no way resemble nerve tissue. In addition to these processes of the odontoblasts, a process arising from the pulp end of the odontoblasts, and a process on eaeh side of the cell communicating laterally with the adjoining odontoblasts. have been described. These additional processes are not dis- cernible in histologic preparations and must therefore be con- sidered for the present at least in the light of histologic specu- lations. Diseases of the Pulp The pulp, because of the character of its blood supply, being devoid of collateral sources of nutrition; because of the lack of adaptability of its vessels to changes in blood pressure; because of the character of its immediate surroundings, hard and un- yielding; because of the liability of its protecting tissues (the enamel, the dentin, and the cementum) to diseases which de- crease their thickness or density, and hence lessen their power to act as barriers against disease-producing influences, thermal, chemical and bacterial, — is susceptible in an exaggerated degree to diseases which in the vast majority of cases impair its vitality permanently. While from a pathologic standpoint the pulp is subject to a number of diseases, each of which will be discussed under its own heading, from the clinical standpoint diseases of the pulp are considered from two main aspects only. The group in which conservative measures can be successfully employed with the view of preserving the pulp, is one; and the group which demands as the only permanent compromise the sacrifice of the organ, is the other. In the first group is included, mainly, hyperemia, when it is a pathologic entity in itself and is nonbacterial in origin. In 50G DENTAL PATHOLOGY the second group are included all diseases of bacterial origin, and those persisted forms of nonbacterial hyperemia which lead to nonseptic pulpitis and death of the organ. The pulp is also subject to retrograde as well as to construc- tive metamorphoses. In the former group are included the fibroid degenerations of Eopewell-Smith, and those presenting similar characteristics as described by Talbot, Latham, Wedl, Wahlkoff and Rothman; also fatty, hyaline and colloid degenerations, recognized only upon postmortem examinations of the pulp.' In the latter group are included calcareous infiltration of the pulp, calcifications of the dentinal tubuli, pulp nodules and secon- dary dentin. General Predisposing Causes In the discussion of diseases of the pulp, the predisposing as well as the exciting causes should be considered. The predispos- ing causes may be general or local. Neither heredity nor sex are of any moment in this connection. Age is considered as a pre- disposing cause mainly because during childhood and. say, up to sixteen years, children do not take care of their teeth in a manner conducive to the prevention of caries, and consequently inflammation of the pulp is more frecpient than later in life, when the development and progress of caries is prevented by hygienic care and filling operations. As the child grows the at- tacks of toothache from pulpitis and pericementitis become les< frequent, but this should not be attributed to the influence of age itself. It is the result of conditions in which age plays no part whatsoever. Degenerations of the pulp are more frequent as age advances, and these degenerations "are not necessarily connected with the actual number of years of the individual's life, but with the age of the tooth and its pulp." Hopewell- Smith has found evidence of retrograde metamorphoses, such as fibroid degenerations, in children's deciduous teeth, identical to Ihose degenerations incidental to old age. 4 The amount and the composition of the blood varies in the presence of such systemic pathologic states as affect the lungs, heart, kidneys, spleen, pancreas, stomach, intestines, the blood, the lymph, the nervous system, etc., and these abnormal condi- sHopewell-Smith, A.: In N. G. Bennett's Science and Practice of Dental Surgery, New V..rk, Win. Wood & Co. iHopewell-Smith, A.: Ibid. THE DENTAL PULP AND ITS DISEASES 501 lions doubtless exerl some influence upon the nutritional proc- esses in ilif pulp. The same must be s;ii stimulated deposit, by means of the odontoblastic pro- longations, inorganic salts in the dentinal tubuli — tricalcium phosphate, mainly. The anatomic changes "which thus result are an increase in the density and in the thickness of the walls of the tubuli, and possibly a decrease in the size of the dentinal fibrillar. This process occurring in a number of tubuli results in an overcalcified area, the transparent zone of Tomes. It is the result, as previously stated, of odontoblastic stimulation, and is brought about by caries of the enamel; caries of the dentin; erosion; abrasion; metallic fillings; involuntary gritting of the teeth; violent brushing of the teeth; and by extremes of tem- perature, such as occur during a meal. Several theories have been advanced in explanation of dentin transparency, or the transparent zone of Tomes. Black 1 attributes this phenomenon to death of the dentinal fibrillar in the transparent zone (hyaline zone) from the irritation caused by the progress of caries. John Tomes, the first investigator to report upon dentin transparency, attributed it to a calcification of the dentinal fibrillar, or an in- filtration of the organic filaments by calcium salts. We consider it as the expression of a vital process — in fact the only view tenable today. Miller's experiments must be accepted as final, or at least so until such time as the weight of accumulated evi- dence to the contrary shall be forthcoming. The transparent zone is not observable in pulpless teeth, unless it he that the phenomenon occurred prior to the death of the pulp following 1 Black: Operative Dentistry, Chicago, Medico-Dental Pub. Co., i. 510 CALCIFIC DEGENERATIONS 511 infectious processes or accidental traumatisms, but occurs in teeth having live pulps following abnormal degrees of irritation brought about by the scries of conditions above enumerated. Miller has reminded us thai the opacity of dentin is the resull of the difference in indices of refraction between the dentin ma- trix (the intertubular substance ), and the dentinal tubules. There are two ways in which the transparency of an area of dentin may be brought about. In the one ease it is by an increase in the amount of calcified substance within the tubuli, thus equalizing (lie coefficient of refraction between these and the dentin ma- trix; or by decalcification of t lie dentin matrix, producing the same result. That decalcification of the dentin matrix does not occur lias been shown by chemical analysis; and as, in addition, a diminution in the caliber of the tubuli has been observed, the conclusion is forced upon us that it is a process characteristic of living dentin in which a degree of transparency is attained by the increase in calcified matter in the tubuli, which to some extent equalizes the coefficients of refraction of these and the dentin matrix. Miller observed the identical phenomenon in human senile teeth in which, doubtless, the pulps had been for many years subjected to mild degrees of irritation, in roots in the process of resorption, and in the abraded teeth of dogs. Secondary Dentin There occurs either in conjunction with the formation of the transparent zone, or at some subsequent time, or else independent of the transparent zone, the formation of additional dentin at the expense of the size of the pulp chamber and root canals (Figs. 406-409). The secondary dentin so formed must be viewed in the light of a stimulation to the pulp of somewhat greater in- tensity than that which follows tubular calcification. Secondary dentin is classified as typical or amorphous, the typical variety bein\s 513 Fig. 407. — Secondary Fig. 408. — Secondary dentin which entirely filled dentin in connection with the pulp chamber, the abraded upper central, original outlines of which can be distinguished from the secondary formation. Abrasion and erosion are responsible for the vol- uminous depositions of sec- ondary dentin. Fig. 409. — Secondary dentin in connection with severe abrasion. Fig. 410. — Pulp the seat of a chronic inflammation, a, an area of round-cell infiltration. 514 DENTAL PATIIOLOGV Pulp Nodules Pulp nodules, or pulp stones, are amorphous masses of calcific matter found in the pulp chamber or in the root canals. It is the result of an activity of the pulp caused by direct or indirecl abnormal stimulations. Pulp nodules, even though they give rise to no symptoms whatsoever during their deposition, and sometimes thereafter, must be regarded as the pathologic mani- Fig. 411. — Chronic inflammation of the pulp. The degeneration of the cells and fibers of the pulp results in the marked areolation seen in the specimen. festations of disturbed intrapulpal metabolism. The pulp nodule is more in the nature of a secretion within the pulp of the sub- stances entering into the composition of the nodule. In at least some cases it follows in the wake of chronic inflammation in limited areas of the pulp. The process of nodule formation is preceded by forms of cell degenerations — hyaline or fatty. In CALCIFIC DEGENERATIONS 515 Fig. 412. — Pulp stones occupying the Fig- 413. — Pulp stone (nodule) in pulp entire pulp chamber. chamber of lower molar, a. Tooth before splitting; b, and c, halves of the tooth with the pulp stone in situ. Fig. 414. — Pulp nodule filling up the entire pulp chamber. The nodule is not attached to the walls of the pulp chamber. Fig. 415. — A pulp nodule in situ. 51G DENTAL PATHOLOGY _„_& Fig. 416. — Decalcified section with pulp stone in situ, a, a, dentin; b. b, pulp stone in situ; c, pulp. Fig. 417. — Decalcified longitudinal section, showing a pulp stone in place. Notice the onion peel arrangement in the substance of the stone. It is not attached to the walls of the root canal, a, a, pulp; b, b, dentin; c, c, pulp stone in situ. 7 = ft i> 3 -a ■A*.,. wo ft , t. J. -«... d:'"- CALCIFIC DEGENERATIONS 517 pulps studied by the author small areas of chronic inflammation have been found which bad existed probably for months and years without giving rise to any symptoms whatsoever (Figs. 410-411). it is therefore probable thai those same areas become in some instances pulp nodules, following calcific infiltration. Fatty degeneration is responsible for the liberation of fatty acids which at first combine with the calcium broughl to the degenerat- ing cells in the blood, the resulting calcium — fatty acid compound being decomposed into soluble phosphate or carbonate by the dis- placement of the fatty acids by phosphoric or carbonic acid. Pulp nodules do not resemble dentin: they are irregularly shaped masses ranging from such a size as to be visible under the mi- *t Fig. 420. — Pulp stones in pulp chamber of upper right first and second molars. croscope only, to a size to fill up the entire pulp chamber (Figs. 412-420i. The teeth in which pulp nodules exist may remain absolutely quiet and comfortable, and again may give rise to severe reflex manifestations in the shape of radiating neuralgia, the pain traveling in the direction of the ear, the eye, the tem- ples, and the back of the neck. Pulp nodules are found in the pulp chamber and in root canals. In these nodules occasionally calcospherites are found. In some instances the pulp contains in the root-canal portion a number of nodnles which are accountable for the so-called lead-wire for- mation, as described by Black. Here also erosion and abrasion are frequently the cause of pulp nodules. The number and size of pulp nodules vary. In some microscopic sections examined by the author as many as fifty pulp stones were counted in one field of a pulp. chapter xli pulp hyperemia General Considerations By pulp hyperemia is understood an abnormal condition in which the vessels of the pulp are engorged. The organ in most of the cases is the seat of active, rather than of passive, conges- tion, and responds to thermal stimuli with a degree of intensity more pronounced than is normal to it. The congestion is brought about either by paralysis of the vasoconstrictor nerves of the blood vessels of the pulp, or by stimulation of the vasodilators, following the infliction of degrees of irritation. (I. V. Black' was of the opinion that all pulp hyperemias are active or ar- terial, while Hopewell- Smith 2 argues that venous hyperemia of the pulp occurs more frequently than arterial. From the clinical standpoint this diversity of views has no significance whatsoever. Hyperemia proper is to he segregated from that hyperemia which is one of the phenomena of pulp inflammation, the former being considered here as a distention of the vessel walls independent of any reaction to septic invasion (Figs. 421 and 422). It is practically in all instances of the active type; that is to say, the beginning is marked by changes in the caliber of the pulp arteries and in the quantity of blood which they hold. It must be noted, however, that as the result of a distention of the arteries and their increased blood contents there occurs a corresponding decrease in the lumen of the veins — a purely mechanical cause which we interpret as the inability of the veins to drain increased blood supply, because of their limited power of accommodation, limited as it is, to overcome exaggerated arterial pressure within tin 1 pulp. The pulp mass must continue constant on account of the unyielding character of its surroundings (the walls of the pulp chamber and root canals"), so that a dilatation of one set of ves- sels — the arterial — must be synchronous with a compression of the other — the venous. •Black, G. V.: Special Dental Pathology. Chicago, Medico-Dental Pub Co =Hopewell-Smith, A.: In X. G. Bennett's Science and Practice of Dental Surgery New York, Wm. Wood \ Co " 518 ITU' HYPEREMIA 519 Etiology The causes of pulp hyperemia are, indirectly, all disease processes or forces responsible for a decrease in either the thick- ness or density, or both, of the protecting tissues of the pulp. The direct causes are the subjection of the pulp to stimuli of a de- gree of intensity greater than is normal for thai pulp. In hy- h'ig. 421. — Section of dental pulp, longitudinal. The distention and congestion of the vessels in the course of hyperemia is here beautifully shown. With the exception of the abnormal caliber of the vessels all the other tissue-elements are of normal appearance. u, a, a. a, distended vessels; b, b, odontoblastic layer. peremia of the pulp, the bacterial factor is excluded, except when indirectly induced by dental caries, when the destruction of portions of the enamel and of the dentin bring about irritation of the pulp by permitting the transmission of thermal impulses, which in the case of a sound tooth would not occur. Also it should be noted that the products <>f fermentation and putrefac- 520 DENTAL PATHOLOGY t ion, especially when concentrated, act as irritants to the pulp, a condition which occurs constantly in a carious cavity. The pulp of each tooth, as pointed out years ago by Jack, has a temperature range peculiar to itself; a decrease of several degrees of temperature in this range, either from the higher or lower maximum, is to be interpreted as hyperemia. For instance, if a pulp, under normal conditions, does not respond to applica- tion of water of a temperature of from 98° down to 50° F., or Fig. 422 — Cross section of hyperemic pulp. No pathologic lesion per se is to be de- tected at this stage of the process. - Some few distended blood vessels containing large n umbers of blood cells are seen on the upper part of the picture, a, a, distended vessels. from 98° up to 128°, such a pulp has a temperature range of 78°. This plan suggests the advisability in all cases in which the possibilities of hyperemia are brought into play (i.e. following the insertion of metallic fillings or the preparation of teeth for crowns), to obtain the temperature range before the hyperemic state develops. In the event of painful symptoms developing, by ascertaining whether or not a decrease in the temperature range PULP HYPEREMIA •">_ 1 has occurred, a corred diagnosis can be more easily established, and the disturbed pulp is definitely located. The thickness or density, or both, of the protecting Tissues of the pulp (enamel, dentin and cementum) are modified by disease processes as well as factors other than these. Among the former we include dental caries, erosion and abrasion; annum' the latter, the removal by mechanical means of closely adjacent portions of the enamel or dentin preparatory to the restoration by crowns or fillings which have much higher degrees of thermal conduc- tivity (such filling materials as gold, or silver and its alloys). Furthermore, while per s< the insertion of a small metallic filling may not perhaps cause hyperemia, the development of an exces- sive degree of heat in the process of polishing such a filling will frequently bring about this pathologic disturbance. Also the presence of a foreign mass, such as a filling of gold or of amal- gam, is in itself irritating to the dentinal fibrillar. Hyperemia or congestion of the pulp may also develop fol- lowing fractures of portions of the croAvns of teeth, also follow- ing the traumatisms incident to the condensation of gold fillings. In the latter instance both the peridental membrane and the pulp may become affected. It may also occur from the action upon the pulp of chemical substances such as formalin, paraformalde- hyde, silver nitrate, zinc chloride, etc., and from the too rapid movement of teeth in orthodontia. The recovery from hyperemia depends upon a recovery of normal tone (contraction) by the vessels of the pulp, and is governed by the length of time the hyperemia has existed, the frequency and intensity of the paroxysms of pain, and the thoroughness with which the pulp environment is favorably changed. If the cause be a metallic filling, this should be re- moved and replaced by a filling of gutta-percha, and the use of foods or beverages of too low or too high a temperature must be most carefully avoided. In other words, the environmental disease-producing factors should be eliminated at once. Abrasion and erosion causing hyperemia, not infrequently neces- sitate the removal of the pulp if the disturbance is not promptly relieved by such methods as counterirritation or the use of co- agulant obtundents. In the absence of infection the pulp is capa- ble of fully recuperating from the effects of a hyperemia. Black 522 DENTAL PATHOLOGY has shown that either moderate or relatively large liquid in- flammatory exudates are disposed of successfully by the pulp if placed under a nonirritating environment. The paroxysms of pain from pulp hyperemia may last from just a few seconds to several minutes, or hours, or even days. In some cases the pain is not exaggerated, although continuous; in others it is both intense and continuous, — at times, for a period of seconds, the pain being unbearable. The pain may be lo- calized in the affected tooth, but may be felt in several teeth or in the entire side of the jaw. It may also be of the radiating type, i.e. toward the temple, the ear, the eye, or the forehead. Occasionally a hyperemia in an upper tooth — the cuspid in par- ticular- — will be reflected to all of the upper teeth posterior to it, and sometimes also to a number of teeth in the lower jaw of the corresponding side. An intense hyperemia with corresponding degree of pain, or a moderate hyperemia lasting for several weeks or months, if permitted to go untreated, ends in the death of the pulp; here the hyperemia has assumed the characteristics of a nonseptic pulpitis. All pain having ceased the patient feels greatly relieved both physically and mentally ; but such a dead pulp may at any time give rise to an acute or a chronic alveolar abscess, and the chronic abscess may be either of the frank type with a sinus, or of the blind type without one. CHAPTER XLI] GANGRENE OF THE PULP— PUTRESCENT PULP General Considerations By gangrene of the pulp (gangrenous decomposition) is meanl death of the pulp en masse. It is the resull of the shutting off of the circulation to the pulp through mechanical, thermal, or chemical factors, or as the result of paralysis of the vessel walls. The shutting off of the circulation at the apex may he caused by (1) blows upon the teeth, (2) tooth movement in orthodontia, (3) the quick separation of teeth preparatory to filling opera- tions, or (4) nonseptic pulpitis leading to thrombosis and con- sequent infarction. The chemical causes are those incident to the application of so-called mummifying or tannifying sub- stances which contain formalin, tannic acid, thymol, zinc chloride, or other tannifying or coagulating substances. In the latter group of cases, the chemical substances used doubtless dehydrate the pulp, and by disturbing its metabolism to a de- gree beyond the possibility of cell recovery lead to cellular death (necrobiosis) of the pulp which, in the absence of bacteria and because of its complete dehydration, remains in the root canals as a shriveled mass. Paralysis of the vessel walls is caused by any form of shock, such as in a greater degree might cause the strangulation of the pulp at the apex. It is doubtful whether a pulp dies because of an actual strangulation (severance) of its blood vessels. Instead, it is more likely that the injury to the vessel walls is the cause of a thrombosis in either the arterial or venous trunk of the pulp. In other words, death of the pulp follows a series of arterial or venous obstructions, rather than a single strangula- tion. The pulp which dies in bulk either remains in a state of dryness or mummification, or becomes infected. In the former condition all fluids in the pulp are absorbed and when the pulp-chamber is opened the pulp has a dried up, parchment-like appearance, with no offensive odor detectable. In the latter stage moist gangrene develops. 523 f>24 DENTAL PATHOLOGY By moist gangrene is meant putrefactive decomposition of the pulp, a process identical to that which occurs in the bodies of dead animals. The bacteria concerned in this process are sapro- phytes — bacteria which depend for their existence upon the prod- ucts of the decomposition of dead nitrogenous matter. It is, however, to be remembered that bacteria, even though parasitic, may. when circumstances demand it, develop saprophytic proper- ties. The organisms which have been found in putrescent pulps are both saprophytic and pathogenic, and it is more than probable that many forms are facultatively pathogenic and saprophytic. Long thread-forms, leptothrix, cocci, bacilli, spirilla? and spi- rochetes have been found. Arkovy found the Bacillus gangrenae pulpae, the Staphylococcus pyogenes albus and aureus, the Strep- tococcus pyogenes and the Bacillus pyocyaneus. The breaking down of the tissue elements of the pulp is a process of simplification resulting ultimately in the formation of hydrogen sulphide, ammonium sulphide, carbon dioxide, and water. The albuminous substances are first changed into pep- tones ; then such animal alkaloids as cadaverin, putrescin, and neuridin are formed; then nitrogenous bases such as leucin and tyrosin ; then aromatic products such as indol, phenol, and cresol ; and finally the simpler compounds H 2 S, C0 2 and H 2 0. In teeth the pulps of which are undergoing putrefactive decom- position, or a combination of suppuration and putrefaction, dis- coloration is liable to occur. In these cases the discoloration 1 is prob- ably due to a combination of factors, such as the formation of compounds of iron and sulphur (black ferrous sulphide); to the action of hydrogen sulphide (an end product of putrefaction) on hemoglobin, resulting in the production of sulphomethemoglobin; and to the decomposition of hemoglobin, as already stated, in the case of unexposed pulps when the seat of nonseptic pulpitis. It has been argued that possibly the combination of ammonia (an end product of putrefactive decomposition, which in the presence of water is changed into ammonium hydroxide) with iron (liberated in the course of the decomposition of hemoglobin) is changed into Fe(OH 2 ), which upon being oxidized is changed 'Kirk, E. C: Discolored Teeth and Their Treatment. American Textbook of Opera- tive Dentistry, Philadelphia, Lea & Febiger. G \N*.i;i ni: OF Tin: PULP .V2.~> into I'.- 'Ml . ,i reddish-brown compound. This may play a pari in the discoloration of teeth whose pulps have under- gone putrefactive decomposition.* A tooth containing a pulp which is the seat of dry gangrene gives rise to no subjective symptom. The roo1 canals arc occupied by a mass n\' dried up tissues which, upon being exposed to the moisture and bacterial flora of the mouth, and to a liberal supply of oxygen (increased oxygen tension I, usually precipitate within a short time an infectious apical pericementitis, either acute or chronic. Teeth in which the pulps have died following nonseptic causes become the seal of putrefactive changes in the presence of: 1. Direct access to the pulp chamber fas through carious cav- ities, etc). 2. Indirect access to the pulp chamber: (a) From under a defective filling. (b) From under a sound filling in a cavity from which all carious matter had not been removed. (c) From infected dentinal tubuli. (d) Through imperfections in the enamel. (e) Through cementum and dentin at the neck of the tooth following caries. 3. By an infection which has reached the pulp via the circula- tion. Pulpitis Pulpitis, in a general way. may be defined as the aggregate of inflammatory phenomena in the dental pulp, which may be either bacterial or nonbacterial in origin ; it is distinguished from hyperemia in that the latter disease occurs in the absence of bacterial irritation and subsequent tissue destruction — two char- acteristic phenomena of pulpitis. This, of course, fails to hold good if the hyperemia is of such severity as to assume the charac- teristics of an inflammation. Nonseptic Pulpitis A nonseptic pulpitis is the result of subjecting the pulp to an exaggerated degree of the conditions responsible for the onset of hyperemia. An untreated hyperemia, in some instances, be- *Buckky. T. P.: Modern Dental Materia Medica, Therapeutics, and Pharmacology, Philadelphia, P. Ijlakiston's Son & Co. 526 DENTAL PATHOLOGY comes a nonseptic pulpitis and ends in death of the pulp. The difference between nonseptic pulpitis and hyperemia, from the standpoint of pathologic anatomy, is that in nonseptic pulpitis occurs a diapedesis of leucocytes with, when very acute, a trans- migration of a few erythrocytes and a transudation of serum ; while in hyperemia diapedesis does not occur, although occasionally a small number of erythrocytes are forced through the vessel walls. In traumatic pulpitis the destruction of tissue by proteolysis does not occur. The pulp cells die following the shutting off of the circulation of the organ by thrombi, or by the products of cell degeneration, fat, cell fragments, etc. If the pulp remains free from bacteria the tooth will remain comfortable, usually until such time as an attempt is made to remove the dead con- tents of the root canal, when not infrequently a dentoalveolar abscess develops as the result of the passage through the apical foramen into the periapical tissues of the products of putrefac- tive decomposition and of bacteria; and also of a change in oxy- gen tension in the root canals. Septic Pulpitis The pulp is very susceptible to the effects of bacterial invasion, and being possessed of a minimum of recuperative powers, be- comes without delay the seat of a destructive inflammation upon being subjected to even the mildest degree of bacterial infection. The virulence and number of the bacteria and the degree of vital resistance of the tissues of the pulp determine whether the in- fection will pursue a rapid course with proportionate rapid tissue destruction, or whether the course will be slow and the destruc- tion of the pulp will consume a longer period of time. Acute- ness and chronicity are differentiated from the standpoint of the duration of the inflammatory process up to the time of the death of the pulp. While determined clinically in most cases by the severity or mildness of the pain, together with the period of time the pain has been present, this symptom is not, however, in all cases, a true index of the degree of infection. In some cases in which death of the pulp occurs in a short time following an in- fection, the pain is neither severe nor paroxysmal, but rather mild and practically continuous, ivhich, bearing in mind our clinical diagnosis, would be, as far as the degree of pain is con- G W'.l.TNl OP THE I'ULP 527 eerned, indicative of chronicity rather than of acuteness; and again, in other cases in which the infectious pulpitis is of long duration, the pain may be just as intense as that which accom- panies the severer in feci ions, which once more would reverse the usual findings. In the presence of a wide opening by caries into the pulp cham- ber, even an acute process of pulp destruction may not give rise to extremely painful phenomena, since the inflammatory exudates find an outlet into the cavity of decay, so that the pres- sure within the pulp Avill at no time reach the maximum — unless it be when the exposure becomes obstructed with food debris. To the contrary, an inflammatory process by less virulent organ- isms in the pulp chamber or root canals, in the absence of drain- age, may discard the yoke of invalidism, and to regain their respective places among the useful units of their communi- ties. Chronic mouth infection — oral focal infections — for the pur- pose of convenience in description we have divided into two groups; (1) the intraosseous and (2) the extraosseous. And be it understood thai by "oral focal infection" we imply an area of chronic infection in the mouth — the teeth and its osseous and sofl investing tissues — from which, through hematogenic or lymphogenic metastases, chronic disease develops in any organ or structure of the body at remote distance from the original focus of infection. In the intraosseous group are included the chronic and subacute infections in the substance of the jaws immediately adjacent to the roots of the teeth. These are consequent upon a chronic in- fection of the periapical peridental membrane — the sinusless chronic dentoalveolar abscess (so-called dental granuloma) — to- gether with the secondary foci of infection arising from this source. In the e xtraosseous group are included all chronic sup- purative diseases of the peridental membrane, alveolar process. gingiva and gums. In most cases of dental disease in which extensive destruction of the hard tissues of the tooth has taken place through caries, with involvement of the pulp as the consequence, a focus of chronic infection, if present, will, of course, be located in tin 1 deeper osseous structures of the jaw. These seats of chronic in- fection, the existence of which has not altogether been unknown in the past, have by some been designated as blind abscesses, br- others, the author included, sinusless chronic dentoalveolar ab- scesses, and by still others denial granulomas. They play a very active part in the etiology of chronic inflammatory disorders in articular structures, muscles, heart, kidney, intestines, etc. In discussing foci of infection in the mouth we are prone to give the preference to these septic nuclei in the deeper structures of the jaw (rarefying osteitis). It is not our aim to minimize their im- portance; nevertheless, we feel constrained to state that these are not by any means the onlv dental or oral sources of o-eneral in- 550 DENTAL PATHOLOGY volvement. Tt has been satisfactorily shown, however, that infec- tion of joints, muscles, the intestinal tract, kidneys, heart, etc., may take place via the hematogenic or lymphogenic routes. In the month are to he found numerous conditions which make possible the absorption of bacteria and their toxins directly into the circulation, in the absence of "blind abscesses"- — namely, in the absence of chronic, acute or subacute pericemental infections. These extraosseous sources of toxin absorption are, in patho- logic significance, equal to, if not greater than, the intraosseous focal areas. The presence upon the surfaces of the teeth of sali- vary calculi which maintain the margins of the gum in a state of constant irritation, either through pressure atrophy or through in- duction of a suppurative process, cause the destruction of the stratified squamous epithelium protective covering, and constitute a prolific source of absorption of bacteria — and bacterial toxins. Almost invariably, when salivary calculi are present in varied amounts, such absorptions are going on constantly, not only from the locations in which the calculi are present, but also from ad- jacent areas which become involved by a process of continuity. Sal- ivary calculi exert a detrimental influence upon soft tissues and favor their invasion by bacteria. They also act mechanically by favoring the lodgment of food particles which, after undergoing fermentation or putrefaction, or both, give rise to either acid or alkaline end-products, which irritate the soft tissues and prepare the field for bacterial invasion by decreasing its vital resistance. Salivary calculi as a source of bacterial and toxin absorption, with possibly future systemic involvement, can not be too strongly emphasized. The other forms of calcareous deposits upon the teeth, namely, those deposits which exist under the free margin of the gums, and which are brought about by some form of irritation of the gingival and septal tissues, eventually lead to the destruction of the peri- dental membrane and alveolus, and likewise constitute a frequent source of absorption of bacteria and bacterial toxins. Any form of injury to the gingiva 1 , such as the rough edges of crowns and fillings; negligence in the care of the mouth permitting the accu- mulation of food particles which undergo decomposition and main- tain the gingival tissues in a state of constant irritation ; the pres- ence of unfilled cavities of decay; defectively contoured fillings; MOUTH [NPECTIONS AND SYSTEMIC DISEASE 551 natural or acquired insufficiency of approximal contact; and olhcr allied abnormal phenomena, are all important causative factors in tins variety of deposits. Subgingival deposits invariably spell in- flammation of gum tissue and eventually the formation of pyor- rhea pockets. The gingiva, the peridental membrane, and llic al- veolar process become the seat of a chronic infection; the peri- dental membrane and the overlying alveolar process become tlie seat of a destructive suppurative inflammation, slow in its develop- ment but, nevertheless, one which continues and in time will lead to the establishment of the pathologic condition which is ordinarily designated as pyorrhea alveolaris. The importance of the study of these conditions is made more understandable by recalling- the list of maladies which clinical ob- servation has shown to be related in etiology to infections about the roots of teeth and their investing and supporting structures. The list includes endocarditis, myocarditis, pericarditis, joint and muscle infections, gastric, intestinal, renal and pulmonary infec- tions, toxemias, insomnia, sinus infections which become secondary foci, etc. Hartzell and Henrici have produced lesions of the heart, kidneys, aorta, and joints of rabbits following intravenous injections of 8 c.c. of a twenty-four-hour broth culture of the strains of strepto- cocci obtained from pyorrhea alveolaris and dentoalveolar abscess. The mouth and teeth, the air sinuses, the tonsils, the postpharyn- geal adenoid tissue, upon becoming the seat of chronic infections, constitute jointly the most common forms of focal infection. From chronic dentoalveolar abscesses and pyorrhea alveolaris have been obtained different strains of streptococci — the hemolyticus, rheu- maticus, and viridans; also the Staphylococcus pyogenes albus and aureus, the fusiform bacillus, and the diplococcus of pneumonia; and from the saliva and pharyngeal mucus, in addition to the above are found the B. diphtheria, the B. tuberculosis, the M. catarrhalis, and a large number of saprophytic organisms. Any one of these pathogenic organisms may migrate into any struc- ture of the body, as previously stated, by the hematogenic and lymphogenic routes, and finding areas of decreased vital resist- ance, start on their campaign of slow destruction. The Streptococcus viridans may occasionally produce acute in- fections even though the organism is one of low virulence and 552 DENTAL PATHOLOGY brings about ehronie rather than acute inflammations. Acute joint inflammations have, however, beer observed in which the Streptococcus viridans was the principal organism. We now direct the reader's attention to the advisability of disregarding the absence of subjective and objective symptoms in the diagnosis of mouth infections, having become long ago convinced thai some of the mosl pronounced cases of systemic involvement had developed in eases in which there were to be found in the mouth no indications of the existence of a chronic inflammatory process. In the course of an investigation by James D. McCoy, a series bout L25 cases was radiographed, several extra- and intra- oral exposures being made of each ••a-'-, making a total of nearly 500 radiograms. In this series the radiograms showed, in each instance, some theretofore unsuspected pathologic condition, such ,i- impacted and incarcerated teeth, incompletely filled root canals, foci of chronic infections, etc. Of the cases exhibiting chronic foci of infection in each instance the condition being unsuspected by the patient) a proportion of somewhat over per cent had systemic manifestations in the form of arthritis or myositis of various degrees of intensity. A clinical investigation covering a series of 125 cases con- stitutes a strong enough nucleus or' data from which to deduct conclusions which should lead to a more definite conception of the role played by mouth infections in the development of joint and muscle inflammation. The fact that tin' existence of these mouth lesions had not been suspected fit any time prior to the radiographic examinations, because of absence of subjective and objective symptoms, is the conclusion in McCoy's work which constitutes a strong link in tin- chain of evidence on the rela- tionship of month infections to systemic infections. The Streptococcus viridans, an organism of low virulence, has been obtained byHartzell and Henrici from chronic dentoalveolar abscesses, and the same investigators 3 have obtained from one case of pyorrhea alveolari-. and dentoalveolar abscess various strains of streptococci, the Staphylococcus albus, Bacillus coli, Bacillus proteus, various spore-bearing aerobes of the Bacillus subtilis type, and Bacillus pyocyaneus; also ;i small Gram-positive Am. Med. Assn , xliv, Xo. 13. MOUTH [NFECTIONS \M> SYST1 MIC DISEASE 553 bacillus and a diphtheroid bacillus. Prom another case they ob- tained a pure culture of Bacillus fecalis alcaligenes. Urlich made au examination of L350 teeth, 82 per cent of which showed apical abscesses. He examined 976 artificially devitalized teeth with rod canal fillings, and of these over 68 per cent showed apical abscesses. A bacterial examination was made in 318 cases and the Streptococcus viridans and the Streptococcus hemolyticus were found 309 times. 6r in 97 per cent of all caves examined. In nine eases of acute arthritis reported by Hartzell and Hen- rid in one series, the patients showed marked improvement im- mediately after the removal of the abscessed teeth. In another report they mention the case of a patient with pyor- rhea alveolaris, apical abscess and a severely painful arthritis which began to recede a few hours after the extraction of the tooth having- the chronic dentoalveolar abscesses. Cultures from the root tip yielded another strain of streptococcus of high viru- lence, killing a rabbit overnight. This rabbit showed a hemor- rhage into one of the mitral cusps and a number of whitish streaks in the myocardium just beneath the pericardium. In these streaks were found, microscopically, the lymphocytes gathered together in the cellular tissues under the pericardium. The streptococci were recovered in pure culture and immediately injected in a smaller dose in another rabbit which died, in two days; the only lesions obtained in this rabbit were numerous mil- iary abscesses in the kidneys, especially the medulla — a case of true pyemia. Hartzell and Henrici 4 have also studied seven cases of endo- carditis. In two of these patients the heart condition was vastly improved by eliminating the mouth infection. One from among the many observations on the relation of local dental infections to arthritis has recently been reported by Morey. 5 In a series of six cases of arthritis of long standing, the symptoms subsided immediately upon, or a short time fol- lowing, the eradication of intraoral foci of infection, the sup- position being that the mouth streptococcus had been carried by the hematogenic route to the points of activity in the articu- 4 Hartzell and Henrici: Jour. National Dental Association, vi, Xo. 12. "•Morey. F. L. : Acting Assistant Dental Surgeon U. S. Navy, in the U. S. Xaval Medical l'ulletin. 554 DENTAL PATHOLOGY lations. No attempt is made by the reporter to connect all cases of arthritis with diseased teeth ; but, on the other hand, he brings forth additional and convincing proof that a large num- ber of cases of arthritis, nephritis, cardiovascular diseases, and inflammations in the gastrointestinal tract, are of dental etiology. Three cases in which infectious arthritis were cured by the removal of teeth having a slight area of infection are reported by Morey : Case 1 Arthritis of the right ankle. Patient unable to benr any weight on his foot for about six months; he had been under treatment most of the time but had not improved very much. A roentgenogram showed a slight area of infection above the right first molar, which had only a small occlusal amalgam filling in it; the patient was advised to have the filling removed and the canals treated, but he preferred to have the tooth extracted. Within two hours after the extraction the pain in the ankle began to subside and the next day he was able to bear his weight on the foot. Case 2 Arthritis of the arms and legs, patient having been in bed for four months, some days feeling slightly improved but gradually growing weaker. No focus of infection could lie found; a roentgenogram of the teeth showed a slightly infected area at the root of one of the molars. The first molars had gold crowns on them and it was thought advisable to remove the teeth that were crowned, as the patient was confined to his bed and it was impossible to open the teeth and treat the roots with any degree of satisfaction. "Within five weeks after the extraction the patient was able to walk around, being free from all pain, and the swelling had disappeared. Case 3 Confined to his bed with arthritis of the knees and ankles. Eemoved the left superior first molar, it having a slight infection above it; also removed a badly broken-down root which was the source of some infection. Patient began to improve within forty-eight hours. Relatively small areas of rarefaction on the roots of teeth con- sequent upon chronic peridental infection are frequently the cause of severe joint infection. In some cases one single slight area of infection, upon its elimination, has brought about re- covery of the case. Hartzell and Henrici report that in the study of a series of seventeen cases of arthritis deformans over one-half of these patients showed improvement, which in a few cases was pro- "Hartzell, Thomas B., and Henrici, Arthur T. : A Study of Streptococci from Pyor- rhea Alveolaris and from Apical Abscesses, Jour. Am. Med. Assn, xliv, No. 13. MOUTH [NFECTIONS WD SYSTEMIC DISEASE .».,.» nounced; other eases, however, became worse under treatment. In a series of seven eases of endocarditis, in two of the patients the heart condition was vastly improved. Other systemic dis- turbances studied by them were three eases of pernicious anemia, five cases of gastric ulcer, and nine eases of active arthritis. In the pernicious anemia eases no definite report was made by the investigators, although they state that one man showed a marked progressive increase in the blood count after removal of some of the abscessed teeth, but that he left the hospital before his dental work was completed, and returned later with a low blood count. The gastric ulcer patients, two of whom had been affected twelve to fourteen years with frequent recurrences in that time, Fig. 436. — Case 1. had no recurrence, since eliminating the mouth infections, dur- ing a period of observation of two years and five months after the dental work was completed. The arthritis patients all showed a marked improvement beginning in some cases a few hours after removing the abscessed teeth. The following reports of cases studied by the author from a series of several hundred will throw some light on the role of mouth infections as sources of systemic intoxications. Case 1 (Fig. 436) Woman, aged thirty-six, had previously been in apparent good health but complained of severe pain in her face. In addition, she complained of a series of symptoms typical of general toxemia. She seemed anemic and decidedly 556 DENTAL PATHOLOGY below par. She sought the services of a dentist for the purpose of ascertain- ing whether any abnormality could be detected in her teeth that would ac- count for the reflex pain from which she had been suffering for some time past. An area of rarefying osteitis was found around the root of the second lower bicuspid, indicative of chronic sepsis in the peridental tissues and within the bony structures. The tooth had been previously treated and the root canal carefully filled. The bicuspid was extracted and almost immediately the pain and toxic symptoms began to improve, and have continued so uninterruptedly ever since. Case 2 (Fig. 437) Man aged forty-five gave a history of continued good health up to the time of the incidence of the symptoms which led to his being placed under our observation. He had evidently been a man of vigorous constitution and non- sedentary in his habits. He complained of loss of appetite, lassitude, and an inability to exert himself to any extent without experiencing a sense of fatigue. Fig. 437. — Case Tlic radiogram (Fig. 437) showed a marked chronic septic condition under the roots of the lower second molar, which evidently had been treated years pre- viously and in which the root canal had not been completely filled. There was a tenderness to percussion in several teeth and consequently a definite diagnosis could not lie made at the time. The radiogram came to our assistance, the offending tooth was extracted, and a complete recovery followed within a period of three or four weeks. Case 3 (Fig. 438) Man, aged about sixty years. This case seems to us to present features of special interest because the septic, conditions about the roots of some of the teeth were evidently responsible for an interruption in the mental balance of the patient. The man, of limited means, had endeavored for some time past MOUTH [NFECTIONS AND SYSTEMIC DIS] \>l. 557 to secure a berth in an old man'- home, bul on accounl of the mental and physical symptoms the authorities of the institution rejected his application. He was referred by bis physician to ascertain whether any abnormality could exist in his jaws ami around his teeth which could be made to accounl for the toxic symptoms from which he was suffering and also for the disturbance in psychic function. We found that which would warrant one in assuming thai the foci of infection in his jaws were at leasl a factor in the production of the pathologic symptoms herein described. On the left side conditions were as follows : A chronic abscess around the roots of the lower fust bicuspid; an incar- cerated root in the upper jaw mesial to the second molar; also foci of in- fection in tin- distal root of the lower third molar, above ami around the loots of the upper second bicuspid and upper third molar. On the right Bide Fig. 438.— Case 3. A, left; B, right. a number of foci of infection could be detected in the lower and upper jaws. All the teeth that were considered responsible for the conditions herein described were extracted and the improvement that followed was so marked that he was permitted to become a member of the household in the institu- tion for the aged, to which admission had been denied him some months pre- viously. Case i (Fig. 439) Woman, aged about thirty, gave a history of rheumatoid arthritis with marked pain in the region of the shoulder blades; pseudoankylosis ; marked anemia, fatigue, lassitude, etc. This case also exhibited marked reflex nervous manifestations. From this case Streptococcus viridans was isolated. The tooth that was considered beyond therapeutic measures (the lower left second molar) 558 DENTAL PATHOLOGY was extracted; some of the other teeth, the seat of chronic septic inflamma- tions, were treated in the approved ways, while the a piers of the single rooted teeth were amputated. The improvement which has followed is most encouraging. Fig. 439.— Case 4. Fig. -140.— Case 5. Case 5 (Fig. 440) Man, aged fifty years, complained of pain in the shoulder on the same side as that upon which was found to exist a chronic septic focus around the apical third of a lower bicuspid tooth. Removal of the tooth was followed by complete recovery. MOUTH INFECTIONS AND SYSTEMIC DISEASE 559 Case 6 Woman, aged aboul forty, gave a history of no pain, bul on the other hand, one of disturbance of nutrition, accompanied by anemia. Being the wife of a physician, her case was studied with particular care by a number of medical practitioners, all of whom reported absence of viscera] Lesion. Several foci of infection were found in the mouth, namely, one around the roots of the lower first bicuspid, one around the roots of the lower right sec 1 molar, and one on the distal side of the upper right second bicuspid. Eradication of these anas was followed by decided improvement. Case 7 Woman, aged thirty years. This patient exhibited symptoms of intense gen- eral toxemia for a number of months. Prior to the onset of these symptoms she reported having been in good health. She was referred to us to ascertain whether the condition of the lower first molar, which had been treated and Fig. 441.— Case 7. the root canals filled, was satisfactory. Suspicion had been aroused because the tooth was slightly tender to percussion. While a slight infection was present in this tooth, the main difficulty was, however, in the second bicuspid (Fig. 441). This patient was in such an exhausted condition as to require anywhere from sixteen to twenty-four hours of sleep a day, and even after such a long period of quietness she would awake with a feeling of fatigue as intense as it seemed to be at the time of retiring. The lower second bicuspid was extracted, and in the course of a few weeks the symptoms entirely dis- appeared. She has since reported that eight hours of sleep satisfy her com- pletely. Case 8 (Fig. 442) Man, aged about forty-five, gave a history of lameness in the right shoul- der, torticollis, and a continued toxic condition. He did not have to state 5G0 DENTAL PATHOLOGY that he was a sick man — it was self-evident. The roots of the first molar showed an intensified septic process. The tooth was extracted, and there followed in due time a marked improvement. Fig. 442.— Case 8. Fig. 443.— Case 9. Case 9 (Fig. 443) Man, aged about forty-five years, had symptoms of toxin absorption and slight pain on the left side of the mandible. A large septic focus was found between and below the roots of the lower first molar. Extraction was fol- lowed by recovery. MOUTH [NFECTIONS AND SYSTEMIC DISEASE .",111 In a series of three hundred eases of gastrointestinal lesions, 50% per cent, or about L52 patients, had mouths in which l'< ORAL MUCOUS MEMBRANE 573 structioD of the superficial epithelium they become infected, and in people pasl the age of thirty or thirty-five they should be considered dangerous, as they are liable to murk the beginning of the development of malignant neoplasms. In making the diag- nosis of these ulcers an accurate history of their development should be secured, and if upon removing all sources of irritation and treating them with weak silver nitrate solutions they do not disappear promptly, the prognosis is serious. If there he no in- duration the ulcer is probably a benign one, but if induration be present it is probably a malignant one. Ulcers of the tongue may also be syphilitic, in which ease the history, the presence of other manifestation of syphilis, and the Wassermann test, will determine the diagnosis. Indurated ulcers in patients past forty years of age suspected of being carcinomatous, should be excised without de- lay. The tongue is frequently the seat of inflammatory disturbances brought about by digestive disorders. In these cases the tongue appears red and smooth, the inflammation being as a rule located in the anterior portion of the tongue. Leucoplakia of the Tongue Leucoplakia is a disease characterized by the presence upon the dorsum of the tongue and mucous membrane of the mouth, particularly the buccal, of patches of a yellowish white color, irregular in shape, and slightly raised above the mucous mem- brane. They may become indurated, and after the white patches are cast off, the under-surface so exposed appears ulcerated. The superficial layers of the stratified squamous epithelium are thickened, while the deep layers exhibit a tendency to proliferate into the deeper structures. The patch may also have a bluish color and whenever it is removed, Avhether it be the white patch or the bluish, it leaves a raw surface behind. There is no pain accompanying the patches. It may be caused by the irritation of tobacco smoke, strong drinks or highly spiced food, or it may be a manifestation of a long standing syphilis. Some authorities consider leucoplakia as a forerunner of cancer — a precancerous lesion — and consequently insist upon the complete excision of the patches, while others believe that leucoplakia is the oral manifes- tation of psoriasis. [NDEX A Abnormalities of teeth, 250 of upper lateral incisor, 267 Abraded surfaces, shape of, 357 Abrasion and malocclusion, 356 Abrasion and pulp exposure, 357 cup-shaped in lower molars, 362 etiology of, 356 from chewing gum, 356 from gritty tooth-powders, 356 from pipe and cigarette stems, 356 from tooth-brush friction, 356 in cuspids, 360 in iiicism-s, 358 of root, 357 pathologic anatomy of, 357 pulp degeneration in, 358 tubular calcification in, 358 Abscess, acute dentoalveolar, 42-1 : i lid chronic, difference in pathol- ogy, 443 bone involvement in, 457 clinical symptoms of, 425 definition of, 424 discharge from, 424 discharging externally, 42!) discharging into maxillary sinus. 427 discharging into nasal cavity, 427 extensive swelling from, 431 involvement of face in, 429 limited swelling from, 431 most painful stage of, 431 protrusion of tooth in, 433 periostitis in, 435 chronic dentoalveolar, characteris- tics of, 443 cultures from, 454 etiology of, 436 fibrous wall of, 451 forms it may assume, 438 looseness of tooth with, 440 leucocytes in mass of, 444 microscopic anatomy of, 444 pathologic anatomy of, 436 sequestrum formation in, 468 sinus formation in, 427 staphylococci in, 452 Streptococci in, 452 sinuses from, 436 Abscess — ('out M. formation, 102 "hot," 103 lateral, 422 periapical chronic, 423 pericemental, -122 pyorrheal, 122 sinusless, chronic dentoalveolar, 549 subacute dentoalveolor, 430 chronic dentoalveolar, systemic in- volvement by bacteria from, 551 Abscesses, blind, 549 chronic, trabeculated, 151 cold, 103 Absence of teeth, 291 Acari, 196 Acarus, scabiei, 206 Acid, dilute, action upon enamel, 219 effects of, on enamel, and perinea bility of, 227 lactic in erosion, 360 Acidity, potential, of salivary depres- sants, 312 producers, .".24 weak, in mouth washes, 332 Acroo dextrin, 322 Actinomyces bovis, 181 Actinomyces Madura?, 182 Actinomycosis, 181 Adamantinoma, 146, r,:\r, A denocareinomata, 143 Adenoma, acimise, 139 alveolar, 139 canalicular, 139 racemose, 139 simple, 139 tubular, 139 Adenomata, 138 Adhesions, 107 Age and dental caries, 320 Age as a predisposing cause of dis- ease, 38 Agenesia, 4 6 of enamel, 256 Agglutinins, 153 Albumen in normal and pathologic saliva, 371 Albuminoids, 28 Alkaloids, animal, 524 cadaveric, 413 57.'. 576 INDEX Albuminosis, 64 Albumins, 28 Alveolar plate, exfoliation of, 462 process, atrophy of, 491 Alveoli, cortical layer of, 161 necrosis of, 462 rarefying osteitis of, 462 Alveolodental periosteum, 402 Ameboid movement, 32 Ameloblasts, 245 Amino-aeids, 27 Ammonium carbonate in hyperacid diathesis, 372 Amyloid degeneration, 56 Anasarca, 95 Anatomy, pathologic, 37 definition of, 213 Anemia, collateral, 82 local, 82 neurotic, 82 idiopathic, 82 obstructive, 82 Angina, Vincent's, 179 Angioma, cavernous, 134 Angiomata, 133 Angiosarcoma, 126 Ankylostomiasis, 203 Anopheles, 188 Anthrax, 176 Anthfacosis, 64 Antibodies, 153 Antigens, 153 Antiseptic power of saliva, 315 Aphthae, 570 Aphthous stomatitis, 570 Apical areas, resorption of, 465 region, pyogenic bacteria in, 412 Aplasia, 16 Arachnida, 196 Argyria, 64 Arterioliths, 381 Arthritis deformans, 554 Arthritis from oral foci of infection, 563 Arthritis, infectious, case histories, 554 Arthropoda, 196 Ascaris lumbricoides, 200, 201 Ascites, 96 chylous, 95 Ateleiosis, 45 Atmospheric pressure, increased, ef- fects of, 4:'. Atrophy, 41 brown, 46 combined, 45 degenerative, 45 discussion of, 2.10 etiology of, 46 Atrophy — Cont 'd. general, 45 gross morbid anatomy of, 46 local, 45 numerical, 4.1 pathologic histology of, 46 pathologic physiology of, 17 simple, 4.1 A u1 plysis, 76 B Bacillus acidophilus, '■'>- I anthracis, 176 coma, 17(5 diphtheria, 173 dysenteric, 175 fusiformis, 179, 4.12 gangrense pulpse, 452 gingivae pyogenes, 4.12 influenza, 178 pestis, 177 of Ducrey, 158 pulpae pyogenes, 4.12 pyoeyaneus, 155 tuberculosis, 164 typhosus, 174 Backward caries, 328 Bacteria, 152 from chronic dentoalveolar abscess, .1.11 higher, 153 in dentinal tubules, 328 lower, 153 on the number of, in mouth, 315 putrefactive, 79 pyogenic in apical region, 412 Bacterial absorption from subgingival space, 380 enzymes in dentin caries. 326 infection, nonreceptivity to, 214 Bacteriemia, 114 Bands of Betzius, 221 Betel-nut chewing, 383 Bicuspid, abrasion of, 362 lower first, abnormalities of, 277 lower first, hypoplasia of, 277 lower second, hypoplasia of, 277 Bicuspids, lower, with two roots, 277 perfect fissures in, 318 second, impaction of, 297 upper first, with three cusps and roots, 271 upper, hypercementosis in, 3.11 upper, hypoplasia of, 274 upper second, abnormalities of, 271 bifurcation of root of, 273 with two or three roots, 274 upper, with three roots, 273 INDEX 577 Biliary, calculi, 70 Blastodermic layers, 34 Blastomycetes, 152 Blastomycosis, 152, 182 Blind abscess, 436 Blood cells, solution of, by saliva, 315 coagulation, 7 1 excess of carbon dioxide in, 362, 363 hemolytic power of, 315 suffusion of, ' S(i supply of peridental membrane, 402 uric aeid suits in, 196 Bone and eeiiirntmii, differences be- tween, 233 cancellated, 455 changes in maxillary sinus, 427 compact, 455 eorpuscles of, 155 endochondral, 156 lamellae of, 455 lesions in pocket formation, .194 normal and pathologic considera- tions, 455 periosteal, 456 spongy, 455 Bright 's disease, 95 Bioblasts, 25 Broncholiths, 70 Bronchopneumonia, 161 Bubonic plague, 177 Burns, degrees of, 42 C Cadaverin, 413, 524 Caisson disease, 4.", Calcareous deposits, 381 in intestines, 381 formations in pulp hypertrophy, 53] infiltration, 68 Caleicosis, 64 Calcification of enamel, direction of, 246 Calcification, tubular, in abrasion, 358 Calcified amorphous bodies in defec- tive fissures. 260 Calcium acid phosphate in erosion, 361 Calculi, biliary, 70 renal, 70 vesical, 70 Canaliculi in cementum, 2::4 Canals, Volkmann's, 455 Cancellated spaces, infection through, 418 Cancer and mouth infection, 561 I lancer, colloid, 140 Candy-makers mouth, 312 < 'a nit ies, 67 Canker sons, 570 Carbohydrate diet, excessive, manifes- tat inn in saliva, 37 I Carbohydrates, degrees of fermenta- tion of, 323 Carbon dioxide, excess of, in blood, 362 Carbuncle, 103 Carcinomata, 139 basal cell, 142 medullary, 1 15 scirrhous, 143 simple, 146 Caries, among civilized races, 311 aiming school boys and girls, 313 ancient theories of, 307 and age, 320 and diet, 311 and general diseases, .'121 and heredity, 321 and inflammation of gingivae and gums, 320 and osteomalacia of pregnancy, 320 and starchy foods, 320 and sulphocyanates, 371 and the constitutional factor, 314 backward, 328 beginning of, 334 chemico-bacterial theory of, 314 chemico-parasitic theory of, 310 coarse foods in relation to, 312 conditions which favor progress of, 317 constitutional factor in, 414 dissolution of enamel in, 322 etiologie factors in, 322 factors which favor, 314 favorable areas for, 314 historical data, 306 how it advances, 357 how limited, 355 immunity from, 315 immunity to, in uncivilized races, 311 in approximal surfaces, predispos- ing causes of, 336 in British races, 313 in candy-makers and millers, 312 in dentin, progress of, 342 in fissures and pits, 33 1 in meat-eating tribes, 312 in prehistoric times, 311 in teeth of uncivilized races. 224 in the Maori rare, 313 lateral, 326, 328 malocclusion and, 319 Miller's conclusions on, 310 578 INDEX < laries — Conl 'd. of dentin, 340 of dentin, bacterial enzymes in, 320 onset of conditions which favor, 320 pathologic processes in, 322 predisposition to, of hypoplastic enamel, 318 predisposing causes of, .".17, 320 pulp infection in absence of, 527 putrefaction theory of, 309 quantity of saliva in relation to, 316 races free from, 312 restricted, 320 role of ptyalin in, 370 salivary stimulants in relation to, 312 statistics on, 313 teeth in malocclusion and, 319 theories on, accepted, ."'in worm theory of, 309 Carious process in dentin, 320 Cessation, 76 Catarrhal stomatitis, 500 Causes of disease, 37 exciting, 37, 211 of hypercementosis, 353 of pericemental inflammation, sep- tic, summary of causes, 421 predisposing, 37, 213 predisposing, of caries, 317 predisposing, of caries in approxi- mal surfaces, 32:! predisposing, of dental caries, 320 predisposing, of dental disease, 215 Cell, 23 anatomy of, 24 chemistry of, 26 growth, 32 nutrition of, 32 physics of, 29 physiology of, 32 staining reactions of, 30 wall, 24 Cells, cementoclastic, 250 giant, 456 plasma, 451 Cementoblasts, 233, 407 Cementoclastic cells, 250 Cementum, 233, 248 and enamel, line of junction, 228 canaliculi of, 234 caries of, 349 changes, conditions which govern, 250 chemical composition of, 240 denudation of, 388 differences from bone, 233 ( 'ementum — Cont 'd. fillers encased in, 234 formation of, 350 ground sections of, 238, 239, 240 how deposited, 233 increases in thickness of, 250 lacuna 1 , 233 lamella;, 233 increase in number of, 355 increase in size of, 355 matrix of, 234 nutrition of, 233 nutrition to, from dentin, 237 resorptions in, 250 Centrosome, 25 Cervicolingual ridge, abnormalities of, 264 fissured, 265 hypoplasia of, 265 ('est odes, 195, 198 Chalieosis, 64 Chancre, soft, 158 Chancroid, 158 Cliemisis, 96 "Chicken-fat" clots, 75 Chicken pox, 191 Chilblain, 42 Chlorides, increase of, in gouty diath- esis, 372 Cholera, Asiatic, 173 Cholesteatoma, 149 Cholesterin, 29 Chorionepithelioma. 149 Chloroma, 128 Chondromata, 120 Chordomata, 121 Chromatin, 26 Chronic gingivitis, 392 Cilia, 32 Ciliary movement, 32 < longenital disease, 40 Circulatory activity, impairment of, 215 changes, 82 Cleft palate, 211 Cloudy swelling, 48 Coagulation, blood, 74 Coagulation necrosis, 73 Coccidiosis, 190 Calco-globulin, 382 Cold, effects of, 42 Colloid degeneration, 52 Colloids, 29, 30 Coma bacillus, 173 Concretions, 69 Concussion, 41 Congestion, hypostatic, 85 Conjunctivitis, epidemic, 179 [NDEX 57«J Constructive changes in cementum, 250 Contact, Lack of, 379 Cough, whooping, 17!) Culex, (mosquito), 188 Cusp, lingual, of lower firsl bicuspid, 277 supernumerary in upper first molar, 280 Cuspid, lower, supernumerary root in, 273 hypoplasia of, 270 short rooted, 270 two rooted, 270, 272 radiograph of, 273 Cuspids, abraded, 360 upper, abnormalities of, 269 longitudinal section of, 228 short rooted, 270 Cusps, three, in upper first bicuspid, 271 Crystalloids, 29, 30 "Currant jelly" clots, 75 Cylindromata, 147 Cytoplasm, 23, 25 Cystic odontomas, 532 Cysts, 149 dental, 532 dental or root, pathologic anatomy of, 539 dentigerous, 410, 441 dermoid, 148 follicular, 534 follicular, pathologic anatomy of, 540 glandular, 150 parasitic, 150 retention, 149 root, 532 softening or necrotic, 150 Czermack, interglobular spaces of, 231 D Death, somatic, 73 Decalcification, tardy, of deciduous teeth, 302 Deciduous enamel, when it begins to form, 246 teeth, calcification of, 248 retention, 291 tardy decalcification of, 302 Deformities, macroscopic, of central incisors, 264 of teeth, macroscopic, 264 Degenerations, 47 amyloid, 56 colloid, 52 fatty, 48 I >egenera1 ions I !on1 \l. granular, 48 hyaline, 54 mucoid, 50 parenchymatous, 48 waxy, bacony, or lardaceous, 56 Dengue, 193 Dental band, 241 Dental caries among civilized races, 311 among school boys and girls, 313 and age, 320 and civilization, 311 and general diseases, 321 and heredity, 321 and inflammation of gingiva and gums, 320 and meat diet, 320 and pregnancy, 320 and starchy foods, 320 and teeth in malocclusion, 319 chemico-bacterial theory of, 314 coarse foods in relation to, 312 conditions which favor onset of, 320 conditions which favor progress of, 317 constitutional factor in, 414 "dry mouth" in relation to, 316 etiologic factors in, 322 factors which favor, 314 historical data, 306 immunizing properties of saliva in, 315 immunity to in uncivilized races, 311 in British races, 313 in candy-makers and millers, 312 in Maori race, 313 in meat-eating tribes, 312 in prehistoric times, 311 on immunity from, 315 pathologic processes in, 322 predisposing causes of, 317, 320 quantity of saliva in relation to, 316 races free from, 312 restricted, 320 salivary stimulants in relation to, 312 statistics on, 313 Dental cysts, 532 ectopia, 304 disease, definition of, 213 predisposing causes of, 215 follicle, chronology of, 245, 254 follicles in syphilitic, 305 granuloma, 355, 436, 549 groove, 241 580 INDEX Dental— Cont'd. hypoplasia and caries, 252 hypoplasia, definition of, 251 microscopic, 252 infantilism, 304 lamina, 241 papillae, 246 ridge, 241 stigmata of syphilis, 303 Dentrifices, cause of dentin discolora- tion, 347 Dentigerous cysts, 410, 441 Dentin, 228 caries, 340 carious process in, 326 caries, progress of, 342 chemical composition of, 233 comparative hardness of, 226 discoloration by dentrifices, 347 elastin in, 230 forming organ, 246 hypoplasia, 256 intertubular substance of, 248 lactic acid in depth of, 328 matrix, 230 matrix liquefaction of, 342 microorganisms in the structure of, 327 nature of tissue, 228 nutrition to, from cementum, 237 pigmentation in caries, 347 secondary, 511 amorphous, 511 amorphous classification of, 511 typical, 511 temporary arrest of calcification in, 2.",:: the softening of, 341 transverse section of, 229 Dentinal fibrillar, 228 tubuli, 228 a field of, 229 anastomosis of, 230 average diameter of, 250 bacteria in. 238 calcifications in, 250 Calcific degenerations of, 510 curves of, 231 in bicuspids and molars, 230 in crown portion, 230 in incisal region, 230 in relation to cusps, 231 in root portion, 230 penetration into enamel, 232 penetration into cementum, 237 putrefactive changes in, 414 relative diameters of, 230 Dentinification, process of, 247 Dentition, complete absence of, 202 deformities of, due to syphilis, 302 Dentoalveolar abscess, acute apical, 424 acute osteomyelitis in, 435 chronic, 436 chronic, bacteria from, 551 chronic forms of, 438 chronic, systemic involvement from, 551 clinical symptoms of, 425 pathologic anatomy of, 433 Deposit, calcareous, 381 subgingival, lesions produced bv, 392 Development of teeth, 241 Diagnosis by percussion, 440 Diapedesis, 99 Diaphanous halo, 345 Diathesis, gouty, increase of chlorides in, 372 hyperacid, ammonium carbonate in, 372 Diet and caries, 311 Diphtheria, 173 Diploeoccus intracellularis meningiti- dis, 156 Disaccharides, 32 4 Discoloration from pulp putrefaction, 524 of enamel, congenital, 259 of teeth, 441 on approximal surfaces of bicus- pids and molars, 334 with nonexposed pulp, 530 Disease, cause of, 37 congenital, 40 contagious, 152 definition of, 21 dental, definition of. 213, 216 predisposing causes of, 215 etiology of, 37 functional, 21, 216 infectious, pathology of, 152 general, definition of, 216 of the gingiva?, gums and mucous membrane, 565 organic, 216 Diseases of peridental membrane. 402 nf suboxidation, 361 suppurative, 154 susceptibility to, 214 toxemic, 172 Dropsy, 95 Ducts of salivary glands, deposits in, 381 l.M'I.X 581 Drugs, irritating, in rool canal work, 408 1 dysentery, amebic, 1 B5 bacillary, 175 E Ear, involvement from impacted t1iir''< blood supply of, 375 histology of, 375 II Habits, as a predisposing cause, 40 Haplobaeteria, 153 Hard and soft teeth, 226 Harelip, 211 Healing by first intention, 106 by second intention, 106 by third intention, 107 Health, definition of, 21 Heat, exciting cause of disease, 41 exhaustion, 42 Helminthes, 195 Helminthiasis, 195 Hematogenic route, periapical infec- tion by, 421 Hemangiomata, 134 Hematidrosis, 85 Hematocele, 85 Hematogenous pigmentation, 63 Hematoidin, 66 Hematoma, 86 Hematemesis, 85 Hematuria, 85 Hemoglobin, 29, 66 Hemopericardium, 85 Hemoperitoneum, 85 Hemophilia, 87 Hemoptysis, 85 Hemorrhage, 85 Hemorrhagic infarct, 86 Hemorrhage, secondary, 86 Hemosiderin, 64, 66 Hemothorax, 85 Hepatization, 160 Hepatogenous pigmentation, 63 Heredity and absence of teeth, 291 and caries, 321 and disease, 40 Herpes labialis, 572 Heterolysis, 76 Heteroplasia, 110 Histologic defects in enamel, 253 Histology, morbid, definition of, 213 of gums and gingivae, 375 pathologic, 37 Howship 's lacuna?, 470 584 INDEX Hutchinson's notch, 266 teeth, 269, 299 triad, 304 Hyaline degeneration. 54 Hyaloplasm, 25 Hydrocephalus, 96 Hydropericardium, 96 Hydroperitoneum, 9(5 Hydropic infiltration, 71 Hydrops, articuli, 96 Hydrorrhaehis, 96 Hydrothorax, 96 Eylomata, 116 Hyperacid diathesis, ammonium car- bonate in, 372 Hypercementosis, 350 and pulp removal, 355 and pyorrhea alveolaris, 355 causes of, 353 etiologv and pathologic anatomy, 352 from mild infection, 354 from occlusion stress, 353 from protruding root filling, 354 from rough edges of fillings, 353 from salivary and subgingival de- posits, 353 from thread biting, 353 from tooth movement, 353 in chronic dentoalveolar abscess, 354 in lower molars, 351 in upper bicuspids, 351 in upper molars, 351 Hyperemia, 83 active, 83 collateral, 83 neuroparalytic, 83 neurotic, 83 of pulp, 505, 518 passive, 84 Hypernephroma, 14^ Hyperostoses, 121 Hyperplasia, 111 Hypertrophy, 111 'false, 111 numerical, 111 of pulp, 530 simple, 111 true. 111 Hyphomycetes, 152 Hypoplasia, 45, 250 of cervieo-lingual ridge, 205 dental, causes of, 252 microscopic, 251 milder forms of, 260 pathologic anatomy of. 258 of deciduous teeth, 258 Hypoplasia — Cont'd. of dentin. 256 of enamel and caries, 317 of enamel producing external de- fect, 255 of lower first bicuspid, 277 of lower cuspid, 270 of lower second bicuspid, 277 of upper cuspid, 269 of upper third molar, 283 Hypoplastic enamel, predisposition to causes of, 318 Idiosyncrasy, 39 Imbrication lines and caries suscep- tibility, 225 Immune, saliva of, 315 Immunity, 153 acquired, 153 from dental caries on, 315 natural, 154 Impaction of third molars, case his- tories, 296 Incisor central, abrasion of, 362 disproportion in size of crown and root, 266 imperfect development of root, 266 macroscopic deformities of, 264 overdeveloped, 266 supernumerary root in, 265 with short root, 267 lower lateral, abnormalities of, 269 lower central, freedom of defects of, 267 upper lateral, abnormalities of, 267 absence of, 291 deflection of root of, 268 peg-shaped, 268 Incisors, abrasion in, 358 supernumerary tuberculated, 287 Incremental lines, 221 Endol, 524 Infantile paralysis, 192 Infantilism, 45 Infarcts, 92 anemic or white, 92 hemorrhagic, 86 hemorrhagic or red, 93 Infection, 152 Infectious protozoa, 185 Infestation, 152 Inhibition, pain a source of, 294 Infiltration, 59 calcareous, 68 fatty, 59 I\IU \ 585 I nlilt rat inn ( 'nut 'd. glycogenic, 71 hydropic, 70 intiTst it Lai, of fluid, 95 pigmentary, 61 round eell, 99 serous, 70 Inflammation, 08 acute, 98 acute, characteristics of, 99 catarrhal, 104 chronic, 98 ehronieity and acuteness of, 424 diphtheritic, 100 edematous or serous, 100 fibrinous, 100 follicular, 105 hemorrhagic, 106 interstitial, 106 of gingiva and gums and dental caries, 320 parenchymatous, 105 phlegmonous, 103 phlegmonous, of face, 431 productive, 106 septic, of peridental membrane, 412 suppurative, 101 Inflammatory exudate, 09, 435 Influenza, 178 Interglobular spaces, 231 abnormal in size and number, 256 abundance of, 319 Interprismatic substance, dissolution of, 325 susceptibility to acids, 219 Interproximal spaces, flat, 319 Ionization, 30 Irritability, 32 Irritation by formaldehyde, 408 gingival, 391 Ischemia, 82 Jaws, necrosis, bacterial causes of, 464 chemical causes of, 464 diagnosis of, 463 mechanical causes of, 463 osteitis of, 470 osteomyelitis of, 469 periostitis of, 467 rarefying osteitis of, 462 K Karyoplasm, 25 K-iryosomes, 26 Keloids, 117 Lactic acid, end producl of fermenta- tion, 315 in depth of dentin, 328 in erosin, 360 Lactose, fermentation of, 323 Lacuna: of cementum, 233, 235 Lamellae of cementum, 233 Leishmaniases, 187 Lepedomata, 1 Hi Leptothrix infections, 180 Leprosy, 167 Leptus autumnalis, 206 Leucin, 524 Leucocytes in chronic dentoalveolar abscess, 444 mononuclear, 448 polymorphonuclear, 99 eosinophil, 447 neutrophile, 444 Leucoplakia of tongue, 573 Leukoderma, 67 Life, simpler forms of, 26 Lime salts, extraction of, from teeth 316 Linin, 26 Lipoids, 29 Lipomata, 122 Liquefaction necrosis, 75 Lock jaw, 172 Lues, 168 Lumpy jaw, 181 Lung dust disease, 61 Lymphangiomata, 135 Lymphatic vessels, obstruction of, 95 Lymphocytes, 99, 447 Lymphosarcoma, 125 Lysins, 153, 76 M Macroscopic pathology, 37 Madura foot, 182 Malacotic enamel, mass density of, 226 .Malaria, 187 Plasmodium of, 187 Malarial pigmentation, 62, 63 Malformations, 208 by defect, 208, 209 by excess, 208 by perversion, 208, 211 due to defective development in anterior median line, 209 due to defective development in posterior median line, 209 Malignant edema, 177 Malocclusion ami abrasion, 356 and dental caries, 319 586 INDEX Maltose from starch, 322 Maori race, caries in, 313 Malta fever, 176 Maltase enzyme, - Maltose, hydrolysis of, 32 Mummification, 79 Mandible, sinuses on lingual aspect, 429 Marrow. 456 red, 456 yellow, 456 Matrix of eementum, 2:;4 Maxillary sinus, abscess discharging 'into. 427 infection from cell. 427 variations in shape and size. 427 Measles, 190 black, 190 German, 191 Meat diet and dental caries, 320 Meat-eating tribes and earies, -'112 Medullary substance, 458 Melanocarcinoma, 146 Membranes, false, 74 Meningitis, epidemic cerebrospinal. 156 Menorrhagia, 85 Mercurial stomatitis, 569 Mesoderm, 35 tissues derived from, 36 Metabolic pigmentation, 62 Metaplasia, 110 Metaplasm, 25 Metastasis. 92 Metazoa. 152. 195 i hagia, s 5 Micrococcus gonorrheal, 157 tetragenus, 1~>~> Microorganisms, pathogenic for man. 152 Microscopic pathology, 37 Mites, 196 Molars and bicuspids, discoloration on approximal surfaces, 334 defective fissures in, 318 first permanent, disturbances affect- ing development of, 253 noneruption of, 293 fourth, 289, 290 impacted third, and disturbed pho- nation, 298 ear involvement from, 297 eye involvement from. 2T»7 facial pain from. 297 lower first, disto buccal cusp, ab- sence of, 281 Molar lower first, supernumerarv root in, 281 lower, hypereementosis in, 351 lower second, abnormalities of, 282 lower second, with four roots, 282 lower third, dwarfed, 282 lower third, supernumerarv root of, 283 second, impaction of, 297 second permanent, origin of enamel organ of, 245 third permanent, origin of enamel organ of. 245 perfect fissures in, 318 supernumerary, 289 third, upper and lower, abnormali- ties of, 283 impacted. 294 case histories, 296 reflexes from, 294 reflex disturbances from. 296 upper first, fusion of roots of. 230 supernumerary cusp in, 280 hypereementosis in. 351 second, abnormalities of. 281 third, dwarfed. 2^2 hypoplasia of, 283 supernumerarv root in, 284 Molds, 152 Mole pigmented. 135 Molluscum contagiosum, 142 Mononuclear wandering cells, origiu of. 449 Monosaccharides. 324 Morbid anatomv. Morula, 34 Motility, 32 Mouth bacteria, number of, 315 infection and cancer. 561 and systemic disease, 544 and tuberculosis. 561 as a source of systemic intoxica- tions, '>'>') dry. and dental caries, 316 washes, weak acids in, 332 Mucin, 28, 369 in plaque formation. 331 precipitation of, 370 Mucoid degeneration. Mucous membrane of gingivae and gums, 375 of hard palate. 375 patch, 136 Mumps, 191 Mycetoma, 182 Mycoses, 152, 180 Myxomata, 119 IN D IX :»7 N NaCI, increased, 95 Nanism, 15 Xasal cavity, abscess discharging into, 127 Nasmytb *s membrane, 246 Necrobiosis, 72 Necrosis, 72 coagulation, 7:; Eat, 77 focal, 78 liquefaction, II, 75 cheesy, 76 of alveoli, 462 of jaws, bacteria] causes of, 464 causes of, 463 chemical causes of, 464 diagnosis of, 463 mechanical causes of, 463 Nematodes, 196 Neoplasm of pulp, 508 Nevus, 135 Neuridin, 413, 524 Neurin, 413 Newman, sheaths of, 230 Nitrogenous decomposition, 413 Nodules, pulp, 514 Nonelectrolytes, 30 Nucleolus, 26 Nucleoplasm, 26 Nucleus, 2-1 Occlusion stress, hypercementosis from, 353 Occupations, injurious, 40 Odontoblastic layer, 230 Odontoblasts, 247, 500 Odontomas, cystic, 532 Oidiomycosis, 183 Opsonins, 153 Ophthalmia neonatorum, 157 Oral disease, definition of, 213 Oral foci of infection, 544 Organic disease, 216 matter, comparison in cementum and bone, 240 Osmosis, disturbed, 95 Osteitis, of jaws, 470 rarefying, 462 Osteoblasts, 407 Osteoclasts, 4n7, 456 Osteogenetic laver of periosteum, 456 Osteomalacia of pregnancy, causes of, 320 Osteomata, 121 heteroplastic, 121 homoplastic, 121 Osteomyelitis, 394 acute, in dentoalveolar abscess, i:;r,, 157, 469 Osteophytes, 121, 467 Oxuris vermicularis, 202 Oxygen ten-inn, change of, in root canal, 414 Pain, continued, action of, 204 Palate, hard, mucous membrane of, 375 Papilla, dental, 246 Papillomata, 135 hard, 136 intracystic, 136 soft, 136 Paralysis, infantile, 192 Paraplasm, 25 Parasites, 152 facultative, 152 Parenchymatous degeneration, IS Parotitis, acute epidemic, 191 Parules, 431 Pasommoma, 147 Pathologic anatomy, 37 definition of, *213 of chronic gingivitis, 392 chemistry, 37 Pathology, cellular, 123 dental, definition, 213 general, definition, 21 general and dental conception of, 216 gross, 37, 216 Pathologic histology, 37 physiology, 216 processes, 45 Pediculus capitis, 196 pubis, 196 vestimenti, 196 Petechia?, 86 Peptides, 27 Peptones, 27 Perforations of root canals, 419 Periapical infection by hematogenic route, 421 Periapical infections, recovery from, 422 Pericemental abscess, 422 of gouty origin, 496 inflammation, acute septic, 412 septic, 412 septic, summary of causes, 421 588 INDEX Pericementitis, acute septic, 412 chronic septic, 412 first symptoms of, 433 nonseptic, Mis aonseptie, caused by protruded root fillings, 410 ' nonseptic, causes of, 408 nonseptic, from arsenic, 4ln nonseptic from pressure, 410 nonseptic, from pulp extirpation, 410 septic apical, 422 bacteria of, 452 etiology of, 45 Pericementum, 402 Peridental membrane, IMS apical fibers, 406 atrophy of, 491 blood "supply of, 402, 407 cysts from chronic infection of, 441 diseases of, 402 effect of mild irritation upon, 352 epithelial remnants in, 442, 527 fibers of, 404 fibers, detachment of, 439 free gingiva fibers, 406 functions of, 402 horizontal fibers of. 405 involvement in gingivitis, 393 nerve supply of, 407 oblique fibers of, 405 relation of, to gingiva, 403 septic inflammation of, 412 structural constituents of, 406 susceptibility to infectious proc- esses, 402 transseptal fibers, 406 thrombi in, 410 Periosteum, 456 Periostitis, acute, in dentoalveolar ab- scess, 431, 435 Pernio, 42 Pertussis, 179 Periostitis, chronic, osteophytes in, 467 of jaws, acute, 467 symptoms of, 469 syphilitic, 470 Phleboliths, 381 Phonation, disturbed, from impacted third molar, 298 Phosphoproteins, 29 Physiochemical processes in tissues, 21 Physiology, pathologic, definition of, 213 Pickerills' calearine fissures, 225 Pigment, malarial, 63 Pigmentary infiltration, 61 Pigmentation, hematogenous, 63 hepatogenous, 63 malarial, 62 metabolic, 62 of dentin in caries, '117 Pigments, metabolic, 63 Pits, caries in, 334 Plague, bubonic, 177 Plaque formation, mucin in, 331 Plaques, gelatinous, 331 Plasma cells, 99, 451 Plasmodium malaria 1 , 187 Plastids, 25 Platyhelminthes, 195 Pneumonia, 159 aspiration, 163 fibroid, 163 hypostatic, 163 lobar or croupous, 159 lobular, 161 purulent, 163 tuberculous, 164 Pneumonokoniosis, 61 Pocket formation, bone lesion in, 39 I Poisons, chemical, 44 Poliomyelitis, acute, 192 Polyarthritis. 193 Polymorphonuclear leucocytes, 445 Polysaccharides, 325 Poulticing, results of, 428 Predisposing causes, 213 of dental caries, 320 Pregnancy and dental caries, 320 Pressure, effect of, 41 Processes, retrograde, 45 Protamines, 28 Proteins, 27 conjugated, 28 simple, 28 Proteoses, 27 Prothrombin, 74 Protoplasm, 23 Protoplasmic movement, 32 Protozoa, 23, 152 classification of, 185 Pseudomelanin, 63 Pseudomucin, 52 Ptyalin, 370 role in caries, 370 Pulex eheopis, 196 irritans, 196 lipines, 196 penetrans, 196 i.\i)i;.\ 589 Pulp abscess, 530 areas of chronic inflammation in, 507 blood vessels of, 504 calcific degenerations of, 510 cells of, 503 description of, 500 clinical aspect of diseases of, 505 congestion, 521 constructive changes in, 506 death, chemical causes of, 523 death, mechanical causes of, 523 death of, en masse, 523 decomposed, 413 degenerations, 508 degeneration in abrasion, 358 diseases of, 505, 500 exciting causes, general, 508 exciting causes of (local), 509 local predisposing causes of, 507 predisposing causes of, 506 exposure in abrasion, 357 gangrene, 523 gangrenous, organisms in, 452 histologic constituents of, 500 hyperemia, 505, 518 active, 518 character of pain from, 522 etiology of, 520 following insertion of gold fill; ings, 521 from erosion and abrasion, 521 in febrile disturbances, 508 passive, 518 hypertrophy, calcareous formations in, 530 epithelial cells in, 531 impairment of vitality, 505 infection in absence of caries, 527 ulcerative form, 530 intercellular substance of, 504 involvements, prophylaxis of, 414 lead-wire formation in, 517 live, abscess in teeth with, 422 moist gangrene, 524 mummification, 523 neoplasm, 508 nerves of, 504 nodules, 514 from erosion and abrasion, 517 normal, 501 Pulp, odontoblastic layer of, 230 putrefaction, 413 discoloration from, 524 products of, 524 putrefactive changes in, 525 putrescent, 523 organisms in, 524 Pulp Cont'd. removal and hypercementosis, 355 reparative power of, .~ u i t retrograde changes in, 506 severe inflammation of, ) l'.~ suppurating, organisms in, 152 suppuration, 1 13, 528 temperature, range of, 520 thrombosis in, 523 Pulpitis, 525 chronic hypertrophic, 530 nonseptie, 525 pathologic anatomy of, 528 septic, 526 character of pain in, 527 Pus, 101 Pus pocket, 394 Pustule, 103 Putrefaction of pulp, 413 products of. 524 Putrefactive changes in dentinal tu- buli, 414 changes in, pulps, 525 Putrescin, 413, 524 Pyemia, 103, 154 Pyogenic bacteria in apical region, 412 Pyorrhea alveolaris and hypereemen- tosis, .'!•"." and malposition of teeth, 379 bacteria in, 551 bacteriology of, 491 by salivary calculi, 474 by subgingival deposits, 476 clinical forms, 473 defective approximal contacts in, 479 food impactions in, 476 general considerations, 473 historical sketch. 471 indicative of, 473 of gouty origin, 495 of systemic origin, 487 osteomyelitis in, 484 substitute terms for, 473 systemic disorders and. 485 systemic factor in, 490 systemic lesions by bacteria from, 551 pockets, study of culture of, 494 E Race as a predisposing cause, 39 Rarefaction areas, 419, 554 Rarefying osteitis, 462 of alveoli, 462 of jaws, 462 590 INDEX Raynaud's disease, 82 Eeflexes from impacted third molars, 294 Regeneration, 108 pathologic, 108 physiologic, 108 Renal calculi, 70 Relapsing fever, 179 Re] roduction, 33 Resorption of apical areas, 465 of eementum, 250 Retrograde processes, 45 Retzius, bands of, 221 in hypoplasia, 262 Ridge, cervieolingual fissured, 265 Rhabdomyoma, 1 30 Rheumatism, acute articular, 192 Rhinoscleroma, 171 Rhinoliths, 70 Rigos' disease, 473 Ringworm, 183 Rocky Mountain fever, 195 Rodent ulcer, 142 abrasion of, 357 bifurcation in uppar second bicus- pid, 27:; cysts, 532 deflection in upper first bicuspid, 271 Root canals, irritating drugs in, 408 perforation of, 419 of central incisor, imperfect de- velopment of, 266 filling beyond apical foramen, ef- fects of, 353 fractures, intraalveolar, 419 fusion of, in upper first molar, 280 of upper second bicuspid, abnor- malities of, 271 perforation, 411 supernumerarv, in central incisor, 265 in lower cuspid, 273 in lower first molar, 281 in lower third molar, 283 in upper third molar, 284 two, in lower bicuspids, 277 in lower cuspid, 270 in lower cuspids, 272 in lower lateral incisor, 269 in upper second bicuspid, 274 Rubeola,' 190 S Saccharomyces albicans, 571 Saliva, 366 abnormal constituents of, 373 Saliva— Cont'd. action on blood cells, 315 albumin in, 371 amount of, 366 color of, in pathologic and normal states, 367 hemolytic power of, 315 immunizing properties of, 315 immunizing properties of, and den- tal caries, 315 inorganic constituents of, 369, 372 manifestation in, of excessive car- bohydrate intake, 374 odor of, in pathologic and normal states, 368 of immunes, 315 of immunes to caries, '■'< 1 5 of susceptibles to caries, 316 on antiseptic power of, 315 organic constituents of, 369 parotid, unmixed, 383 quantity of, in relation to caries, 316 reaction of, 373 solution of blood cells by, 315 sulphocyanates in, 371, 372 taste of, in normal and pathologic states, 368 viscosity of, 316 in relation to caries, 316 Salivary calculus, agglutinin of, 384 destruction of investing tissues by, 388 Salivary deposits and hypereementosis, 353 as cause of gingivitis, 389 clinical symptoms of, 389 color of, 386 denudation of eementum by, 388 effects Of, 389 from betel-nut chewing, 383 in salivary glands, 381 lesions caused by. :;s7 location of, 381 origin of, 381 size of, 386 theories on formation of, 381 where first formed, 388 depressants, 366 depressants of potential acidity, 312 glands, deposits in, 381 stimulants, 366 in relation to caries, :!12 Sapremia, 151 Saprophytes, 152 INDEX 591 Saprophj t ic bactei ia, action of, 1 1 '■'■ organisms in acute dentoalveolar abscess, 133 Sarcoma, alveolar, 125 gianl celled, 128 melanotic, 127 round cell, 124 spindle-celled, 127 Sarcomatous cylindromata, 126 Scarlatina, H'l S.-arlct fever, 191 Scalorrhea, 367 Schizomycetes, 152 Scler eter, enamel, 228 Sclerotic enamel, mass density of, 226 Secondary denl in. ."1 1 " Self -cleaning, " as applied to teeth, 319 Septal gingivae, 377 Septal tissues and caries, 337 Septic pericemental inflammation, acute, 112 Septicemia, 154 Sequestrum formation in chronic dentoalveolar abscess, 4(38 Serous infiltration, 71 Serum, antidiphtheritic, 173 antitetanic, 172 Sharpey's fillers, 156 Sheaths of Newman, 230 Shock, 41 Shreger, lines of, 222 Sialorrhea, .".'';7 silicosis, 64 Sinus formation, 427 Sleeping sickni ss, 186 Smallpox, 194 Sodium phosphate, acid, in erosion, 360 Solution, 30 Somatic death, 73 Specific gravity of enamel, compared ■with density, 22."> pyogenes albus, 155 pyogenes aureus, 155 Starch, 325 conversion of, into maltose, 322 Starchy foods and dental caries, 320 Stellate reticulum, 244 Stomatitis aphthous, 570 pathologic anatomy of, 570 catarrhal, 566 pathologic anatomy of, 567 mercurial, ">t'u Stratum intermedium, 2 I I Streptococci, in chronic dentoalveolar abscess, 452 Streptococcus erysipelatis, 156 mucosus, 4o2 pyogenes, 155 rheumaticus, 156 viridans, 156, 452, 551, 552 Stricture, 157 Strongyloides intestinalis, 202 Subgingival deposits, 390 and hypereementosis, 353 color of, 390 detection of, ::!»2 etiology of, 390 lesions produced by, '■'<'.>- preliminary step in formation, 396 -pa.,, bacterial absorption from, 380 penetration of bacteria through, 422 Submental fistula. 430, 4:;4 Sugars, double, 324 multiple, 325 Sugars, relative fermentability of, 323 simple, 324 Sulphocyanates, amount of, in saliva, ' 372 "Sulphur granules," 181 Sunburn, 43 Sunlight, bactericidal action of, 43 Sunstroke, 42 Supernumerary cusp in upper first molar, 280 molar, 289, 290 peg-shaped tooth, 287 root in central incisor, 26."> root in lower first molar, 281 root in upper third molar, 284 tuberculated incisors, 287 teeth, 287 Suppurative inflammation, 101 Suppuration, description of, 413 in pulp, 413 Swelling from dentoalveolar abscess, 431 592 INDEX Syphilis, 168 dental manifestations of, transmis- sion to fetus, 253 hereditary, dental stigmata of, 303 pathognomonic signs of, 303 primary stage, 169 secondary stage, 160 tertiary stage, 169 transmission of, 299 Syphilitic stigmata, 299 Syringomyelia, 96 T Tapeworms, 195, WS Teeth, abnormalities of, 250 abraded, discoloration of dentin in. 347 absence of, 291 calcium salt content of, 226 classification of, as to hardness, 226 deciduous, calcification of, 248 geminated, 284 hyperplasia of, 258 retention of, 291 time of appearance of enamel or- gans for, 24." development of, 241 extraction of lime salts from, 316 fully calcified, noneruption of, 294 geminated, 284 Hutchinson 's, 299 macroscopic deformities of, 264 malposition in pyorrhea alveolaris, 379 mass density of. 227 permanent, calcification of, 248 " self -cleansing, ' ' 319 specific gravity and density, differ- ence between, 226 supernumerary, 287 Tenderness to pressure in pericemen- tal infection, 425 Teratomata, 148 Tetanus, 172 Thrombi, 74 agglutinative, 88 annular, 88 arterial, 88 ball, 88 calcified, 89 canalized, 89 capillary, 88 cardiac, 88 glutinative, 88 hyaline, 88 infective, 89 in peridental membrane, 410 Thrombi— Cont 'd. lymphatic, 88 marantic, 88 obliterative, 88 organized, 89 parietal, 88 polypoid, 88 portal, 88 primary, 88 propagated secondary), 88 proximal, 88 red. 88 saddle, 88 stratified, 88 types of, 87 valvular, 88 venous, 88 white, 88 yellow, 88 Thrombosis, 87 Thrush. 571 pathologic anatomy of, 572 Ticks, 196 Tinea, circinata, 184 favosa, 183 sycosis, 184 tonsorans, 184 trichophytina, 183 versicolor, 184 Tissue ehanges, progressive, 111 Tissues, investing, destruction of, by salivary calculi tobaeosis, 64 Tomes, fibers of, 505 granular layer of, 231 zone of 344 zone of, possible etiology of, 346 Tongue, affections of, 572 leueoplakia of, 573 ulcers of, 572 Tooth brush friction and abrasion, 356 development, first evidence of, 242 follicle, fibrous envelope of, 233 impaction, 291 incarceration, 291 movement, following extraction, 379 peg-shaped, supernumerary, 287 powders, gritty, and abrasion, 356 protrusion, 436, 433 sensory organ of, 501 Toxemia, 154 Toxic products from burned tissue, 42 Toxins, 153 intracellular, 153 soluble, !'>■] Transparent zone, 344, 510 Transudation, 95 Traumatisms, 39 INDKX :,!i:; Trematodes, L95, 196 Treponema pallidum, L68 Trichinosis, 204 Trie! ephalus dispar, 202 Trichomycetes, L80 Trichophyton, 183 Trypanosomes, pathogenic, 186 Trypanosomiasis, 186 Tuberculosis, 164 ;iinl mouth infection, •"(>! secondary, 167 Tubular calcification in abrasion, 358 Tubuli, dentinal, 228 a field of. 220 anastomosis of, 230 average diameter of, 348 calcific degeneration of, 510 curves of, 231 in bicuspids and molars, 230 in incisal region, 230 in relation to cusps, 231 penetration into enamel, 232 relative diameters of, 230 Tumors, 113 benign, 115 classification of, 116 habit of growth theory, 114 inclusion theory, 113 irritation theory, 113 nervous theory, 114 parasitic theory, 114 predisposing causes, 114 primary, 115 secondary, 115 theories of origin, 113 Typhoid fever, 174 Typhus fever, 194 Ty rosin, 524 U Ulcer, 104 follicular, 104 fungous, 104 gangrenous, 104 indolent, 104 i leer -Cont 'ii. of tongue, 572 peptic, 104 phagedenic, l ( 'l rodent, 1 1 1' serpiginous, 104 specific, 104 Ulceration form of infection of pulp, 530 Uric acid salts in Mood, 496 Vaccination, 154 Varicella, 191 Variola, 194 Verrucas, 136 Vesical calculi, 70 Vincent's angina, 179 Viscosity of saliva, 316 Vital resistance, 214 conditions which lower, 214 lowered, 214 Volkmann's canals, 455 W Wandering cells, 99 Warts, 136 Wheals, 95 "White" clots, 75 Wombstones, 132 Worms, round, 196 Xanthoma, 128 X-rays, effects of, 44 Yeasts, 152 Z Zone of Tomes, 344 COLUMBIA UNIVERSITY LIBRARIES This book is due on the date indicated below, or at the expiration of a definite period after the date of borrowing, as provided by the library rules or by special arrangement with the Librarian in charge. 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