Oral submucous fibrosis (or OSF) is a chronic,complex,irreversible,highly potent pre-cancerous condition characterized by juxta-epithelial inflammatory reaction and progressive fibrosis of the submucosal tissues (lamina propria and deeper connective tissues). As the disease progresses, the jaws become rigid to the point that the sufferer is unable to open his mouth.[1][2] The condition is linked to oral cancers and is associated with areca nut chewing, the main component of betel quid. Areca nut or betel quid chewing, a habit similar to tobacco chewing, is practiced predominately in Southeast Asia and India, dating back thousands of years.
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In 1952, J. Schwartz coined the term atrophica idiopathica mucosa oris to describe an oral fibrosing disease he discovered in five Indian women from Kenya.[3] S.G. Joshi subsequently coined the termed oral submucous fibrosis (OSF) for the condition in 1953.[4]
Oral submucous fibrosis is clinically divided into 3 stages (Pindborg J.J.):[5]
Stage 1: Stomatitis
Stage 2: Fibrosis
a- Early lesions, blanching of the oral mucosa
b- Older lesions, vertical and circular palpable fibrous bands in and around the mouth or lips, resulting in a mottled, marble-like appearance of the buccal mucosa
Stage 3: Sequelae of oral submucous fibrosis
a- Leukoplakia
b- Speech and hearing deficits
Khanna and Andrade in 1995 developed a group classification system for the surgical management of trismus:[6]
Group I: Earliest stage without mouth opening limitations with an interincisal distance of greater than 35 mm.
Group II: Patients with an interincisal distance of 26-35 mm.
Group III: Moderately advanced cases with an interincisal distance of 15-26 mm. Fibrotic bands are visible at the soft palate, and pterygomandibular raphe and anterior pillars of fauces are present.
Group IVA: Trismus is severe, with an interincisal distance of less than 15 mm and extensive fibrosis of all the oral mucosa.
Group IVB: Disease is most advanced, with premalignant and malignant changes throughout the mucosa.
Chronic exposure to beetel nuts, chilli, pepper and prolonged deficiency of iron and zinc may lead to an alteration in oral mucosa, which causes hypersensitivity to these irritants.
This hypersensitivity reaction may often results in a juxta-epithelial inflammation that leads to increased fibroblastic activity resulting in formation of collagen fibres in lamina propria.
These collagen fibers are non degradable and the phagocytic activity is minimized.
In the initial phase of the disease, the mucosa feels leathery with palpable fibrotic bands. In the advanced stage the oral mucosa loses its resiliency and becomes blanched and stiff. The disease is believed to begin in the posterior part of the oral cavity and gradually spread outward.
Other features of the disease include:
Dried products such as paan masala and gutkha have higher concentrations of areca nut and appear to cause the disease
The incidence of the disease is higher in people from certain parts of the world including South-East Asia, South Africa and Middle East.[7]
Biopsy screening is mandatory before treatment. Treatment includes:
Treatment also includes following:
The treatment of patients with oral submucous fibrosis depends on the degree of clinical involvement. If the disease is detected at a very early stage, cessation of the habit is sufficient. Most patients with oral submucous fibrosis present with moderate-to-severe disease. Moderate-to-severe oral submucous fibrosis is irreversible. Medical treatment is symptomatic and predominantly aimed at improving mouth movements.
Recently scientists have proven that intralesional injection of autologous bone marrow stem cells is a safe and effective treatment modality in oral sub mucosal fibrosis. It has been shown autologous bone marrow stem cell injections induces angiogenesis in the area of lesion which in turn decreases the extent of fibrosis thereby leading to significant increase in mouth opening.[8][9]
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