Chapter 7,8,9, 20 -11

CHAPTER 7

Developmental disturbances of the oral region

Figure 7 – 1: Commissural lip pits. (Neville et al 2003).

Figure 7 – 2: Paramedial lip pits with cleft lip and palate. (Langlais & Miller 2003).

Figure 7 – 3: Double lip. Horizontal fold of redundant mucosal tissue, located on the inner aspect of upper lip. (Neville et al

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2003).

Figure 7 – 4: Congenital median fissure of the lower lip. (Bork et al 1993).

Figure 7 – 5: Mucocutaneous pigmentation of Peutz – Jegher’s syndrome. (Lamey & Lewis 1991).

Figure 7 – 6: Down syndrome. Swollen lip with radial folds and indistinct vermilion border. (Bork et al 1993).

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Figure 7 – 7: Cheilitis glandularis. A long – standing enlarged lower lip with a pale, dry surface containing multiple small raised papules (enlarged duct openings) is characteristic of this condition. (Sapp et al 1997).The other causes of large lip are either due to granulomatous diseases like cheilitis granulomatosa, Melkersson-Rosenthal syndrome, Crohn‘s disease, leprosy, sarcoidosis, or due to allergic reaction to allergens as seen in the followings pictures.

A B

Figure 7 – 8: Chelitis granulomatosa. Enlarged lower lip, which is apparent in frontal (A) and lateral (B) views. The condition also produces difficulties in eating and speaking. (Sapp et al 1997).

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Figure 7 – 9: Melkersson - Rosenthal syndrome:Cheilitis granulomatosa in association with facial paralysis and fissured tongue. (Bork et al 1993).

Figure 7 – 10: Top. Photomicrograph of non caseating specific granulomatous inflammation. Most are epithelioid histiocytosis and langhans multinucleated giant cells. Bottom. Focal granuloma composed of histiocytes, and a multinucleated giant cell (arrow) surrounded by lymphocytes, plasma cells, and edematous connective tissues. (Silverman et al 2001).

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Figure 7 – 11: Crohn’s disease. Persistent macrocheilia. (Cawson et al 2001).

Figure 7 – 12: Leprosy (lepromatous type). Nodules can form on the lips , these may later break down to form ulcers. (Cawson et al 2001).

Figure 7 – 13: Sarcoidosis. (Scully & Cawson 2006).

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Figure 7 – 14: Acquired angioedema. Patient with swelling of the lips and right cheek with transepithelial oozing and crusting of transudate that began three days after receiving penicillin during root canal treatment. (Sapp et al 1997).

Figure 7 – 15: Macrostomia. www.dentalmedsoft. com.

Figure 7 – 16: Fordyce granules 0f upper lip. (Neville et al 2003).

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Figure 7 – 17: Fordyce granules. Sebaceous glands forms creamy granules in the buccal mucosa. (Langlais & Miller 2003).

Figure 7 – 18: Fordyce granules. Histology shows a typical sebaceous gland opening directly on to the surface through a short duct. (Cawson et al 2001).

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Figure 7 – 19: Focal epithelial hyperplasia. Typical site (the lower lip) and appearance of a soft pinkish plaque which, in this case, stands out from the surrounding (racial) mucosal pigmentation. (Cawson et al 2001).

Figure 7 – 20: Focal epithelial hyperplasia. (Right) low power shows parakeratosis, acanthosis and mitosis – like intranuclear degeneration (mitosoid cells); (left) high power view of mitosoid cell. (Cawson et al 2001).

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Figure 7 – 21: White sponge nevus. Typical appearance of irregular white thickening of the entire buccal mucosa . The patient’daughter was similarly affected. (Cawson et al 2001).

Figure 7 – 22: White sponge nevus. (Upper) low power view showing acanthosis and the edematous superficial layer of irregular thickness; (lower) high power view showing vaculated superficial epithelial cells of the plaque. (Cawson et al 2001).

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Figure 7 – 23: Familial gingival fibromatosis. In contrast to phenoytoin – induced hyperplasia, the overgrowth of the gingivae is smooth and uniform. The upper teeth have erupted but are buried within the fibrous overgrowth. (Cawson et al 2001).

Figure 7 – 24: Familial gingival fibromatosis (elongation of rete ridges, proliferation of cellular fibrous tissue and lack of inflammatory changes). (Cawson & Odell 2002).The drug- induced gingival hyperplasia are seen in the following three pictures:

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Figure 7 – 25: Patient with generalized gingival hyperplasia due to the administration of cyclosporine. (Sapp et al 1997).

Figure 7 – 26: Phenoytoin – induced gingival hyperplasia. Typical fibrous overgrowth of the interdental papillae produces discrete bulbous swellings. Despite the deep false pocketing the gingivae are not inflamed and the normal stippled surface is enhanced. (Cawson et al 2001).

Figure 7 – 27: Nifedipine – associated hyperplastic gingivitis. (Soames & Southam 2005).

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Figure 7 – 28: Acromegaly showing coarsening of facial features and macrognathia. (Soames & Southam 2005).

Figure 7 – 29: Mandibular prognathism associated with acromegaly. (Soames & Southam 2005).

Figure 7 – 30: Enlargment of the maxilla in Paget’s disease of bone, it is of unknown etiology. (Soames & Southam 2005).

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Figure 7 – 31: Micrognathia. www.dentalmedsoft. com.

Figure 7 – 32: Cleft lip. (Neville et al 2003).

Figure 7 – 33: Cleft palate. (Neville et al 2003).

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Figure 7 – 34: Cleft uvula. (Neville et al 2003).

Figure 7 – 35: (Left); Cleft palate, broad midline defect is present. (Right) cleft lip and palate. Complete unilateral cleft of palate, alveolar bone and lip joining the oral and nasal cavities. (Cawson & Odell 2002).

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Figure 7 – 36: Hemifacial hypertrophy. The patient exhibits extensive disproportionate growth of the whole left side of the cranium, midface, and mandible (upper view); the left side of the tongue (middle view); and a severe malocclusion (lower view). (Sapp et al 1997).

Figure 7 – 37: Macroglossia. Large tongue shows pressure indentations from the teeth. (Langlais & Miller 2003).The causes of acquired (secondary) macroglossia are acromegaly and cretinism,cystic lesions the in tongue, amyloidosis (figure 7- 38) and tumors in the tongue like hemangioma (figure 7-39) or lymphangioma. (7-40).

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Figure 7 – 38: Macroglossia due to amyloidosis. (Bork et al 1993).

Figure 7 – 39: Macroglossia due to haemangioma. (Cawson & Odell 2002).

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Figure 7 – 40: Macroglossia. The tongue of the young patient is excessively large due to the presence of a lymphangioma. (Sapp et al 1997).

Figure 7 – 41: Ankyloglossia. The tongue of the patient has reduced mobility caused by the large band of fibrous tissue extending from the ventral surface of the tongue to the lingual gingiva of the mandible. (Sapp et al 1997).

Figure 7 – 42: Bifid tongue. www.dentalmedsoft. com.

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Figure 7 – 43: Fissured tongue (scrotal tongue). (Neville et al 2003).

Figure 7 – 44: Moderatly fissured tongue. (Cawson et al 2001).

Figure 7 – 45: Median rhomboid glossitis. A well defined area of depapillation in the midline of the tongue. (Cawson et al 2001).

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Figure 7 – 46: Lingual varicosities. The under surface of the tongue and floor of the mouth is a common finding with age. (Neville et al 2003).

Figure 7 – 47: Mucosal varix. (Neville et al 2003).

Figure 7 – 48: Benign migratory glossitis. Sharply defined areas of depapillation surrounded by creamy, slightly elevated margins. (Cawson et al 2001).

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Figure 7 – 49: (Left), benign migratory glossitis in young infant. (Right), benign migratory glossitis: Multiple patches on a mildly fissured tongue. (Cawson et al 2001).

Figure 7 – 50: Hairy tongue. There are numerous elongated papillae with dark brown pigmentation. (Neville et al 2003).

Figure 7 – 51: Lingual thyroid nodule. Accessory accumulasion of thyroid gland tissue within the body of the tongue. (Neville et al 2003).

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Figure 7 – 52: The clinical and radiographical pictures of complete anodontia in four years old female with hereditary ectodermal dysplasia. There is neither any deciduous tooth nor any permanent tooth. (Personal case).

Figure 7 – 53: The clinical and radiographical pictures of seven years old girl with many missing permanent teeth.(Personal case).

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A B Figure 7 – 54: A. Anhidrotic ectodermal dysplasia showing conical teeth, giving an undesirable. Dracula – like appearance. B. Another case showing typical fine and scanty hair and loss of support for the facial soft tissues. (Cawson & Odell 2002).

Figure 7 – 55: Hypodontia. Congenitally absent left maxillary central incisor resulting in underdevelopment of the maxilla and severe malocclusion. (Sapp et al 1997).

Figure 7 – 56: Supernumerary teeth. (Neville et al 2003).

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Figure 7 – 57: Top, supernumerary teeth. An erupted supernumerary left mandibular central incisor. Bottom, hypodontia, note retention of deciduous teeth where permanent successional teeth are absent. (Neville et al 2003).

Figure 7 – 58: Supernumerary teeth. A fully developed normal extra- premolar that has erupted lingually to the arch. (Sapp et al 1997).

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Figure 7 – 59: A paramolar, a buccally placed supernumerary molar tooth. (Cawson & Odell 2002).

A BFigure 7 – 60: A. Supernumerary teeth. An erupted miniture conically shaped extra tooth is present in the midline of the anterior palate (mesiodens). B. A similarly located extra tooth that is impacted and unable to erupt. (Sapp et al 1997).

Figure 7 – 61: Cleidocranial dysplasia. This man can bring his shoulders together .His daughter was similarly affected.The radiograph shows absence of clavicles in this disorder. (Neville et al

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2003).

Figure 7 – 62: Cleidocranial dysplasia. (Neville et al 2003).

Figure 7 – 63: Cleidocranial dysplasia. Many buried teeth can be seen in this radiograph. (Neville et al 2003).

Figure 7 – 64: Natal teeth. Two normally sized mandibular incisors that

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were present at birth. (Langlais & Miller 2003).

Figure 7 – 65: Microdont in the third molar position. (Regezi & Sciubba 1999).

Figure 7 – 66: Occlusal view of a macrodont (molar) and a peg lateral. (Regezi & Sciubba 1999).

Figure 7 – 67: Bilateral gemination. Abnormally shaped crown that is extra wide due to the development of two crowns from one tooth

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germ. (Langlais & Miller 2003).

Figure 7 – 68: Gemination. (Neville et al 2003).

A BFigure 7 – 69: A. Gemination. The patient exhibits an extra wide lower central incisor that is most likely caused by gemination because there is a normal number of incisors in the arch. B. Fusion. Patient with an extra wide lower incisor most likely caused by fusion because the arch contains three incisors instead of four. (Sapp et al 1997).

Figure 7 – 70: Bilateral fusion. An abnormally shaped tooth that may appear

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as an extra wide crown resulting from the union of two adjacent tooth germs by dentin during development. (Langlais & Miller 2003).

Figure 7 – 71: Fusion. (Neville et al 2003).

Figure 7 – 72: Concrescence. Two upper molars fused together by cementum. (Cawson & Odell 2002).

Figure 7 – 73: Cocrescence. Molars adhered to each other by fusion of their cementum. (Sapp et al 1997).

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A BFigure 7 – 74: Taurodontism. A. Radiograph of a molar with an enlarged coronal pulpal chamber and lowered bifurcation area of roots. B. Similar abnormality, formed tooth that has been cut in a sagittal plane, to illustrate the abnormal shape of the tooth and its pulpal chamber. (Sapp et al 1997).

A B Figure 7 – 75: Dens invaginatus. Radiograph of lateral incisors exhibiting a mild form of the defect in a tooth with a dilacerations of the root (A), and a moderate form in which the tooth is conically shaped and exhibits the characteristic appearance of a tooth within a tooth (dens in dente) (B). Both teeth have the commonly associated periapical lesions. (Sapp et al 1997).

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Figure 7 – 76: Dens evaginatus of lower second premolar. (Langlais & Miller 2003).

A BFigure 7 – 77: Talon cusp. A. In this specific form of dens evaginatus, cuspal projections are present bilaterally and arise from the cingulum of the lateral incisors, resembling eagle’s talons. (Sapp et al 1997). B. Accessory cusp: Protostylid. (Langlais & Miller 2003).

Figure 7 – 78: Dilaceration. A severely bent root of the maxillary central incisor that prevented the eruption of the tooth. (Sapp et al 1997).

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Figure 7 – 79: Supernumerary roots of first molar (left) and canine (right). (Langlais & Miller 2003).

Figure 7 – 80: Enamel pearl. There is a small mass of enamel at the root bifurcation. (Cawson & Odell 2002).The etiology of developmental abnormalities of enamel are either genetic,environmental\systemic, or local causes as seen in the following pictures:

[Figure 7 – 81: Amelogenesis imperfecta. Inherited enamel defect. (Bork et al 1993).

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Figure 7 – 82: Amelogenesis imperfecta (hypoplastic type). The enamel is thin, rough in texture, and stained, but there is hard and relatively normal in structure. Three sisters were similarly affected and the trait was traced back through three generations. (Cawson et al 2001).

A B CFigure 7 – 83: A. Focal hypoplastic amelogenesis imperfecta. The enamel is of normal thickness and hardness with diffuse pitting. B. Generalized hypoplastic amelogenesis imperfecta. The enamel is evenly reduced in thickness but of normal hardness, resulting in spacing and alteration of the shape of teeth. C. Hypocalcified amelogenesis imperfecta. The enamel is soft and easily chipped away, leaving exposed dentin that is easily stained, worn, and caries prone. (Sapp et al 1997).

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A B Figure 7 – 84: Hypomaturation amelogenesis imperfecta. A, sever form with enamel of normal thickness but that exhibits loss of translucency and hardness, resulting in some chipping of incisal edges. B, in the mild form the teeth may be relatively normal but contain white flecks in the incisal third of the teeth (snow – capped teeth). (Sapp et al 1997).

Figure 7 – 85: Turner tooth. Top, radiograph of first maxillary premolar exhibiting radiolucency due to hypoplasia acquired during development of the crown. Middle, gross appearance of the tooth illustrated in top with a brownish – yellow, irregular shape and surface of crown. (Sapp et al 1997). Lower, maxillary first premolars. (Langlais & Miller 2003).

Figure 7 – 86: Enamel hypoplasia. (Neville et al 2003).

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Figure 7 – 87: Enamel hypoplasia. (Neville et al 2003).

Figure – 88: Dental fluorosis, moderate effects from an area of endemic fluorosis. (Soames & Southam 2005).

Figure 7 – 89: Mottled enamel (fluorosis). In this severe example, the enamel has widespread pitting defects and brown discoloration. (Cawson et al 2001).

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Figure 7 – 90: Environmental enamel hypoplasia , unlike the hereditary types, defects are linear and thought to correspond to a short period of amelogenesis disturbed by a severe illness. (Neville et al 2003).

Figure 7 – 91: Tetracyclin staining, note the brown intrinsic stain. (Langlais & Miller 2003).

Figure 7 – 92: Tetracycline pigmentation. The newly erupted permanent teeth are yellow but the deciduous teeth have changed to a dirty gray. Tetracycline had been given for long periods during the mother’s pregnancy and during the child’s infancy. (Cawson et al 2001).

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A B Figure 7 – 93: A. Congenital syphilis. Hutchinson’s incisors. These taper towards the tip and show the typical notched edges. The anterior open bite is also characteristic. B. Mulberry molars: Multiple nodules have formed instead of cusps and the pitted areas have been replaced with amalgam. (Cawson et al 2001).

Figure 7 – 94: Enamel hypoplasia appear as a horizontal band associated with measles in early childhood. (Soames & Southam 2005).

Figure 7 – 95: Erythropoietic porphyria. The characteristic reddish – brown stains of the enamel is produced by deposition of porphyrin in the developing dental tissues. (Cawson et al 2001).

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Figure 7 – 96: Rickets. Enamel hypoplasia; patient was vitamin – D deficient from age 1 – 2 ½ years. (Bork et al 1993).

Figure 7 – 97: Top, dentinogenesis imperfecta. The teeth are grayish in color but, unlike the tetracycline – stained teeth in previous figures, are abnormally translucent. Bottom, dentinogenesis imperfecta: In this 14 – year – old, the teeth have worn down to gingival level but the pulp chambers have become obliterated as part of the disease process. Some enamel remains around the necks of the posterior teeth. (Cawson et al 2001).

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Figure 7 – 98: Dentinogenesis imperfecta. This radiograph shows the characteristic short roots and relatively bulbous crown. (Cawson et al 2001).

A B Figure 7 – 99: Dentin dysplasia type I. A. Patient exhibits normally shaped and colored teeth. B. Dentin dysplasia type I. Panoramic radiograph depicting the oblitration of the pulp except for the occasional “chevron” radiolucency, shortened and W – shaped roots, and periapical radiolucency. (Sapp et al 1997).

Figure 7 – 100: Dentin dysplasia type II. Periapical radiographs indicating teeth with relatively normal roots and pulpal chambers that contain large pulp stones. (Sapp et al 1997).

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Figure 7 – 101: Regional odontodysplasia. Patient exhibiting a localized area of the mandible in which two abnormal teeth are present surrounded by an increase in the soft tissue. (Sapp et al 1997).

Figure 7 – 102: Regional odontodysplasia. Panoramic radiograph revealing several faint outlines of teeth in the posterior maxilla with large pulpal chambers and lacking root formation. (Sapp et al 1997).

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CHAPTER 8

Genetic, metabolic, and other non –neoplastic bone diseases.

Figure 8 – 1: Osteogenesis imperfecta. Genetic disease of bone , the radiograph shows multiple fractures. (Cawson et al 2001).

Figure 8 – 2: Osteogenesis imperfecta. Higher power view shows only woven bone and large numbers of osteoblasts but no compact bone. (Cawson et al 2001).

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A B

CFigure 8 – 3: A. Osteopetrosis. Generalized hereditary condition, the radiograph showing such extreme bone density that the teeth are barely visible. B. Osteopetrosis necrosis of the body of the mandible following extraction of the teeth from the same patient. C. Osteopetrosis radiograph of the same patient showing the line of separation of the sequestrating alveolar bone. (Cawson et al 2001).

Figure 8 – 4: Osteopetrosis radiograph. The bone is excessively thick and dense as a result of defective resorption. (Neville et al 2003).

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Figure 8 – 5: Osteopetrosis. Absence of differentiation into cortex and medulla. The bone is dense but penetrated by vascular channels and small amounts of fibrous marrow. Few osteoclasts are present. (Cawson et al 2001).

Figure 8 – 6: Cleidocranial dysplasia. In this rare familial disorder, absence of clavicles allowing shoulders to be brought forwards (look also to figure 7-61, 7-62,and 7-63). (Soames & Southam 2005).

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Figure 8 – 7: Both figures represent retention of deciduous teeth with multiple impactions of permanent teeth in cleidocranial dysplasia. (Soames & Southam 2005).

Figure 8 – 8: Achondroplasia. May be inherited as an autosomal dominant trait,the retrusive middle third of the face is due to defective growth of the base of the skull. (Soames & Southam 2005).

Figure 8 – 9: Cherubism. Autosomal dominant lesion, the facial features resemble a cherub due in part to symmetric bilateral enlargement of the posterior mandible. (Sapp et al 1997).

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Figure 8 – 10: Cherubism. Both rami, much of the body of the mandible and the posterior maxillae are expanded by multilocular radiolucent lesions which have displaced and destroyed developing teeth. (Cawson & Odell 2002).

Figure 8 – 11: Cherubism. Top, microscopic appearance of an early – stage lesion containing giant cell tissue with little evidence of fibrous tissue and bone formation. Bottom, mature stage in older patient reveals a reduction in the proportion of giant cell tissue and an increase in fibrous tissue and bone formation. (Sapp et al 1997).

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Figure 8 – 12: Cherubism. It produce some elevation of the floor of the orbit, causing the pupils to be elevated upward. (Neville et al 2003).

A BFigure 8 – 13: Hyperparathyroidism. A. There is an area of bone destruction simulating a multilocular cyst. B. A periapical view reveals the relative radiolucency of the bone and loss of lamina dura around the roots. (Regezi & Sciubba 1999).

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Figure 8 – 14: Hyperparathyroidism in the humerus of the same patient with a parathyroid adenoma. Note also the loss of trabecular pattern and cortex. (Cawson & Odell 2002).

Figure 8 – 15: Hyperparathyroidism. Multinucleate osteoclast – like giant cells are lying in a hemorrhagic fibrous tissue. The appearances are indistinguishable from giant cell granuloma histologically. (Cawson & Odell 2002).

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Figure 8 – 16: Paget’s disease. A rare example of severe mandibular involvement. (Cawson & Odell 2002).

Figure 8 – 17: Paget’s disease. Generalized enlargement of the maxilla. (Neville et al 2003).

A BFigure 8 – 18: Paget’s disease. A, involvement of the maxilla produces this characteristic massive overgrowth of the alveolar ridges, sometimes partially burying the teeth. B, radiograph showing that the maxillae and base of the skull have become thickened with characteristic fluffy margins and excessive amounts of bony tissue. (Cawson et al 2001).

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Figure 8 – 19: Paget’s disease .The bone have a characteristic cotton- wool appearance.(Neville et al 2003).

Figure 8 – 20: Paget’s disease. Periapical radiograph of teeth exhibiting loss of lamina dura. (Neville et al 2003).

A BFigure 8 – 21: Paget’s disease. A. Mandibular involvement as seen in the radiograph is rare and shows patchy sclerosis combined with gross hypercementosis of the remaining teeth. B. Paget’s disease, early stage. There are many osteoclasts and osteoblasts associated with active resorption and formation of new bone, producing the characteristic mosaic pattern of bluish reversal lines within the bone. (Cawson et al 2001).

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A BFigure 8 – 22: Juvenile fibrous dysplasia. A. Facial asymmetry due to expansile lesion of right maxilla. B. Diffuse buccal and lingual expansion of right alveolar process exhibiting displacement of first premolar and retained primary molar. (Sapp et al 1997).

A B

CFigure 8 – 23: Fibrous dysplasia. A. Intraoral appearance of the bony swelling which has remained virtually unchanged after many years (B). C. Radiograph shows the uniform ground – glass appearance of the affected areas, which involves and has destroyed the normal appearance of the lamina dura surrounding the teeth. (Cawson et al 2001).

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Figure 8 – 24: Fibrous dysplasia. Slender trabeculae of woven bone, said to resemble Chinese characters in shape, lying in a very cellular fibrous tissue. With maturation there is progressively more bone formation. (Cawson & Odell 2002).

Figure 8 – 25: Adult monostotic fibrous dysplasia. Clinical appearance of an unusually large lesion of the mandible.(Sapp et al 1997).

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Figure 8 – 26: McCune – Albright syndrome. Large café – au – lait macule with polyostotic fibrous dysplasia. (Bork et al 1993).

Figure 8 – 27: Polyostotic fibrous dysplasia. Top, clinical appearance of patient exhibiting disproportionate bone growth caused by multiple fibrous lesions of the craniofacial bones and café – au – lait pigmentation. Bottom, expansile lesions of the mandible and maxilla are evidence in all quadrances. (Sapp et al 1997).The other fibro –osseous lesions like cemento-osseous dysplasia were seen in chapter- 6,while the fibro-osseous neoplasms like cemento-ossifying fibroma are seen in chapter-14.

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CHAPTER 9

Regressive alterations of teeth

Figure 9 – 1: Attrition. Wear of tooth substance as a result of tooth to tooth contact during mastication or parafunction. (Neville et al 2003).

Figure 9 – 2: Attrition (ground section). The incisal edge has been worn away, exposing the dentin. The dentinal tubules in the exposed area are sclerosed and appear dark in transmitted light. (Cawson et al 2001).

Figure 9 – 3: Abbrasion. Wear of tooth substance by friction with the

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foreign substance independent of occlusion. (Neville et al 2003).

Figure 9 – 4: Abbrasion. (Neville et al 2003).

Figure 9 – 5: Attrition and abrasion. Chronic physical trauma to the teeth produced by chewing and over – vigorous use of a toothbrush respectively. The incisal edges of the teeth have worn into polished facets, in the centers of which the yellowish dentin is visible. The necks of the two nearest teeth have been deeply incised by tooth brushing, also exposing dentin. The pulp has been obliterated by secondary dentin formation but its original site can be seen in the center of the exposed dentin. (Cawson & Odell 2002).

Figure 9 – 6: Erosion(corrosion). Loss of hard dental tissues by some

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chemical process that does not involve bacterial action. (Neville et al 2003).

Figure 9 – 7: Erosion. (Neville et al 2003).

Figure 9 – 8: Erosion. (Neville et al 2003).

Figure 9 – 9: Abfraction. Microstructural loss of tooth substance in areas of stress concentration,occlusal loading forces lead to a breaking away of the extremely thin layer of enamel rods. (Neville et al 2003).

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Figure 9 – 10: Pink tooth.(Neville et al 2003).

Figure 9 – 11:Pathological internal resorption of tooth,which is starting from the pulpal surface.(Neville et al 2003).

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Figure 9 – 12: Resorbing dentin surface with resorption lacunae and osteoclast – like cells. (Soames & Southam 2005).

Figure 9 – 13: External resorption. (Neville et al 2003).

Figure 9 – 14: External resorption. (Neville et al 2003).

Figure 9 – 15: Pulp stone.(Neville et al 2003).

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Figure 9 – 16: Lamellated (false) pulp stones.(Soames & Southam 2005).

A BFigure 9 – 17: Hypercementosis. A. Maxillary molar exhibiting massive deposits of cementum on all roots. B. Radiograph of maxillary molars in an area of chronic inflammation exhibiting extensive hypercementosis. (Sapp et al 1997).

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Figure 9 – 18: Ground section, approximately 100 m thick, of an old tooth. The section has been placed over a pattern, which can be seen through the apical translucent sclerotic dentin. ( Nanci 2003).

A BFigure 9 – 19: Difference in pulp volume between halves of young tooth (A) and an old tooth (B). ( Nanci 2003).

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