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On the Indian subcontinent, the use of smokeless tobacco in various forms is very popular. This habit, which usually involves the chewing of a betel quid (combined areca nut, betel leaf, tobacco and slack lime), has led to the development, in a large proportion of users, of a unique generalized fibrosis of the oral soft tissues, called oral submucous fibrosis. While not producing soft tissue masses in the usual sense, the fibrosis may be confused with generalized fibromatosis, hence, is included in this section of the present chapter.
The condition is found in 4/1,000 adults in rural India, and is caused by
the areca nut in the quid. Additionally, it is estimated that as many as
5 million young Indians are suffering from this precancerous condition as
a result of the increased popularity of the habit of chewing pan masala.
It results in a marked rigidity with progressive inability to open the
mouth. There is a fibroelastic transformation of the
juxta-epithelial connective tissues and an increased risk of oral carcinoma
from the tobacco of the quid.
Submucous fibrosis typically affects the buccal mucosa, lips, retromolar areas and the soft palate. Occasional involvement of the pharynx and esophagus is seen. Early lesions present as a blanching of the mucosa, imparting a mottled, marble-like appearance. Later lesions demonstrate palpable fibrous bands running vertically in the buccal mucosa and in a circular fashion around the mouth opening or lips. As the disease progresses the mucosa becomes stiff, causing difficulty in eating and considerably restricting the patient's ability to open the mouth (trismus). If the tongue is involved, it becomes stiff and has a diminished size.
petechiae are seen in more than 10% of cases and most patients complain of a
burning sensation, often aggravated by spicy foods. Salivary
flow is diminished and blotchy melanotic mucosal pigmentation is often seen.
More than a fourth of affected persons develop precancerous leukoplakia
of one or more oral surfaces. Once present, oral submucous fibrosis does not
regress, either spontaneously or with cessation of betel quid chewing.
Pathology and Differential Diagnosis
The early cases of oral submucous fibrosis present as chronic inflammatory cell infiltration of subepithelial connective tissues. This otherwise nonspecific infiltrate usually contains a number of eosinophils, cells seldom found in oral inflammation. Older lesions demonstrate a reduced vascularity, reduced numbers of inflammatory cells, and dense bundles and sheets of collagen immediately beneath the epithelium. The eventual thick band of hyalinized subepithelial collagen shows varying extension into submucosal tissues, typically replacing the fatty or fibrovascular tissues normal to the site.
Minor salivary glands in the area of habitual quid placement often demonstrate a chronic inflammatory infiltrate and replacement of acinar structures by the hyalinized fibrosis. The hyalinized stroma can be distinguished from the amyloid infiltration of amyloidosis through the use of Congo red staining and thioflavin-T staining under polarized and immunofluorescent light.
The epithelium is atrophic, with or without excess surface keratin, and demonstrates intercellular edema. A fourth of the biopsied cases will demonstrate epithelial dysplasia at the time of biopsy. When squamous cell carcinoma is seen, it has the same features of carcinoma as those seen in persons without the betel quid chewing habit.
Treatment and Prognosis
There is no effective treatment
for oral submucous fibrosis and the condition is irreversible once
formed. Plastic surgery may be required to allow for improved
opening of the mouth. Surface leukoplakias are handled by close follow-up
and repeated biopsies of areas of severe involvement. All dysplasias and
carcinomas are treated in the routine manner for those entities. Epidemiological
studies have shown that as many as 10% of oral submucous fibrosis patients
develop an oral carcinoma. Since the tobacco is the component of the quid
most associated with cancer development, cessation of the quid chewing habit
or eliminating the tobacco from the quid will reduce the risk of oral cancer.
Likewise, a certain proportion of precancerous keratoses will diminish or
disappear with habit cessation.
References (Chronologic Order)
Note: General references can be found by clicking on that topic to the left.
Pindborg JJ, Mehta FS, Gupta PC, Daftary DK. Prevalence of oral submucous fibrosis among 50,915 Indian villagers. Brit J Cancer 1968; 22:646-654.
Pindborg JJ. Oral precancer. In: Barnes L (ed). Surgical Pathology of the Head and Neck, Marcel Dekker Co, NY; 1985: 279-331.
Murti PR, Bhonsle RB, Pindborg JJ, et al. Malignant transformation rate in oral submucous fibrosis over a 17-year period. Community Dent Oral Epidemiol 1985; 13:340-341.
Sinor PN, Gupta PC, Bhonsle RB, et al. A case-control study of oral submucous fibrosis with special reference to the etiologic role of areca nut. J Oral Pathol Med 1990, 19:94-98.
Borle RM, Borle SR. Management of oral submucous fibrosis: a conservative approach. J Oral Maxillofacial Surg 1991; 49:788-791.
Bouquot JE, Glover ED, Schroeder KL. Leukoplakia and smokeless tobacco keratosis are two separate precancers. In: Varma AD (ed). Oral oncology. Delhi: MacMillan India, Ltd, 1991; vol 2:67-69.
Jayanthi V, Probert CSJ, Sher KS, Mayberry
JF. Oral submucous fibrosis - a preventable disease. Gut 1992; 33:4-6.Murti PR, Gupta PC, Bhonsle RB, et al. Smokeless
tobacco use in India: effects on oral mucosa. In: Stotts RC, Schroeder KL,
Burns DM. Smokeless tobacco or health, an international perspective. NIH
Publ 93-3461; US Dept Health Human Services, Natl Instit Health, Bethesda,
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