A unique book that collects similar disease manifestations, related histopathological features, similar confusable cell names, phenomena, radiographic pictures, and important syndromes. The book is indispensable for the last-minute review of the pathology before you are subjected to written, oral, practical, chair-side exams or board certification.

Oral Manifestations in Various Skin Conditions A great number of pathologic conditions of the skin have accompanying oral manifestations that may precede or occur concurrently with or independent of the cutaneous eruption. In general, such lesions do not bear strict comparison with the skin lesions, because of the considerable difference in moisture, temperature, exposure to trauma, lack of a keratin layer, and the presence of secondary infection. In the differential diagnosis the prevalence of purely local lesions of a vesicular or bullous type (e.g., recurrent aphthous ulcers) should be kept in mind. One of the familiar dermatoses in which the oral mucosa may participate is lichen planus, which is a chronic inflammatory disorder with no malignant potential. It has the appearance most commonly of rectangular white plaques associated with erythema and erosions; less often seen are ulcerations and hyperkeratotic plaques. The pathogenesis has not been completely elucidated, but it involves a T cell–mediated immune response causing a cytotoxic reaction by activating CD8 T cells against epithelial basal cells. The diagnosis is confirmed through a review of the patient history, physical examination, and histologic findings. The presence of the purplish, polygonal, or angular skin papule eruptions improves the accuracy of the diagnosis. In a majority of cases, however, the oral lesions precede those of the skin surfaces, and, not infrequently, the disease may remain confined to the mouth. Most often, the cheek mucosa displays the characteristic fine, lacelike pattern of bluish white lines and small, pinhead-size, elevated papules, although the tongue, palate, and gingiva may be similarly affected. The latter locations, as compared with the cheek, usually show coarser plaques and aggregated papules. The lips are least commonly involved. Occasionally, an erosive form may be observed, which is painful and characterized by a caked, whitish material covering a red base in which bleeding is easily induced. The radiating and interlaced grayish white lines are the most significant signs in the diagnosis. These lesions are most often seen in HIV/AIDS and other immunosuppressed conditions. Differentiation from syphilis, moniliasis, and glossitis migrans is easily made, but differentiation from other local leukokeratoses is sometimes difficult, and biopsy then becomes a helpful adjunct. The histopathologic picture in lichen planus shows moderate keratosis or parakeratosis, a “sawtooth” arrangement of the rete pegs, and a very typical band of lymphocytes chiefly concentrated beneath a vague basal cell zone. This lymphocytic infiltrate is sharply demarcated from the rest of the stroma. Pemphigus begins in over 50% of cases with manifestations on the oral mucosa, where large, painless vesicles or bullae develop. The thin-walled blebs rupture in a short time, leaving a superficial ulcer rimmed with tattered, grayish shreds of thin membrane. Signs of inflammatory reactions are absent in the early stages but may present themselves later in the form of a slightly red halo. The onset is insidious, chronicity and recurrence being typical even when unaccompanied by skin signs. As the disease progresses, confluent areas become raw and oozing, and salivation, pain, and bleeding increase; mastication and swallowing are impaired. Erythema multiforme major may affect, along with the skin, the mucous membranes of the mouth, eyes, and anogenital regions. Erythema multiforme minor presents similarly but without any mucosal involvement. Both the major and minor forms have the distinctive target skin lesions. The earliest vesicular lesions in the mouth are sometimes indistinguishable from those of pemphigus. A diffuse bullous stomatitis ensues, with a heavy yellowish pseudomembrane, a marked variation in the size of the lesions, and, often, a bluish red areola around the lesions. The lips are usually swollen, ulcerated, and covered with hemorrhagic crusts. The severity of the disease varies. Recurrence is common and tends to be seasonal. Although the development of erythema multiforme has been linked to many factors, including but not limited to, medications, malignancy, autoimmune disease, and herpes simplex virus infection, the virus is the precipitating agent in over 90% of cases. Stevens-Johnson syndrome is a rare acute, life-threatening mucocutaneous disease that is nearly always triggered by a drug. Most often the offending agents are allopurinol, anticonvulsants, antimicrobial agents, and nonsteroidal medications. The cutaneous reaction includes extensive keratinocyte cell death causing separation of areas of skin at the dermal-epidermal junction. The oral mucosa and the vermillion border are almost invariably involved with painful hemorrhagic erosions covered with a grayish white membrane. Stomatitis and mucositis lead to impaired oral intake, with consequent malnutrition and dehydration. The degree of body surface area involved in the skin separation process in Stevens-Johnson syndrome is up to 10%. Toxic epidermal necrosis is a further progression of the cutaneous process, resulting in involvement of more than 30% of the body surface area. If the involvement is between 10% and 30%, the disease is classified as a combination of Stevens- Johnson syndrome and toxic epidermal necrosis. Acquired epidermolysis bullosa is an autoimmune subepithelial blistering disease that primarily affects elderly individuals; it has no predilection for gender or race. The skin eruption is generalized and favors skin folds and flexural areas. The initial presentation is an area of localized erythema or urticarial papules that coalesce into plaques and subsequently turn into dark-red vesicles and bullae in a few weeks. Oral blisters can develop; they are few in number and are less severe and more transient than the cutaneous lesions. Hereditary epidermolysis bullosa is a heterogeneous group of genetic bullous disorders characterized by blister formation in response to mechanical trauma. The dystrophic and junctional types are more serious and include organ involvement, skin breakdown, and scarring. Enamel hypoplasia is present in, and limited to, the junctional form, causing pitting of the deciduous and permanent surfaces of the teeth. Dental caries is prominent in both the junctional and dystrophic forms of the disease. None of the serious cutaneous or oral manifestations have been described in the simplex form of the condition. Langerhans cell histiocytosis (histiocytosis X) is a rare disorder characterized by organ infiltration of Langerhans cells. Papules, vesicles, nodules, and a seborrheic-like pattern on the scalp and diaper area are the primary cutaneous findings of the disease. Dental problems are seen in 30% of patients, and they include a destructive periodontitis resulting from osseous infiltration of the Langerhans cells. Ultimately this can cause destruction of the dentition support system from the maxilla and mandible and loosening of the teeth (floating teeth). Periodontal involvement characterized by gingival recession and pocket formation ultimately leads to alveolar bone loss, culminating in loss of dentition. Congenital erythropoietic porphyria is a rare autosomal recessive disorder that is phenotypically depicted as an abnormality of heme biosynthesis. A pale oral mucosa and teeth that appear a red-maroon color (erythrodontia) are the primary dental abnormalities seen. The pattern of discoloration is distinct and aids in the diagnosis. The incisors are nearly completely stained, whereas the canines are colored at the cusp tips and the molars demonstrate varying degrees of discoloration. The coloring of the teeth is thought to be from an affinity of porphyrins for the calcium phosphate rich teeth. Congenital syphilis is a result of transplacental infection by Treponema pallidum. Cutaneous findings of red macules and papules, a papulosquamous eruption, or a desquamating dermatitis are seen in less than half of the infants infected, but hemorrhagic bullae on the palms and soles are pathognomonic of the infection. Rhinitis, mucous patches on the lips, mouth, tongue, and palate, and condylomata mainly in the anogenital area and angles of the mouth are characteristic. Ectodermal dysplasias constitute a group of hereditary conditions characterized by one or more ectodermal structures, including the skin. The typical areas affected are the hair (hypotrichosis, partial or complete alopecia), nails (dystrophic, hypertrophic, or abnormally keratinized), tooth enamel (defects or absent), and hypoplastic or aplastic sweat glands. Dental defects are characteristic and a core manifestation of the disease, including anodontia, polyodontia, dysplastic teeth, retained primary teeth, deficient enamel development (amelogenesis imperfecta), and underdevelopment of the alveolar ridge. Tuberous sclerosis (Bourneville disease) has an autosomal dominant inheritance. It results in the formation of hamartomatous lesions in several organ systems, including the skin, brain, kidney, ear, lung, bone, and eye. Characteristic oral lesions include gingival fibromas and dental enamel pits caused by a reduced amount of enamel present during dentition development. The pits are large defects in the enamel without a change in color or texture of the enamel surrounding the pit, producing a pockmarked appearance. Nevoid basal cell carcinoma syndrome is an autosomal dominant predisposition for the development of epitheliomas, medulloblastomas, and other developmental abnormalities. The hallmark of the disease, however, is the presence of multiple odontogenic keratocysts. Finding the keratocysts in a young child is diagnostic of the condition.

Benign Tumors of Oral Cavity Tumors of the oral cavity are very diversified. Only a select few can be discussed here. A fibroma may be found on the gingiva, lips, palate, and buccal mucosa. It is hard or soft and pale or reddish, depending on the density of collagen and the abundance of vascular elements. The gingival fibroma (fibrous epulis) is usually derived from the periosteum. It is sessile or pedunculated, well defined, and slow growing. The papilloma is soft and pedunculated or, when arising from an area of leukoplakia, hard with a warty, keratinized epithelium. The epithelial projections may grow beyond the basal layer and may occasionally curl inward into the stroma and become fixed at their bases, suggesting that they are potentially malignant. They are found in the same areas as the fibromas and also on the tongue. The hemangioma, either cavernous or capillary in structure, is primarily seen on the tongue but may arise in any part of the mouth from blood vessel endothelium. It may be congenital or familial, or it may develop at a later period in life. Multiple hemangiomas can occur anywhere in the mucous membrane of the intestinal tract, but the lip, tongue, gum, and rectum are sites of predilection. The color is light red to dark purple, with a tendency to blanch on pressure. Some large hemangiomas appear more globular than flat and are lobulated on their free mucosal surfaces, with a tendency toward displacement of bone by osteolysis. Extension occurs through endothelial proliferation along the nourishing blood vessels, usually more widespread than is apparent on clinical inspection. Significant blood loss has been reported from incidental minor procedures such as tooth extractions. The benign giant cell tumor, or epulis, is a not uncommon gingival or, more rarely, an intraosseous growth, which originates from the periodontal membrane or periosteum and has a tendency to recur unless this tissue is widely excised. The superficial form is apparently an exaggerated granulation process, with numerous giant cells eroding the bone trabeculae; older lesions contain more adult fibroblasts and fewer hemorrhages. Extravasation of erythrocytes releasing hemoglobin, which is transformed to hemosiderin, explains the occasional brown color. The central giant cell tumor may show features of resorptive inflammation but behaves like a neoplasm and may be identical to the giant cell tumor of the long bones, though it has little relation to giant cell sarcoma. The tumor can, however, infiltrate bone and displace teeth. It is nonencapsulated but does not metastasize. Essentially, it is composed of spindle cells with a varying amount of collagen fibers, hemorrhagic debris, and multinucleated cells. Occasionally, a giant cell tumor on the gum or in the bone is a manifestation of hyperparathyroidism. The so-called pregnancy “tumor” is a hyperplasia, developing in the course of a chronic gingivitis, which is not infrequently observed in pregnant women but sometimes also with other hormonal alterations (e.g., puberty). Bleeding, particularly of the interproximal papillae, with light raspberry to dusky red coloration, is an early sign, followed by a hypertrophic swelling of the papillary gingiva, ranging from a slight bloating to a tumor of 1 to 2 cm. It may envelop more than one tooth. The growth regresses with proper oral hygiene and adjusted toothbrush technique, though surgery may be required because of constant bleeding. Generally, tumors that are not too large disappear after delivery. The ameloblastoma, sometimes termed adamantinoma or adamantoblastoma, is an epithelial neoplasm occurring chiefly in the mandible (region of the third molar, ramus, or premolar, in that order of frequency); it belongs to the group of odontogenic tumors (as do the myxoma and cementoma) (not illustrated). According to generally accepted belief, the ameloblastoma originates from remnants of the enamel or dental lamina, but from less differentiated cells (preameloblasts) than those producing a follicular cyst. The tumor is mostly polycystic, sometimes monocystic, and occasionally solid. It is this solid form that on rare occasions has been found to metastasize. The growth of this other-wise benign tumor is very slow. Microcystic infiltration, roentgenologically revealed by tiny locules or notching, enlarges the jaw; the only sign is often a tiny bony capsule distending the surrounding tissue. Eventually, expansion into the orbit, antrum, and even cranium may take place. The most common variety, microscopi- cally recognizable, is the ameloblastic type, character- ized by follicles resembling enamel, with its outer layer of cylindrical cells and stellate reticuloma in the center. Occasionally, solid strands of undifferentiated cells or sheaths of stellate cells or an accumulation of squamous and prickle cells may be found. A microscopic descriptive grading of ameloblastoma is necessary for proper management of each case and for the choice between local or radical removal. The recurrence rate of ameloblastoma is extremely high, but true malignancy is extremely low. Made up of mixed ectodermal and mesodermal tissue, the odontoma, also odontogenic in origin, may be a hard or soft tumor, depending upon the presence or absence of calcified accretions. The hard odontoma is composed of abnormally arranged enamel, dentin, and cementum, in a soft fibrous matrix that is gradually replaced by the calcified elements, leaving a capsule. Complex odontomas contain a bizarre conglomeration of hard structures without finite shape; compound odontomas include both rudimentary and apparently normal supernumerary teeth, at times numbering several dozen. These structures may erupt and imitate the normal dentition. Myxoma of the jaw (not illustrated), derived from embryonal tissue of the dental papilla, is also a benign odontogenic tumor, as is the cementoma, a special form of fibroma, which appears usually at the apices of the lower anterior teeth. Multiple cementomas appear only in women, suggesting an estrogenic influence. Osteoma (not illustrated) is a compact osteogenic tumor, and fibroosteoma is a diffuse one. Both are slow-growing benign neoplasms; a conservative surgical approach is used when the tumors may lead to deformities.

This practical manual of oral histology and oral pathology specially suited for BDS undergraduate students . This book provide opportunity to learn and...

Advanced Bell Stage EO- Enamel Organ OEE- Outer Enamel epithelium SR- Stellate Reticulum SI- stratum Intermedium IEE- Inner Enamel Epithelium EM- Enamel Matrix CL- Cervical Loop A- Ameloblast ( showing Reversal of polarity) OEE Folds ( Invagination of OEE- Reversal of nutrition) DP- Dental Pulp OD- Odontoblast D- Dentin UMC- Undifferentiated mesenchymal cells DS- Dental Sac Contributed by Dr. Vimi Mutalik Advanced Bell stage by Vimi Mutalik is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License

This dental notes contains all the necessary high-yield points about Ameloblastoma. Helpful for Dental Board Exam, NBDE, & NEET MDS Exam.

Benign Tumors of Oral Cavity Tumors of the oral cavity are very diversified. Only a select few can be discussed here. A fibroma may be found on the gingiva, lips, palate, and buccal mucosa. It is hard or soft and pale or reddish, depending on the density of collagen and the abundance of vascular elements. The gingival fibroma (fibrous epulis) is usually derived from the periosteum. It is sessile or pedunculated, well defined, and slow growing. The papilloma is soft and pedunculated or, when arising from an area of leukoplakia, hard with a warty, keratinized epithelium. The epithelial projections may grow beyond the basal layer and may occasionally curl inward into the stroma and become fixed at their bases, suggesting that they are potentially malignant. They are found in the same areas as the fibromas and also on the tongue. The hemangioma, either cavernous or capillary in structure, is primarily seen on the tongue but may arise in any part of the mouth from blood vessel endothelium. It may be congenital or familial, or it may develop at a later period in life. Multiple hemangiomas can occur anywhere in the mucous membrane of the intestinal tract, but the lip, tongue, gum, and rectum are sites of predilection. The color is light red to dark purple, with a tendency to blanch on pressure. Some large hemangiomas appear more globular than flat and are lobulated on their free mucosal surfaces, with a tendency toward displacement of bone by osteolysis. Extension occurs through endothelial proliferation along the nourishing blood vessels, usually more widespread than is apparent on clinical inspection. Significant blood loss has been reported from incidental minor procedures such as tooth extractions. The benign giant cell tumor, or epulis, is a not uncommon gingival or, more rarely, an intraosseous growth, which originates from the periodontal membrane or periosteum and has a tendency to recur unless this tissue is widely excised. The superficial form is apparently an exaggerated granulation process, with numerous giant cells eroding the bone trabeculae; older lesions contain more adult fibroblasts and fewer hemorrhages. Extravasation of erythrocytes releasing hemoglobin, which is transformed to hemosiderin, explains the occasional brown color. The central giant cell tumor may show features of resorptive inflammation but behaves like a neoplasm and may be identical to the giant cell tumor of the long bones, though it has little relation to giant cell sarcoma. The tumor can, however, infiltrate bone and displace teeth. It is nonencapsulated but does not metastasize. Essentially, it is composed of spindle cells with a varying amount of collagen fibers, hemorrhagic debris, and multinucleated cells. Occasionally, a giant cell tumor on the gum or in the bone is a manifestation of hyperparathyroidism. The so-called pregnancy “tumor” is a hyperplasia, developing in the course of a chronic gingivitis, which is not infrequently observed in pregnant women but sometimes also with other hormonal alterations (e.g., puberty). Bleeding, particularly of the interproximal papillae, with light raspberry to dusky red coloration, is an early sign, followed by a hypertrophic swelling of the papillary gingiva, ranging from a slight bloating to a tumor of 1 to 2 cm. It may envelop more than one tooth. The growth regresses with proper oral hygiene and adjusted toothbrush technique, though surgery may be required because of constant bleeding. Generally, tumors that are not too large disappear after delivery. The ameloblastoma, sometimes termed adamantinoma or adamantoblastoma, is an epithelial neoplasm occurring chiefly in the mandible (region of the third molar, ramus, or premolar, in that order of frequency); it belongs to the group of odontogenic tumors (as do the myxoma and cementoma) (not illustrated). According to generally accepted belief, the ameloblastoma originates from remnants of the enamel or dental lamina, but from less differentiated cells (preameloblasts) than those producing a follicular cyst. The tumor is mostly polycystic, sometimes monocystic, and occasionally solid. It is this solid form that on rare occasions has been found to metastasize. The growth of this other-wise benign tumor is very slow. Microcystic infiltration, roentgenologically revealed by tiny locules or notching, enlarges the jaw; the only sign is often a tiny bony capsule distending the surrounding tissue. Eventually, expansion into the orbit, antrum, and even cranium may take place. The most common variety, microscopi- cally recognizable, is the ameloblastic type, character- ized by follicles resembling enamel, with its outer layer of cylindrical cells and stellate reticuloma in the center. Occasionally, solid strands of undifferentiated cells or sheaths of stellate cells or an accumulation of squamous and prickle cells may be found. A microscopic descriptive grading of ameloblastoma is necessary for proper management of each case and for the choice between local or radical removal. The recurrence rate of ameloblastoma is extremely high, but true malignancy is extremely low. Made up of mixed ectodermal and mesodermal tissue, the odontoma, also odontogenic in origin, may be a hard or soft tumor, depending upon the presence or absence of calcified accretions. The hard odontoma is composed of abnormally arranged enamel, dentin, and cementum, in a soft fibrous matrix that is gradually replaced by the calcified elements, leaving a capsule. Complex odontomas contain a bizarre conglomeration of hard structures without finite shape; compound odontomas include both rudimentary and apparently normal supernumerary teeth, at times numbering several dozen. These structures may erupt and imitate the normal dentition. Myxoma of the jaw (not illustrated), derived from embryonal tissue of the dental papilla, is also a benign odontogenic tumor, as is the cementoma, a special form of fibroma, which appears usually at the apices of the lower anterior teeth. Multiple cementomas appear only in women, suggesting an estrogenic influence. Osteoma (not illustrated) is a compact osteogenic tumor, and fibroosteoma is a diffuse one. Both are slow-growing benign neoplasms; a conservative surgical approach is used when the tumors may lead to deformities.

Manifestations of diseases of the oral cavity Pain- the oral cavity- richly supplied with sensory nerve endings- pain is a feature of all diseases, including disorders of the teeth Changes of the oral mucosa- such as ulcerations, vesicular lesions (blisters), changes in colour Ulcers- occur in many diseases, including infections, allergy, trauma, and neoplasns Blisters- infections, such as herpes virur, and immunologic diseases Leukoplakia- white plaques on the mucosa- in hyperkeratosis, in dysplasia Melanin pigmentation- Peutz-Jeghers syndrome-is rare congenital syndrome with autosomal dominance, characterized by melanotic pigmentation of mucosal and skin surfaces, and increased risk of carcinoma of pancreas, breast, lung and ovary, in addition patients have multiple polyps in small intestine and colon Addison disease -uncommon condition characterized by melanin pigmentation of skin and mucosa following destruction of the adrenal cortex, this results in increased stimulation of pituitary gland, high level of ACTH and MSH Mass lesions- solid or cystic Non-neoplastic disorders of the oral mucosa Developmental anomalies White lesions and patches Infections Pseudotumors Developmental anomalies Oral mucosa is subject to the same range of developmental anomalies such as skin, and may be involved in head and neck syndromes, but also there are anomalies confined to the oral mucosa itself 1. Fordyce spots- heterotopic development of sebaceous glands in oral mucosa- produce yellow spots and nodules 2. Peutz-Jeghers syndrome- (periorifacial lentiginosis)- autosomal dominant condition with nearly complete penetrance, it is composed of melanocytic macular pigmentation of the lips, oral mucosa, skin together with intestinal polyposis, most numerous hamartomatous polyps in small intestine, the polyps have a low malignant potential, those in colon with higher risk -the patients are in higher risk of malignancies at other sites, including ovary, uterus and breast -the facial pigmentation is around lips, eyes and nose and may disappear in adulthood -mucosal pigmentation tends to persist to adulthood 3. Congenital epulis- present at birth as mass attached to the gingiva, histologically composed of large granular cells with eosinophilic cytoplasm, covered by stratified hyperplastic squamous epithelium- completely benign White patches. White sponge naevus- is rare autosomal dominant inherited condition, may be congenital or develop later in life mainly affects buccal mucosa, may involve lips and other oral mucosa family history can be detected in all cases histologically: there is acanthosis, parakeratosis, and edema with hydropic degeneration of the cells in the stratum spinosum, epithelium is not dysplastic, there is no inflammation, no relation to tumor Frictional keratosis- is a common cause of intraoral white patches and may be due to sharp edges of teeth or to cheek and lip sucking, it is a response to low grade irritation microscopy may show acanthosis or epithelial atrophy, thick layer of orthokeratosis and prominent granular cell layer, or less commonly hyperparakeratosis with absent granular cell layer there is no significant dysplasia, but sometimes inflammation of the underlying corium, no relation to tumor development clinically- the lesions tend to form diffuse keratotic plaques smoking related keratosis- smoking can result in intraoral plaque formation histologically-atrophic or hyperkeratotic epithelium with patchy inflammation and melanin pigment in the underlying corium- pigmentary incontinence-release of melanin from demaged cells there is no significant dysplasia may be seen in reverse smokers, who hold the burning end of cigarette inside the mouth, this one may be associated with dysplasia acute oral candidosis-oral infections with candida albicans are common, it forms creamy white plaques which can be rubbed off to leave a dry, red mucosa histologically-loose parakeratotic plaques infiltrated by leukocytes (intraepithelial microabscesses) with hyphae- difficult to be seen in HE stained sections but are readily visualised by staining with PAS or silver impregnation methods, such as Grocott wide variety of factors predispose to infection, such as depressed cellular immunity, and inhibition of normal oral flora by broad spectrum antibiotics chronic hyperplastic candidosis (candidal leukoplakia)-Candida albicans can be present in persistent, adherent white plaques- solitary or multiple microscopy- shows a parakeratotic plaque infiltrated by leukocytes, acanthosis and inflammatory infiltrate in the corium, epithelium has elongated rete ridges with thinning of the suprapapillary epithelium giving a resemblance to cutaneous psoriasis, candidal hyphae can be visualized within parakeratotic layer hairy leukoplakia- patients infected with HIV frequently develop painless, white plaques on the lateral border of the tongue and occassionally elsewhere in the mouth microscopy-shows irregular parakeratosis with or without candidal hyphae, vacuolated cell with dark pyknotic nuclei (koilocytes) in the stratum spinosum, no inflammatory infiltrate in the corium, Epstein-Barr capsid antigen can be detected in the epithelial cell nuclei similar lesions have been reported occasionally in patients receiving immunosupressant drugs following organ transplantations geographic tongue- relatively common idiopathic condition typically characterized by areas with loss of papillae, mild chronic inflammation in corium, leukocytic microabscesses in the epidermis Infections- viral, bacterial and fungal infections of the oral mucosa are comparatively infrequent given the number of microorganisms present in the mouth Viral: 1) herpes simplex stomatitis- caused by HSV type 1- common viral infection- usually is subclinical in only few per cent of infected indiviuals, there are more severe symptoms presenting as widespread gingivostomatitis, characterized by multiple vesicles and ulcers- in children and young adults- systemic symptoms- like fever are present locally severe, painful, but self-limited disease- healing occurs within two weeks, recurrent infections may be associated with abnormalities of cell-mediated immunity HS virus passes up the nerve trunks and infects the ganglia in acute phase, it remains in latent form for long time there Herpes labialis-in some patients- attacks of reactivation of the infection as painful localized vesicular and ulceral lesion -reactivation is always precipitated by exposure to sunlight, fever, common cold, etc. 2) herpangina -is uncommon infection of the oral mucosa by coxsackie virus A, occurs as vesicular lesion on the palate 3) aphtous stomatitis- common lesion characterized by recurrent attacks of painful shallow ulcers on the oral mucosa- nonspecific acute infiltrate cause is unknown- no infectious agent has been identified- self-limited lesion 4) viral warts- viral warts of the oral mucosa present as a lesion similar to condyloma accuminatum histologically: features suggestive of viral etiology such as koilocytosis, numerous mitoses, viral inclusions can be present- detection of HPV DNA sequences within the tissue using in situ hydridization technique assists in diagnosis- HPV type 6, 11 and 16 will be present (human papilloma virus) Bacterial: 1.) Acute ulcerative gingivitis: painful condition with ulceration of the interdental papillae between teeth, the ulcers have irregular margins and are covered with fibrinous exudate -etiology is unclear, and is partly relate to poor oral hygiene -smears from ulcers show mixed population of spirochetes, and fusiform bacteria 2.) Actinomycosis- infection of oral mucosa by actinomyces presents as swelling of the mucosa, the organisms are normally present in the mouth- infection is opportunistic 3.) Tuberculosis- infection of oral mucosa by tbc bacili is now uncommon, presents with tuberculosis ulcers that are secondary to pulmonary tuberculosis 4.) Syphilis- syphilitic infection of the oral mucosa is rare in this country, the chancre of the primary infect may occur on the lips or inside the mouth, mucous patches and ulcers may develop in secondary stage, and tertiary syphilis may present with gumma in the tongue or palate Fungal: 1) candidosis -is caused by Candida albicans, which is present as normal commensal of the mouths of about one-half of the population clinical infection of the oral mucosa is an example of opportunistic infection- occurs for example in patients with increased susceptibility (with immunosupression, in AIDS, in newborns, in patients receiving anti-cancer therapy or long-lasting antibiotic therapy, patients with diabetes mellitus) morphology: edema of the epithelium, ulcerations, Candida produces inflammation, white patches- the budding yeasts and pseudohyphae of Candida can be identified in smears and biopsy specimens from the lesions Pseudotumors and hyperplastic lesions of the oral mucosa Epulis -pseudotumors of gingiva -these are reactive lesions of gingiva, grossly- polypoid masses, most common types are Granulomatous epulis- pyogenic granuloma -reactive inflammatory proliferation of nonspecific granulation tissue grossly: small, bright red nodule with ulceration of the mucosal surface it occurs quite commonly in pregnancy-and it resolves spontaneously Giant cell epulis -distinctive lesion of gingiva composed of multinucleated giant cells and spindle mononuclear cells, giant cell epulides tend to be highly vascularized, there can be considerable amounts of hemosiderin, osseous metaplasia is rather common not true neoplasm-most likely a reactive lesion, however, the lesion tends to recur after excision Fibromatous epulis -composed of fibroblasts and myofibroblasts, the lesions show variable degree of cellularity and collagen, dystrophic calcification may occur, osseous metaplasia is common-osteofibromatous epulis Congenital epulis- usually seen in newborn as a polypoid lesion in the anterior maxilla, often protrude from the mouth as a reddish swelling, histologically - the lesion is composed of large eosinophilic cells with granular cytoplasm- the lesion is entirely benign Fibrous hyperplasia –common tumor-like swelling of oral mucosa, these lesions are considered to be a response to low grade irritation polypoid swellings may be sessile and pedunculated microsopically consist of collagen bundles and moderately cellular fibrous tissue Papillary hyperplasia –typically seen in hard palate, belong to spectrum of denture-related , induced stomatitits Generalized gingival fibrous hyperplasia –familiar or drug induced Hereditary gingival fibromatosis- rare condition with AD trait, may be associated with hypertrichosis, neurological problems, such as epilepsy Drug-induced gingival hypertrophy- seen in about half of patients treated with anti-epileptic drug phenytoin for long period, other drug may roduce similar- cyclosporin Orofacial granulomatosis – characterized by chronic granulomatous inflammation of oral mucosa, the cause is unknown, dg after exclusion of Crohns disease, tbc and sarcoidosis Melkersson-Rosenthal disease-cheilitis granulomatosa,fissured tongue, facial nerve palsy Precancerous conditions and tumors of the oral mucosa The most important neoplasm of the mouth is squamous cell carcinoma- despite the accessibility of the mouth to visual inspection, most oral cancers are detected late and their prognosis is comparable to that of squamous cell carcinoma of the esophagus other malignancies and benign tumor are rare, except of squamous cell papilloma, and salivary gland-derived tumors of the oral mucosa Benign tumors of oral mucosa Benign tumors in the oral cavity may arise - from squamous epithelium, from mesenchymal tissue, from the minor salivary glands Squamous papilloma- are usually small, sessile or pedunculated lesions tehy are composed of fibrovascular core, extensions of which are covered by acanthotic stratified squamous epithelium- no evidence of dysplasia, but koilocytic metaplasia may be present majority of papillomas are viral in origin- koilocytosis is a feature of viral infections -koilocytes- clear cell with polymorphic hyperchromatic nucleus pushed to one side there is no tendency for malignant change Fibroma, lipoma, neurofibroma- benign mesenchymal tumors Granular cell tumor- (myoblastoma)- is not uncommon tumor of the skin and mucosal surfaces, they arise particularly in the mouth, where the dorsum of the tongue is a typical site, histologically-striking pseudoepitheliomatous hyperplasia of the overlying epithelium with usually incospicuous granular cell tumor in the corium (simulates squamous cell carcinoma), the tumor consists of large cells with abundant finely granular cytoplasm- these cells were once thought to originate from muscle cells, however despite the fact that they seem to fuse with muscle, they appear to be of Schwann cell origin Oral pre-malignancies There is a wide range of mucosal disorders in which squamous cell carcinoma has been shown to develop more easily Pre-malignant lesions- which show histologically detactable mucosal changes Pre-malignant conditions- more widespread or systemic disorders affecting oral mucosa where cancer is statistically more likely to develop- although the site is unpredictable pre-malignant lesions include: for example leukoplakia, palatal changes associated with smoking, and pre-malignant conditions- sideropenic atrophy and dysphagia caused by iron deficiency LEUKOPLAKIA- this is a term best defined clinically to denote a white patch or plaque according to this definition - heterogenous group of lesions among which epithelial dysplasias- have pre-malignant potential in most cases leukoplakia represents only simple hyperkeratosis resulting from chronic irritation, in minority of cases- there is dysplasia- persistent leukoplakia should be biopsied Epithelial dysplasia- lesions characterized by disordered cell maturation and proliferation associated with increased risk of progression to maligancy histologically-irregular hyperplasia of cells with basal cell morphology, rete ridges show a drop-shaped configuration, loss of both polarity of cells and normal stratification of the epithelium, nuclear changes, such as increased nuclear-cytoplasmic ratio, hyperchromatism and pleomorpism, mitoses in the upper layers of epithellium, abnormal mitoses, individual cell keratinisation often in deep layers (dyskeratosis or premature keratinisation), and loss of celllular cohesion -three degrees of dysplasia can be distinguished- mild, moderate, and severe Malignant tumors of oral mucosa 1) Oral squamous cell carcinoma -accounts for over 90% of all malignant tumors of oral cavity- more common in older men it is important to consider the site of involvement -most commonly it arises in the lower lip (40%), lateral margin of the tongue (20%), floor of mouth (15%)- involvement of the upper lip, palate, gingiva and tonsillar area is less common etiologic factors include cigarette and pipe smoking, alcohol, the lip is more commonly affected in white-skinned people exposed to prolonged sun light- particularly high male predominance grossly- the oral cancer mainly presents as an ulcer, lump, or red or white lesion histologically- majority of oral cancers are well or moderatelly differentiated squamous cell carcinomas well-differentiated carcinoma- is composed of epithelial islands which resemble normal stratified squamous epithelium, except that they are invading the underlying tissues and show aberrant abnormal keratinization, there is often a prominent keratin formation in the infiltrating islands, usually strong host response of lymphocytes in the stroma, the tumor may be frankly deeply invasive poorly differentiated carcinoma- are associated with poorer prognosis, keratin formation is minimal, malignant cells do not exhibit distinction between basal and suprabasal population, mitoses are more frequent, and host response is usually less conspicuous than in better differentiated carcinomas poorly differentiated carcinomas are sometimes difficult to be distinguished from other malignancies, such as high grade lymphomas, malignant melanomas and sarcomas- correct diagnosis can be helped by means of immunohistochemistry using antibodies against epithelial markers (cytokeratin), mesenchymal markers (vimentin, desmin, actin), and melanoma markers, etc patterns of spread- muscle, adipose tissue and other connective tissue tend to be invaded readily by oral cancer, salivary gland tissue and bone provide some resistence to invasion lymph node spread is a relatively late feature of oral cancer- the pattern follows the main anatomical drainage pathways from the primary site- most commonly involved is submandibular lymph node prognosis and treatment : depends on the stage of the disease and on the site of primary tumor compared with favourable prognosis for lip cancer- treated by surgery alone or combination of surgery and radiotherapy- five-year survival is around 70% intraoral cancer has poor prognosis- 5-year survival lower than 40% other significant adverse factor is the size of tumor at presentation lymph node metastases, old age (more than 70), and poor histological differentiation- adverse prognostic factors 2) verrucous carcinoma- is a variant of oral squamous cell carcinoma with predominantly exophytic growth pattern, with minimal invasion, microscopy- shows acanthosis with low degree of epithelial atypia, the advancing margin of the tumor forms pushing margin rather than the finger-like invasion of squamous cell carcinoma it tends to have a rather indolent course with minimal if any capacity for metastases- very good prognosis- treatment - only surgery, radiotherapy should be avoided

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Cysts of Jaw and Oral Cavity Nonepithelialized cysts of the mandible or maxilla may result from trauma with intermedullary hemorrhage, or they may be manifestations of monostotic and polyostotic fibrous dysplasia (disseminated or localized osteitis fibrosa) and generalized osteitis fibrosa, also called cystic osteodystrophy (von Recklinghausen disease). Because the latter conditions are systemic disorders of the bones or endocrine system (primary or secondary hyperparathyroidism), they will not be discussed in this volume. The lesions are more often solid than fluid in content and are recognized as cysts chiefly by their radiographic appearance. The epitheliated cysts of the jaws are etiologically divided into radicular, follicular, and facial cleft cysts. The periapical or radicular cyst has an inflammatory basis and evolves from a granuloma at the root apex of a tooth devitalized by caries or trauma. Bacteria and toxins of the infected pulp canal stimulate proliferation of epithelial remnants left in the periodontal membrane from Hertwig sheath, after it has been ruptured and fragmented by the developing tooth. Eventually, this epithelium lines the necrotic center of the granuloma and thickens, tending to isolate the inflammatory process. A fibrous capsule develops outside the epithelial sac, and the lumen increases by transudation of fluid. Round cell infiltration of the cyst membrane, including the adjacent connective tissue and cellular debris, pus, macrophages, and cholesterol crystals are usually found histologically. Even if the tooth with the granuloma is removed, the cyst remains and may even expand more rapidly as a sterile lesion. The dentigerous or follicular cyst arises from the enamel epithelium of the dental follicle forming around the crown of an unerupted tooth. It is a benign, noninflammatory cyst thought to be developmental in origin. Infection is present only when contiguous teeth are coincidentally abscessed. The pathogenesis of follicular cysts begins with retrograde changes and edema in the enamel organ, which, by expansion, assumes various shapes above the developing crown. A simple follicular cyst forms before enamel is excreted, arresting tooth maturation or growing entirely separate from the tooth. A dentigerous cyst arises at a later phase, after amelogenesis, and gradually envelops the crown, thus interfering with eruption. The tooth may be forced by the cyst fluid to a site remote from its normal position in the jaw. A follicular cyst is usually unilocular, but multilocular forms occur. The most frequent location is the mandibular third molar region. Until the cyst attains a large size and expands the cortical plate of bone, the cyst may remain unrecognized. The buccal, palatal, or alveolar bone may then bulge outward, or the maxillary sinus or nasal cavity may be invaded. The wall of the cyst becomes parchment thin and yields a crackling sound on palpation. Due to the pressure of the cyst and the crowding of roots, the adjoining teeth are tilted when viewed on radiographic imaging and unerupted teeth are displaced in total. Teeth are not devitalized and resorption of roots is not encountered. A smooth, encapsulating layer of cortical bone, a unilocular shape, and the absence of root erosion distinguish a cyst from an invasive neoplasm, ameloblastoma, benign giant cell tumor, and osteitis fibrosa localisata or generalisata. However, a cyst secondarily infected from an adjacent tooth shows an obliterated capsule and appears infiltrative. Also, a few cysts may be multilocular and cannot be completely distinguished from ameloblastoma without biopsy examination. A layer of compact bone borders the cyst sac, which is composed of fibrous connective tissue lined with epithelium. The latter is stratified squamous, ranging from thin to a considerable thickness; in some cysts, it may be simple columnar. The fluid content is clear and straw colored, with an iridescent sheen imparted by cholesterol crystals, or thick and cheesy from epithelial and hemorrhagic debris. Facial cleft cysts, also called fissural cysts, form at the junction of the embryonic segments that fuse to make up the jaws. They may be found at the median fissure of the palate, maxillary bones or mandible (midline or median cyst), or nasoalveolar junction. The nasopalatine cyst, because it is formed in the incisive canal or the incisive foramen from remnants of the fetal nasopalatine communication, may be grouped with the facial cleft cyst. Irritation or mucous secretions likely play an etiologic role in the more superficial type. Ordinarily, a nasopalatine cyst presents no clinical swelling, unless it is very large, and is detected only on radiographic examination. A radiolucent area appears in the midline between the apices of the central incisor teeth and is often misinterpreted as a radicular cyst. The size varies from slight enlargement of the incisive fossa to one of a few centimeters, involving a higher part of the incisive canal. If retention of serous or mucoid secretion produces swelling in the region of the interincisive papilla, discharge from the two tiny orifices on the side of the papilla may be expressed. Secondary infection may occasionally ensue, producing a fluctuant swelling of the palatal mucosa, resembling a dentoalveolar abscess. Mucopurulent discharge then appears at the incisive outlets on pressure. In edentulous mouths, resorption of the alveolar ridge may expose a nasopalatine cyst that escaped previous detection. Cysts of the oral mucous membranes are retention cysts of the mucous glands or their ducts or, occasionally, the sublingual salivary gland. The mucocele may appear on the inner surface of the lips or cheeks, especially at a level parallel to the occlusal plane, where chewing injuries cause obstruction of the mucous ducts. A round, translucent, sometimes bluish swelling may range from a very minute size to a centimeter. In the tongue, the glands of Blandin and Nuhn may form more deeply seated mucoceles, which reach a considerable size, presenting a swelling on the anterior ventral surface. The ranula is named for its resemblance to a frog’s belly; the term is a rather loose one applied to cystic swellings of the floor of the mouth. A common error is to attribute a ranula to obstruction of the submandibular (Wharton) duct, which in the presence of a typical ranula is found patent. The most frequent cause is the occlusion of an excretory duct of the sublingual gland. In a few cases, a ranula may arise from the incisive glands in the midline or from the ciliated cysts that carry epithelium (Bochdalek “glands”), which are derived from the primitive thyroglossal duct. A typical ranula begins in the lateral anterior floor of the mouth immediately beneath the mucous membrane. It usually grows slowly, but rapidly developing cystic swellings (acute ranulas) are also known. The color is bluish gray, with numerous small vessels well outlined. Palpation gives a decided impression of fluid confined by an elastic membrane; the wall may rupture spontaneously but soon refills. As it reaches large proportions it crosses the midline and shows a division marked by the frenulum, also displacing the tongue and impeding speech. A ranula will sometimes bulge downward toward the chin because a portion of the sublingual gland perforates the mylohyoid muscle. Dermoid cysts, owing their origin to inclusion of ectodermal structures by the mesoderm during the embryonic development of the head, usually become visible only in the second or third decade of life. They are located in the midline beneath the chin or between the geniohyoid muscles deep in the floor of the mouth, or in a lateral position beneath the angle of the jaw. The cyst consists of a fibrous capsule lined with a stratified, squamous epithelial membrane, with a cheesy or semisolid mass containing sebaceous material and hair filling the lumen. Theoretically, teeth and other appendages may be present. The dermoid may reach large proportions and protrude in the neck or beneath the tongue as a soft or semifirm doughy lump that pits on pressure and is not fluctuant. The color tends to be waxy or yellowish when the mucosa is thin enough to reveal it.

INCREMENTAL LINES OF DENTIN: E- Enamel D- Dentin PD- primary Dentin SD- Secondary Dentin LVE- Lines of Von Ebner CLO- Contour Lines of Owen PC- Pulp Chamber Incremental Lines of Dentin by Vimi Mutalik is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License. Based on a work at www.oralpathology.in.

Oral Manifestations in Hematologic Diseases Though oral manifestations in hematologic disorders typically appear after disease progression, bleeding from or texture or color changes of the oral mucosa can be the presenting symptom. The prominent oral signs of thrombocytopenic purpura include widespread capillary oozing from the gingival margin of all the teeth. From adherent clots a fetid odor may emanate. Spontaneous hemorrhages of greater severity may arise, especially in areas of inflammation. Petechial spots also appear as purplish red patches on the lips and other mucosa. Erosion and ulcerations are seen only in debilitated, advanced cases. In the acute phases of agranulocytosis, ulcerative lesions of the mouth and pharynx, accompanied by dysphagia, are frequently seen and may be the initial presentation of the disease. The disease may be acute or chronic (cyclic and recurrent); it may be primary or a sequel of a systemic infection, hormonal dysfunction, or idiosyncratic drug reaction. Because the myeloid cells are arrested in maturation, the mucous membranes are subject to rapid invasion of bacteria. With sudden onset the oral mucosa is involved by necrotic ulcers, which show little or no surrounding erythema. All types of gingivitis and stomatitis with gangrenous areas have been observed in the pharynx, tonsils, and hard palate. Malodourous breath and excessive salivation can be seen in severe presentations. The frequency of oral lesions in chronic leukemia is appreciable and varies considerably in severity. Beginning insidiously, pallor of the mucous membrane may be followed by soft hypertrophy and ulceration of the gingivae, with spontaneous bleeding, and fusospirochetal infection in necrotic papillae, producing a foul odor. A blackish, pseudomembranous exudate may cover the tongue, gingivae, and fauces. Enlargement of the gingiva begins usually in the lower interior region. Teeth may loosen, and pulpal liquefaction or abscessed pulps with odontalgia may appear. In the lymphatic form the lymphoid structures of the floor of the mouth and tongue, together with the submandibular lymph nodes, may become enlarged. In general, the acute leukemias produce symptoms more severe than the chronic variants. In polycythemia vera (erythremia, or Vaquez disease), the skin and oral tissues show a vivid purplish red discoloration. Superficial vessels are distended, and the gingivae are swollen and bleed frequently. Petechiae are often noted. In pernicious anemia, the oral mucosa accepts a pale or greenish yellow color, except for the tongue, which is bright red. The latter is in a state of chronic inflammation, characterized by irregular, fiery-red patches resembling a burn, near the tip and the lateral margins (Hunter or Moeller glossitis). A sensation of burning, itching, or stinging is always present, and patients complain of paroxysmal pain or tenderness to food intake or to cold and hot fluids. These symptoms appear in the early stages of pernicious anemia, sometimes prior to or during periods of hematologic remission. The later stages of the oral manifestations, including the gradual loss of the papillae and progressive atrophy of the tongue, are rarely encountered. Tongue manifestations of the disease must be distinguished from other forms of glossodynia and glossopyrosis, from allergic lesions, from the lingual anifestations in syphilis, and from geographic tongue.

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