Per Jens J Pindborg and Satyavati Sirsat (1966) (Pathological definition)- '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 a juxta-epithelial inflammatory reaction followed by a fibro-elastic change of the lamina propria, with epithelial atrophy leading to stiffness.'[5]
Per Mohit Sharma and Raghu Radhakrishnan (2019) - 'An insidious, chronic potentially malignant fibrotic disorder affecting the entire oral cavity and sometimes the pharynx and oesophagus. Although occasionally preceded by and/or associated with vesicle formation, it is always associated with a juxta-epithelial inflammatory reaction followed by a fibroelastic change of the lamina propria with epithelial atrophy leading to stiffness of the oral mucosa, progressive decrement in mouth opening and inability to eat'[6]
Per Chandramani More and Naman Rao (2019) (Clinical definition)- 'A debilitating, progressive, irreversible collagen metabolic disorder induced by chronic chewing of areca nut and its commercial preparations; affecting the oral mucosa and occasionally the pharynx and esophagus; leading to mucosal stiffness and functional morbidity; and has a potential risk of malignant transformation.'[7]
The incidence of the disease is higher in people from certain parts of the world including South and South East Asian, South Africa and the Middle Eastern countries.[8]
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. Other causes include:
"Exposure to areca nut (Areca catechu) containing products with or without tobacco (ANCP/T) is currently believed to lead to OSF in individuals with genetic immunologic or nutritional predisposition to the disease."[9]
This hypersensitivity reaction results in a juxta-epithelial inflammation that leads to increased fibroblastic activity and decreased breakdown of fibers. The fibroblasts are phenotypically modified, and the fibers they form are more stable, produce thicker bundles that progressively become less elastic. once the original loosely arranged fibrous tissue is replaced by the ongoing fibrosis, the movability of the oral tissues is reduced, there is loss of flexibility and reduced opening of the mouth.
These collagen fibers are non degradable and the phagocytic activity is minimized.
According to a recent cross sectional study the time taken for return of salivary pH to baseline levels after chewing areca nut containing mixtures is significantly longer in habitual users with OSF when compared to unaffected users.[9] Prolonged Alkaline pH induces death fetal fibroblast type and replacement by a profibrotic fibroblast.[9] The patterns of intraoral fibrotic bands produced by alkaline chemical injury mimic those produced by areca nut chewing.[10] Sharma et al., have equated the pathogenesis of OSF to an over-healing wound, to explain its evolution as well as malignant transformation.[10][11] Increased mechanical stiffness through YAP/TAZ pathway accelerates the malignant transformation of OSF.[12] The atrophic epithelium in OSF has been attributed to the senescence of basal stem cell layer and the development of hyperplastic epithelium through senescence escape.[11][13]
Oral submucous fibrosis is clinically divided into three stages:[14]
Khanna and Andrade in 1995 developed a group classification system for the surgical management of trismus:[15]
interdependent regulators, they could be used as diagnostic makers and a prognostic mirror of oral submucous fibrosis cases[16]
Biopsy screening although necessary is not mandatory most dentist can visually examine the area and proceed with the proper course of treatment.
Treatment includes:
Treatment also includes following:
The treatment of patients with oral submucous fibrosis depends on the degree of clinical involvement.[23] 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. Severe oral submucous fibrosis is irreversible. Moderate oral submucous fibrosis is reversible with cessation of habit and mouth opening exercise. Current modern day medical treatments can make the mouth opening to normal minimum levels of 30 mm mouth opening with proper treatment.
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.[24][25]
In 1952, T.Sheikh coined the term distrophica idiopathica mucosa oris to describe an oral fibrosing disease he discovered in five Indian women from Kenya.[26] S.G. Joshi subsequently coined the termed oral submucous fibrosis (OSF) for the condition in 1953.[27]
This entry is adapted from the peer-reviewed paper 10.3390/ijms21218104