Diminishing reactive adipogenesis leads to disease progression of oral submucous fibrosis.

Oral fibroblasts, similar to dermal fibroblasts, have the potential to resist the local insults like trauma to the oral mucosa by differentiating into adipocytes and secreting antimicrobial peptide cathelicidin (Camp) and this physiologic process in known as reactive adipogenesis. We hypothesize that in oral submucous fibrosis (OSF), due to constant secretion and up-streaming of transforming growth factor-beta (TGF- β), oral fibroblast lose their adipogenic differentiation potential and Camp production, which leads to progressive fibrosis in OSF. The implication of this hypothesis could open some promising vistas on still unexplored innate immune systems harboured by oral mucosa. Restoring and maintaining the adipogenic and protective potential of oral fibroblasts by inhibiting TGF- β receptors could hinder the disease progression of OSF.