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(BQ) Part 2 book Shafer''s textbook of oral pathology presentation of content: Physical and chemical injuries of the oral cavity, regressive alterations of the teeth, healing of oral wounds, oral aspects of metabolic diseases, allergic and immunologic diseases of the oral cavity, diseases of specific systems, forensic odontology,... and other contents.
Section III Injuries and Repair 2082 Chapter 12 Physical and Chemical Injuries of the Oral Cavity B Sivapathasundharam Chapter Outline Injuries of Teeth Associated with Tooth Preparation Effect of Tooth Preparation Reaction To Rotary Instrumentation Effect of Heat Effect of Restorative Materials Physical Injuries of the Teeth Physical Injuries of the Bone Physical Injuries of Soft Tissues Nonallergic Reactions to Drugs and Chemicals used Systemically Occupational Injuries of the Oral Cavity Occlusal Trauma 2083 Injuries of the oral cavity may be caused by physical or chemical causes Physical injuries may be iatrogenic, self-inflicted, traumatic, or occupational The most important iatrogenic cause is the repair of tooth affected by dental caries or other developmental defects and restoration of missing tooth Iatrogenic cause also includes X radiation and laser radiation Self-induced or factitious injuries are due to overzealous oral hygiene practices, caused by psychotic or neurotic condition, or habitual Traumatic causes include a fall, fight, road traffic accidents, and sports injuries Although chemical injuries are caused by environmental elements such as toxic levels of chemicals in the water, air, or consumables, the restorative and endodontic materials used in the routine dental practice play an important role Injuries of Teeth Associated with Tooth Preparation The teeth, particularly the dentin and pulp, may be injured not only by dental caries, but also from those procedures necessary for the repair of lesions involving dental hard tissues Preparation of the teeth for receiving the restorations include cutting, grinding, and etching with acids etc These physical and chemical methods of tooth preparation as well as the various medicaments and filling materials which are inserted into the prepared tooth, have their own effects Effect of Tooth Preparation 2084 The effect upon the dental pulp of restorative procedure alone is difficult to assess except in the sound tooth, since the carious lesion itself produces demonstrable changes in both the dentin and the pulp Even when a sound tooth is prepared for experimental purpose, care must be taken in observing the effects to separate those which are due solely to the tooth preparation from those which are due to the restorative materials applied Tooth preparation is usually done by rotary instruments such as tungsten carbide burs and diamond burs of different sizes and shapes Lasers and air abrasion are also used alternatively Pulpal responses to these various procedures depend on the heat generated by friction, cutting of odontoblastic processes and drying of dentinal tubules, thickness of remaining dentin, vibration, removal of minerals and exposure of the organic matrix of dentin, and formation of smear layer Reaction to Rotary Instrumentation Stainless steel burs revolving at low speed were used in the past for cavity and crown preparation As the hardness of the enamel is high, these burs could not abrade instead they cut or chip away the tooth material Also a considerable amount of pressure is applied during the procedure, which results in excessive heat production and evaporation of the contents of the dentinal tubules High speed rotary instrumentation with tungsten carbide and diamond burs has replaced the steel burs in recent years Nevertheless stainless steel burs are used in procedures involving bone 2085 The reaction of the dental pulp to cutting of dentin with a dental bur has been studied by Fish in both dogs and monkeys When dentin is injured, there is stasis of the contents of the dentinal tubules, which lose their fluid communication with the pulp because of the formation of secondary dentin Involved dentinal tubules are occluded by the deposition of calcium which separates these sclerosed dentinal tubules physiologically from the rest of the tooth The cavities prepared by Fish in the teeth of dogs or monkeys were cut with steel burs which were kept wet to prevent the complication of heat-induced damage to the pulp In some cases the cavities were then filled with copper oxyphosphate cement and in other instances they were left open and exposed to the oral fluids The animals were sacrificed after varying periods of time, and sections of the filled teeth were prepared for microscopic study Three general reactions to cavity preparation were noted: (1) the production of secondary dentin, (2) changes in the odontoblasts associated with injured tubules, and (3) general changes in the pulp Fish carefully pointed out that the reaction of the tooth with the formation of a calcified barrier and secondary dentin production is always strictly confined to the pulp surface of the injured dentinal tubules There is never overlap of uninjured tubules, and for this reason the changes may be regarded as a specific reaction to injury of the dentinal tubules The pulp reaction to superficial injury of the dentin varies in degree of severity, depending partially upon the depth of the prepared cavity and partially upon the elapsed time between cutting the cavity and extraction of the tooth for study In mild reactions the odontoblasts become distorted and reduced 2086 in number Small vacuoles may appear between them, probably lymph exudate Capillaries in the damaged area may be prominent In more severe injuries, there may be complete disorganization of and hemorrhage in the odontoblastic layer (Fig 12-1) The bulk of the pulp tissue away from the cut tubules may exhibit little or no reaction Figure 12-1 Effect on dental pulp of cavity preparation by steel bur Cavities were prepared in human teeth and filled with gutta-percha A section of pulp from an intact normal tooth is shown in (A), while the injured area in the pulp six days after cavity preparation is seen in (B) Courtesy of Drs David F Mitchell and Jensen JH J Am Dent Assoc, 55:57, 1957 In more serious injuries there is a greater infiltration of the injured locus by polymorphonuclear leukocytes, which gradually become replaced by lymphocytes The majority of the severe pulp injuries are probably associated with irritation brought about by the open cavities, with the sudden exposure of large numbers of open dentinal tubules to oral fluids and bacteria 2087 Even after such severe injuries the majority of damaged pulps undergo spontaneous healing or at least enter a quiescent phase and produce no signs or symptoms of persisting damage (Fig 12-2) The factors responsible for this phenomenon, especially from the clinical aspect, are unknown Figure 12-2 Effect of cavity preparation by steel bur on dental pulp A calciotraumatic line (1) and reparative dentin (2) are found beneath the cavity nine weeks after preparation Courtesy of Drs David F Mitchell, JH Jensen J Am Dent Assoc, 55: 57, 1957 It appears that dentin has a heat-dissipating action which reduces the temperature rise within the pulp to only a fraction of the actual temperature applied to the tooth This is due to the low thermal conductivity of dentin, which acts as an effective insulating medium Nevertheless the application of heat to a dental pulp already injured from a 2088 carious lesion of the dentin, but not an actual pulp exposure, may be sufficient to affect adversely the repair or healing of the pulp even though an apparently successful restoration is given to the tooth The preparation of tooth under the constant application of water to cool the cutting instrument and tooth will prevent many of the serious consequences due to heat, and this procedure is strongly recommended High-Speed Instrumentation The development of high-speed dental engines and hand-pieces necessitated investigation of the possible effects which their use might have on pulp tissue, and numerous reports of such studies have been published Bernier and Knapp reported a study on high-speed instrumentation utilizing various speeds up to 100,000 rpm They found evidence of mild pulpal damage, but, in addition, observed a new type of lesion which they termed the ‘rebound response’ This consisted variously in: (1) an alteration in ground substance, (2) edema, (3) fibrosis, (4) odontoblastic disruption, and (5) reduced predentin formation in a region directly across the pulp opposite the cavity site or at a distant pulpal site, and thought to be caused by waves of energy transmitted to the pulp focused into a certain region by the pulpal walls The significance of this phenomenon is still not clear Swerdlow and Stanley in their study involving 450 human teeth found that speeds over 50,000 rpm with coolants were 2089 less injurious to the pulp than lower speeds They concluded that the combination of high speed, controlled temperature, and light load produced minimal pathologic pulpal alteration When heavy loads were used, even coolants did not minimize inflammatory responses Extending this investigation to 13 operative techniques, Diamond and his coworkers found that the 300,000 rpm air-water spray—No 35 carbide bur technique—provided all the cutting efficiency of a high-speed instrument without producing extended or burn lesions and caused the highest incidence of reparative dentin formation, a favorable protective reaction A speed of 250,000 rpm with water coolant was reported by Nygaard-Ostby to produce even less pulpal reaction than the conventional (6,000 rpm) machine without water-spray Caviedes-Bucheli and coworkers in their study found that substance P expression is increased in tooth where cavity preparation is done and concluded that it may have an important clinical significance in terms of inflammation and pain experience The practicability of use of accelerated hand-piece speeds has been accurately summarized by Stanley and Swerdlow, who stated: ‘In principle, high speed techniques approach the ideal but at the same time these methods can be easily abused… properly used, ultraspeed is an extremely safe and efficient method of reducing tooth structure’ Effect of Air Abrasive Technique In the air abrasive technique, aluminum oxide sprayed under pressure is used as an abrasive for the cavity preparation and surface treatment The main drawback of this procedure is, it does not allow the operators’ stereognostic ability to control 2090 the depth of cutting However Ferrazzano et al, based on their study in 60 mandibular third molar concluded that the macroscopic size and shape of cavities is connected to working distance, while working time is important to determine the depth of preparation Also the abrasive dust is a potential health hazard to the operator and the patient Nowadays it is used only to clean the pit and fissures prior to the application of sealants Effect of Ultrasonic Technique The use of ultrasonic equipment for cutting cavities in teeth has been advocated because it involves less heat, noise, and vibration in contrast to rotary instruments Essentially, the technique consists in the conversion of electrical energy into mechanical energy in the form of vibration of a tiny cutting tip, approximately 29,000 vibrations per second with an amplitude of about 0.0014 inch Aluminum oxide abrasive in a liquid carrier is washed across this tip, and the vibration of the particles in turn results in a rapid reduction of tooth substance The effects of this technique, as used in cavity preparation, on the tooth and dental pulp have been evaluated by a number of investigators whose results are in essential agreement Zach and Brown, Healey and his coworkers, and Lefkowitz among others have found that there are no remarkable differences in the reaction of the dental pulp to the preparation of cavities by the steel bur, the diamond stone or the ultrasonic instrument This again emphasizes that only the dentinal injury itself is important, not how this injury is produced 2091 hereditary opalescent dentin, 55 Hutchinson’s, 52 impacted, 61 resorption and, 581 internal resorption, 585 macrodontia, 40 mesiodens, 41 microdontia, 39 Moon’s molars, 51 mottled, 53 mulberry molar, 52, 53 multiple unerupted, 61 natal, 48 neonatal, 48 odontodysplasia, 58 orthodontic tooth movement and, 532 peg lateral, 40 pellicle, 385 pigmentation, erythroblastosis fetalis and, 770 porphyria and, 628 tetracycline therapy, 560 predeciduous, 48 premature eruption, 59 pseudoanodontia, 46 regional odontodysplasia, 58 reimplanted, resorption and, 582 replantation, 606 resorption, external, 581 internal, 585 rootless, 57 shell, 55 stains, 386 submerged, 42, 528 3855 supernumerary, 47 supernumerary roots, 45 talon cusp, 42 taurodont, 45 transplantation, 608 transplanted, resorption and, 606 Turner’s, 53 twinning of, 40 Toothbrushing, dental caries and, 465 Torticollis, 719, 860 Torula histolytica, 370 Torulosis, 370 Torus, mandibularis, 159 palatinus, 158 Toxic epidermal necrolysis, 816 Toxoplasmosis, 378, 787 Trace elements, metabolism of, 622 Transitional cell carcinoma, 125 Transparent dentin, 577 Transplantation of teeth, 606 Traumatic crescent of gingiva, 393 Traumatic cyst, 529–531 Traumatic neuroma, 200, 201 Traumatic ulcers, 535 Traumatism, periodontal, 565 Treacher Collins syndrome, 8, 720, 738 Trench mouth, 395, 396 Treponema pallidum, 328 Trichinosis, 378, 780 Trichloroacetic acid, 554 Trichomoniasis, 378 Trifacial neuralgia, 853 Trigeminal neuralgia, 853, 856, 858, 862 3856 Trigeminal neuritis, 854 Trigeminal neuropathy, 854 Trigger zones, 854 Trismus, 328, 354, 866 Trisomy, 728 syndrome, 728 Trotter’s syndrome, 854 True cementoma, 301, 736 Trümmerfeldzone, 644 Trypanosomiasis, 378, 780 Trypsin, 593, 603, 918, 948 Tuberculoma, 322 Tuberculosis, 319 lupus vulgaris, 320 miliary, 320 osteomyelitis, 322 scrofula, 320 tuberculoma, 322 Tuberculum impar, 30 Tularemia, 326, 327, 334 Tumors, 81–210, 223–252, 259–306 acidophilic adenoma, 231 acinic cell adenocarcinoma, 234 adamantinoma, 276 adenoacanthoma, 124 adenoameloblastoma, 286 adenoid cystic carcinoma, 238 adenoid squamous cell carcinoma, 124 adenolymphoma, 229 adenomatoid odontogenic tumor, 286 adenosquamous carcinoma, 124 African jaw lymphoma, 184 aggressive fibromatosis, 162 3857 alveolar soft-part sarcoma, 199 ameloblastic carcinoma, 301 ameloblastic dentinosarcoma, 306 ameloblastic fibrodentinoma, 297 ameloblastic fibroma, 289 ameloblastic fibro-odontoma, 291 ameloblastic fibrosarcoma, 305 ameloblastic odontoma, 293 ameloblastic odontosarcoma, 306 ameloblastic sarcoma, 305 ameloblastoma, 276 amputation neuroma, 200 aneurysmal bone cyst, 140 angioblastoma, malignant, 278 angiomyoma, 188 angioreticuloendothelioma, 167 arteriovenous aneurysm, 147 basal cell adenoma, 229 basal cell carcinoma, 238 basaloid mixed tumor, 238 benign cementoblastoma, 301 benign chondroblastoma, 154 benign lymphoepithelial lesion, 249 benign osteoblastoma, 157 Burkitt’s lymphoma, 184 calcifying epithelial odontogenic tumor, 283 canalicular adenoma, 232 carcinoma in situ, 94 cellular adenoma, 228 cementoma, true, 301 chondroma, 224 chondromyxoid fibroma, 154 chondrosarcoma, 171 3858 mesenchymal, 171 clear cell carcinoma of salivary glands, 210 common wart, 81 congenital epulis of newborn, 194 craniopharyngioma, 277 cylindroma, 238 cystic hygroma, 151 dentinogenic ghost cell tumor, 295 denture injury, 540 dermoid cyst, 70 desmoplastic fibroma, 162 ductal papilloma, 233 encephalotrigeminal hemangiomatosis, 149 endothelial myeloma, 169 epidermoid carcinoma, 103 epithelial-myoepithelial carcinoma, 240 erythroplakia, 94 esthesioneuroblastoma, 208 Ewing’s sarcoma, 169 exostoses, multiple, 160 fibrodentinoma, ameloblastic, 297 fibro-osteoma, central, 135 fibrosarcoma, 160 fibrous histiocytoma, 163 fibroxanthoma, 162 atypical, 162 giant cell fibroma, 132 giant cell granuloma, central, 137 peripheral, 136 giant osteoid osteoma, 157 gingival epithelial hamartoma, odontogenic, 297 granular cell myoblastoma, 193 malignant, 199 3859 hemangioendothelioma, 166 hemangioma, 146 hemangiopericytoma, 166 hemorrhagic sarcoma of Kaposi, 167 hereditary hemorrhagic telangiectasia, 148 hibernoma, 143 histiocytosis ‘X’, 169 Hodgkin’s disease, 186 Kaposi’s sarcoma, 167 keratoacanthoma, 102 Lane tumor, 123 leiomyoma, 192 vascular, 192 leiomyosarcoma, 195, 196 leukoedema, 195 leukoplakia, 93 lipoblastomatosis, 143 lipoma, 141 liposarcoma, 165 lymphangioma, 151 lymphoepithelial lesion, benign, 249 lymphoepithelioma, 125 malignant ameloblastoma, 276, 301 malignant lymphoma, 177 malignant melanoma, 207 malignant schwannoma, 207 melanoameloblastoma, 204 melanotic neuroectodermal tumor of infancy, 204 metastatic, 208 Mikulicz’s disease, 249 Mikulicz’s syndrome, 249 ‘mixed’ tumor, 224 monomorphic adenoma, 240 3860 mucinosis, oral focal, 153 mucoepidermoid carcinoma, 235 mycosis fungoides, 179 myeloma, multiple, 187, 188 myoblastoma, granular cell, 193 myoepithelioma, 228 myxoma, 152 nasopharyngeal angiofibroma, 150 neuroectodermal tumor, melanotic, of infancy, 204 neurofibroma, 202 neurofibromatosis, 202 neurofibrosarcoma, 207 neurolemmoma, 203 neuroma, multiple endocrine neoplasia syndrome and, 200 nodular fasciitis, 162 non-Hodgkin’s lymphoma, 178 odontoameloblastoma, 293 odontogenic, see Odontogenic tumors odontogenic adenomatoid tumor, 286 odontogenic fibroma, central, 133 odontogenic gingival epithelial hamartoma, 297 odontogenic myxoma, 299 odontogenic sarcoma, 305 odontoma, 204 olfactory neuroblastoma, 208 oncocytoma, 231 ossifying fibroma, central, 135 peripheral, 136 osteochondroma, 155 osteoclastoma, 138 osteogenic sarcoma, 174 osteoid osteoma, 155 osteosarcoma, 174 3861 extraosseous, 176 parosteal, 175 periosteal, 176 oxyphilic adenoma, 231 papillary cystadenoma lymphomatosum, 229 papilloma, 91 paraganglioma, nonchromaffin, 199 pigmented ameloblastoma, 204 pigmented cellular nevus, 85, 86, 204 Pindborg tumor, 283, 285 pituitary ameloblastoma, 277 plasma cell myeloma, 187 plasmacytoma, 190 pleomorphic adenoma, 224 polypoid squamous cell carcinoma, 123 ‘pregnancy, ’ 145, 336 primary lymphoma of bone, 183 progonoma, 204 proliferative myositis, 162 pseudoadenomatous basal cell carcinoma, 238 pseudoglandular squamous cell carcinoma, 124 pseudosarcomatous fibromatosis, 162 Rathke’s pouch tumor, 277 Rendu-Osler-Weber syndrome, 148 reticulum cell sarcoma, 183 retinal anlage tumor, 204 rhabdomyoma, 193 rhabdomyosarcoma, 196 salivary gland, see Salivary glands, tumors of sarcoma botryoides, 197 schwannoma, 193 serous cell adenocarcinoma, 234 sialadenoma papilliferum, 234 3862 sicca syndrome, 250 Sjögren’s syndrome, 250 spindle cell carcinoma, 126 squamous acanthoma, 83 squamous papilloma, 81 squamous odontogenic tumor, 287 squamous cell carcinoma, 245 Sturge-Weber syndrome, 149 submucous fibrosis, 97 synovial sarcoma, 164 teratoma, 70 torus, mandibularis, 159 palatinus, 158 transitional cell carcinoma, 125 traumatic neuroma, 200 true cementoma, 301 vascular nevi, 58 verruca vulgaris, 81, 82 verruciform xanthoma, 143 verrucous carcinoma, 121 von Recklinghausen’s disease of skin, 202 Warthin’s tumor, 229 Turner’s teeth, 53 Twinning of teeth, 40 Tyrothricin, effect on dental caries, 463 Tzanck cells, 826 Tzanck test, 351, 826 U Ulcer, traumatic, 535, 538 Ulcerative colitis, pyostomatitis vegetans and, 336 Unerupted teeth, multiple, 61 3863 Unicameral bone cyst, 141, 529 Urea, dental caries and, 462 in saliva, 433 Urticaria, giant, 675 Uveoparotid fever, 38, 672 hyperplasia of palatal glands and, 38 Uvula, cleft, 19 V V-Z virus, 351 Vaccine, dental caries and, 463 Valley fever, 369 Van Buchem’s disease, 725 van der Woude’s syndrome, 17 Vanadium, dental caries and, 439 Vancomycin, dental caries and, 463 Vanishing bone, 736 Vaquez’s disease, 773 Varicella, 340, 343, 344, 350, 351 Varicelliform eruption of Kaposi, 342 Varices, lingual, 33 Variola, 348 Vascular hemophilia, 792, 793 Vascular leiomyoma, 167, 192, 193 Vascular purpura, 787, 793 Venereal wart, 349 Venous lake, 129, 146 Verocay bodies, 204 Verruca acuminata, 349 Verruca vulgaris, 81–82 Verruciform xanthoma, 143 Verrucoma, 83 3864 Verrucous carcinoma, 83, 91, 121, 122 Vertebrate dentitions, 902 Vertebral venous plexus, 208 Vesicular pharyngitis, 345 Vidian nerve neuralgia, 855 Vincent’s angina, 319, 396 Vincent’s infection, 369, 381, 395 Viral infections, 339 acute lymphonodular pharyngitis, 346 aphthous fever, 347 aphthous pharyngitis, 345 Behỗets syndrome, 670 benign lymphoreticulosis, 333 cat-scratch disease, 333 chickenpox, 350 classification, 390 condyloma acuminatum, 349 cytomegalic inclusion disease, 355 epidemic parotitis, 351 epizootic stomatitis, 347 foot-and-mouth disease, 347 German measles, 348 hand, foot and mouth disease, 346 herpangina, 345 herpes simplex, 360, 340 herpes zoster, 360 HIV infection, 357 hoof and mouth disease, 347 human immunodeficiency virus, 357 infantile paralysis, 355 measles, 347 molluscum contagiosum, 349 morbilli, 347 3865 mumps, 351 oral candidiasis, 358 periodontal lesions, 359 poliomyelitis, 355 Reiter’s syndrome, 671 rubella, 348 rubeola, 347 salivary gland virus disease, 355 shingles, 351 smallpox, 348 varicella, 350 variola, 348 venereal wart, 349 verruca acuminata, 349 vesicular pharyngitis, 345 zona, 351 Vitamin A, 18, 37, 592, 634 cleft palate and, 18 deficiency and xerostomia, 37 deficiency of, 592 enamel hypoplasia and, 52 excess of, 636 metabolism of, 647 Vitamin B complex, 89, 644–647 B6, 646 B12, 647 biotin, 647 choline, 647 dental caries and, 647 folic acid, 647 inositol, 647 leukoplakia and, 89 niacin, 646 3866 pantothenic acid, 646 pyridoxine (B), 646 riboflavin, 645 thiamine, 762 Vitamin C, 51, 402, 642 deficiency of, 402, 642 dental caries and, 601 enamel hypoplasia and, 51 Vitamin D, 636–640 deficiency of, 636–637 dental caries and, 438–439 enamel hypoplasia and, 439 hypophosphatasia, 640 hypophosphatemia, familial, 638 osteomalacia, 637 phosphate diabetes, 638, 718 pseudohypophosphatasia, 640 refractory rickets, 638, 718 renal osteodystrophy, 640 renal rickets, 640 resistant rickets, 638 Vitamin deficiency diseases, 634 xerostomia and, 37 Vitamin E, 641 Vitamin K, 642 Volatile oils, 392, 554, 678 Vomiting, chronic, erosion of teeth and, 574 von Recklinghausen’s disease of skin, 202 von Willebrand’s disease, 793 W Waldenström, macroglobulinemia of, 796 3867 hyperplasia of palatal glands and, 38 Wandering rash of the tongue, 31 Wart, common, 229 Warthin’s tumor, 229–231 Warty dyskeratoma, 819, 820 Waterhouse-Friderichsen syndrome, 655 Weber-Cockayne syndrome, 832 Webster’s classification, 898 Wegener’s granulomatosis, 674 Werlhof ’s disease, 788 White folded gingivostomatitis (dysplasia), 821 White sponge nevus, 597, 821, 822 Whitlow, herpetic, 342 Wickham’s striae, 680, 809, 810 Wilson’s disease, and copper deficiency, 623 Wiskott-Aldrich syndrome, 179, 790 Wound healing, 591–610 after biopsy, 594 after extraction, 598 after fracture, 604 after gingivectomy, 598 factors affecting, 591 X Xanthoma, verruciform, 143 Xanthomatoses, 633 Xeroderma pigmentosum, 127 Xerostomia, 37 Sjögren’s syndrome and, 37 X-ray radiation and, 37 X-ray radiation, 125, 548, 550, 592 aplastic anemia and, 759 3868 bone, effects on, 550 dental caries and, 445 extraction wound healing and, 598 hairy tongue and, 32 leukemia and, 403 oral mucosa, effects on, 548 salivary glands, effects on, 549 skin, effects on, 548 teeth, effects on, 549 tissue, general- effects on, 548 wound healing and, 592 xerostomia and, 37 Z Zinc, 461, 523, 623 Zinc chloride-potassium ferrocyanide, dental caries and, 461 Zinc oxide and eugenol, effects on tooth, 523 Zinc phosphate cement, effects on tooth, 523 Zona, 351, 654, 657 Uploaded by [StormRG] 3869 ... To Rotary Instrumentation Effect of Heat Effect of Restorative Materials Physical Injuries of the Teeth Physical Injuries of the Bone Physical Injuries of Soft Tissues Nonallergic Reactions... odontoblastic processes and drying of dentinal tubules, thickness of remaining dentin, vibration, removal of minerals and exposure of the organic matrix of dentin, and formation of smear layer Reaction... to injury of the dentinal tubules The pulp reaction to superficial injury of the dentin varies in degree of severity, depending partially upon the depth of the prepared cavity and partially upon