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ORAL SUBMUCOUS FIBROSIS

ORAL SUBMUCOUS FIBROSIS. DEFINITION. (J.J Pindborg and Sirsat 1966)

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ORAL SUBMUCOUS FIBROSIS

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  1. ORAL SUBMUCOUS FIBROSIS www.rxdentistry.co.in

  2. DEFINITION (J.J Pindborg and Sirsat 1966) It is an insidious chronic disease affecting any part of the oral cavity and sometimes the pharynx. Although occasionally preceded by and /or associated with vesicle formation ,it is always associated with juxta-epithelial inflammatory reaction followed by a fibro-elastic changes of the lamina propria with epithelial atrophy leading to stiffness of the oral mucosa and causing trismus and inability to eat. www.rxdentistry.co.in

  3. History • The condition of oro -pharyngeal OSMF of oral cavity was prevalent even in the days of Shushrutha (600 B.C). • Shushrutha, the greatest practitioner of ancient medicine stated in his book "Shushrutha Samhita' a condition called 'VIDARI' in his classification of diseases of mouth and throat. • The features of which suit the symptomatology of OSMF. www.rxdentistry.co.in

  4. First described among five East African women of Indian origin under the term Atrophia idiopathica (tropica) Mucosae Oris by Schwartz 1952 • Joshi in 1953 is credited to be the first person who described it and gave the present term “Oral sub-mucous fibrosis”. • In the year 1954, Su. 1. P. from Taiwan described similar condition, which he called "Idiopathic Scleroderma of mouth" www.rxdentistry.co.in

  5. Paymaster (1956) described the pre-cancerous nature of the condition. Other names that have been suggested are: • Diffuse oral sub-mucous fibrosis (Lal D.1953) • Sclerosing stomatitis (Behl 1962) • Idiopathic palatal fibrosis (Rao 1962) www.rxdentistry.co.in

  6. EPIDEMIOLOGY • OSMF is a crippling fibrotic disorder seen commonly in India and Indian subcontinent. Sporadic cases are seen in Malaysia, Nepal, Thailand and South Vietnam. • Incidence of OSMF in India is 0.2-0.5% of population. • Persons between 20 and 40 years of age are most commonly affected ,but ages have ranged from 2 to 89 years of age • No cast or religious community is especially affected www.rxdentistry.co.in

  7. Case reports also include occurrence of this condition in a 4 yr old Indian immigrant girl in Canada, who had been chewing arecanut since the age of 2 yrs. • Prevalence rate in India ranges from 0.2 to 1.2% www.rxdentistry.co.in

  8. ETIOLOGY www.rxdentistry.co.in

  9. Etiology of OSMF: Exact etiology is unknown. The suggested factors are, 1. Chronic Irritation Chilies Lime Betel nut Tobacco Chewing 2. Deficiency disease. 3. Defective iron metabolism 4. Bacterial Infection 5. Collagen disorder 6. Immunological disorders 7. Genetic disorder. www.rxdentistry.co.in

  10. Chronic irritation: • Pathogenesis of OSMF lies in the continuous action of mild irritants. Chillies: • "Capsaicin" a active extract from capsicum. • The active principle irritant of chillies (Capsicum annum and Capsicum frutescence) . www.rxdentistry.co.in

  11. The suspicion that chilli is an etiological agent arose on the basis of ecological observations and was strengthened by the clinical and histological characteristics of this condition , i.e. • Blood eosinophilia, • Tissue eosinophils in the biopsy specimen and presence of sub epithelial vesicles suggested an allergic nature of this disease possibly due to chilli intake. www.rxdentistry.co.in

  12. There are some ecological arguments against the chilli hypothesis for example from Mexico or other South American countries where chilli consumption is widespread, there is no report of this condition. • The overall assessment is that there is no evidence substantiating the etiologic role of chilli in OSMF www.rxdentistry.co.in

  13. Lime: • Betel nut & lime mixture is used for chewing. This also contains arecoline, lime and tannic acid, These cause local irritation and damage to the mucosa with vesicle and ulceration on susceptible individual. • Lime in betel quid causes constant aberration of oral mucosa, allowing direct access to the carcinogens www.rxdentistry.co.in

  14. Tobacco Chewing • It is a known irritant and a causative factor in oral malignancies • N’-nitrosonornicotine is produced by bacterial and enzymatic nitrosation of nicotine and can be found by reaction of salivary nitrates with nornicotine • N’-nitrosonornicotine levels increased 44% when tobacco was mixed with saliva • N’-nitrosonornicotine extracted from chewing tobacco with saliva is approximately 1000 times that found in cigarette smoke www.rxdentistry.co.in

  15. Betel nut: • Considered to be one of important etiological factor for OSMF • In India arecanut is chewed by itself or in the form of various areca nut preparations such as supari, mawa , manipuri , pan masala and in betel quid either with or without tobacco www.rxdentistry.co.in

  16. The factors that contribute to the pathogenesis in habitual betel nut chewers. 1. The amount of tannic acid (14-18%) contained in the betel nut. 2. The influence of mixed calcium powder. 3. Action of arecoline contained in the betel nut affecting the vascular nerve of oral mucosa and causing neurotropic disorder www.rxdentistry.co.in

  17. Arecanut contain different type of alkaloids- arecoline, arecadine, guvacoline, guvacine and isoguvacine. • Nitrosation of arecoline leads to the formation of arecanut specific nitrasamine. All arecanut specific nitrosamines are found to be powerful carcinogens and alkylate DNA. www.rxdentistry.co.in

  18. KHANNA AND ANDHARA , have suggested pathogenesis of OSMF by dual action of arecanut. They suggested that , • Arecoline , stimulate fibroblastic proliferation and collagen synthesis. • The flavonoids catechin and tannins stabilize the collagen fibrils rendering them resistant to degradation by collagenase. • The attendent trismus is a result of juxtaepithelial hyalinization and secondary muscle involvement (i.e. muscular degradation and fibrosis) • The habit of chewing areca nut leads to muscle fatigue www.rxdentistry.co.in

  19. Deficiency disease • Vitamin B12 and Iron deficiency are associated with OSMF. The deficiency could be due to the fact that defective nutrition due to impaired food intake in advanced cases of OSMF, may be the effect rather than the cause of the disease www.rxdentistry.co.in

  20. Defective iron metabolism • Impaired cellular utilization of iron explains the presence of hypochromic microcytic anemia. There is no definite proof to support the hypothesis that defective iron utilization by oral mucosa and sub-mucosa is the cause of OSMF www.rxdentistry.co.in

  21. INFECTIONS • Mukherjee and Biswas (1972) suggested that there is: • Rise in mucoprotein and mucopolysaccharide level • Rise in anti-streptolysin - O titre in OSMF patients. (But these works are not confirmed) www.rxdentistry.co.in

  22. Collagen disorder: • Rao (1962) suggested that OSMF is a localized condition of collagen disease. • He linked it to scleroderma, rheumatoid arthritis, duputreyens contracture and intestinal fibrosis. Histological features were found to be similar in OSMF and scleroderma. www.rxdentistry.co.in

  23. HARMONAL FACTORS • There would appear to be predisposition in female with a ratio of women to men of 3:1 (Pillai R et al “pathogenesis of Oral submucous fibrosis”, cancer 1992 ;69:2011-2017) www.rxdentistry.co.in

  24. IMMUNOLOGICAL DISORDER: • Oral Submucous fibrosis is a high risk pre-cancerous condition. Raised ESR and globulin levels are found, indicative of immune inflammatory disorder. • Serum immunoglobulin levels IgA, IgG and IgM levels are raised. These suggest an antigenic stimulus in absence of any infection. • Increased circulating immune complex in OSMF www.rxdentistry.co.in

  25. Genetic predisposition to the disease , involving the HLA antigens ,A10,DR3,DR7and probably B7 and the haplotypic pairs A10/DR3 and A10/B8 has been demonstrated. www.rxdentistry.co.in

  26. The increased evidence of CD4 and HLA-DR-positive cells and high ratio of CD4 to CD8 in OSF tissue suggest an ongoing cellular immune response leading to imbalance of immunoregulation and alteration in local tissue architecture. www.rxdentistry.co.in

  27. Mast cells • Mast cells are characterized by numerous cytoplasmic granules. Its cytoplasm contains mucopolysaccharides, histamine and heparin. • Many patients with early stage of OSMF give history of feeling of itching sensation which could be due to release of histamine exact role of mast cells in inflammation is not known. www.rxdentistry.co.in

  28. TOBACCO LIME VOLATILE LIQUIDS VOLATILE OILS ARECANUT MULTIFACTORIAL PATHOGENESIS HYPERSENSITIVITY CHEMICAL BURN MECHANICAL TRAUMA TANNIN& AFLOTOXIN ARECOLINE GENETIC REDISPOSITION ALTERED IMMUNITY DEGRADATION OF COLLAGEN INCREASED SYNTHESIS OF COLLAGEN FIBROBLAST FORMATION IRREVERSIBLE FIBROSIS CACINOMA EXPOSURE CONTINOUS www.rxdentistry.co.in

  29. Brief review : pathogenesis of OSMF • Section of fibroblasts with a high amount of collagen production during long term exposure to arecanut ingredients. • Stimulation of fibroblast proliferation and collagen synthesis by arecanut alkaloids or by fibrogenic cytokines secreted by activated macrophages and T lymphocytes in the OSF tissue www.rxdentistry.co.in

  30. Decreased secretion of collagenase and deficiency in collagen phagocytosis by OSF fibroblasts • Production of collagen with a more stable structure (collagen type I trimer) by OSF fibroblast. • Stabilization of collagen structure by catechin and tannin from arecanut and an increase in collagen cross linkage caused by up regulation of lysy oxidase by OSF fibroblast www.rxdentistry.co.in

  31. Malignant transformation rate is 7.6% (JIAOM, vol-iv;no.3& 4 July-Dec.1993, p 12-15) www.rxdentistry.co.in

  32. CLINICAL FINDINGS • The data regarding the sex predilection is conflicting. Earlier it was thought to be common in females. • But at present ,study ratio shows 2.3: 1 =M:F • Age group common is 2 to 3rd decade of life • But cases have been reported from 4 year to 86 yrs www.rxdentistry.co.in

  33. Prodromal symptoms : • Onset is insidious. The most common initial symptoms are: • Burning sensation on eating spicy food • Blisters on the palate • Ulceration or recurrent stomatitis • Excessive salivation • Defective gustatory sensation • Dryness of mouth. www.rxdentistry.co.in

  34. Later, • Difficulty in opening mouth • Inability to whistle, blow • Difficulty in swallowing • When fibrosis involves pharynx- referred pain to the ear. • Changes in tone of the voice due to vocal cord involvement • Some times deafness due to occlusion of eustachian tubes www.rxdentistry.co.in

  35. COMMON SITES INVOLVED • Buccal mucosa, faucial pillars ,soft palate, lips and hard palate. • The fibrous bands in the buccal mucosa run in a vertical direction ,sometimes so marked that the cheeks are almost immovable. • In the soft palate the fibrous bands radiate from the pterygomandibular raphe or the faucial pillars and have a sear like appearance www.rxdentistry.co.in

  36. The uvula is markedly involved , shrinks and appears as a small fibrous bud. • The faucial pillars become thick , short, and extremely hard. • The tonsils may be pressed between the fibrosed pillars • The lips are often affected and upon palpation , a circular band can be felt around the entire rima oris • When gingiva is affected , it is fibrotic, blanched and devoid of its normal stippled appearance. www.rxdentistry.co.in

  37. BLANCHING LOWER LABIAL MUCOSA AND FLOOR OF MOUTH www.rxdentistry.co.in

  38. INVOLVING LOWER LABIAL MUCOSA www.rxdentistry.co.in

  39. UVULA SHRUNKEN GIVING HOCKEY STICK APPEARANCE www.rxdentistry.co.in

  40. PALE AND BALD TONGUE www.rxdentistry.co.in

  41. INTERINCISAL OPENING MEASUREMENT www.rxdentistry.co.in

  42. SOFT PALATE www.rxdentistry.co.in

  43. TRISMUS www.rxdentistry.co.in

  44. Clinically signs of OSMF can be grouped as: • Stage I : Stage of stomatitis & vesiculation • Stage ll : Stage of fibrosis • Stage III : Stage of sequelae complication www.rxdentistry.co.in

  45. Stage of stomatitis & vesiculation • It is earliest stage and characterized by recurrent stomatitis and vesiculation. Patient complaints of burning sensation in the mouth & inability to eat spicy food. • On examination vesicles on palate are seen. • They rupture and form superficial ulcers. • Some amount of fibrosis is also present. www.rxdentistry.co.in

  46. Stage ll: Stage of fibrosis • There is inability to open mouth completely and stiffness in mastication. As disease advances there is difficulty in blowing out cheek & protruding tongue. Sometimes pain in ear and speech is muffled.On examination there in increasing amount of fibrosis in the submucosa. This causes blanching of mucosa. • Lips & checks become stiff & loose their normal resistance. Shortening & disappearance of uvula in advanced cases. • Dorsum of tongue shows atrophy of papillae. • Mucosa of floor of mouth show blanching & stiffness www.rxdentistry.co.in

  47. Stage of sequelae & Complication • Patient presents with all the complaints as in stage II. Also there may be evidence of leukoplakia. • Changes in mucosa are whitish or brownish black- • Pindborg et al (1967) found the OSMF was found in 40%cases of oral cancer than in general population 1.2%. www.rxdentistry.co.in

  48. CLINICAL GRADING OF SEVERITY OF OSMF www.rxdentistry.co.in

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