Immunoexpression of alpha smooth muscle actin correlates with serum transforming growth factor‐β1 levels in oral submucous fibrosis. Issue 4 (21st October 2019)

• Record Type: Journal Article
• Authors: Singh, Iqbal; Juneja, Saurabh; Tandon, Ankita; Jain, Anshi; Shetty, Devi Charan; Sethi, Aashka
• Is Part Of: Journal of investigative and clinical dentistry. Volume 10:Issue 4(2019)
• Page Start: n/a
• Page End: n/a
• Publication Date: 2019-10-21
• Subjects: enzymelinked immunosorbent assay -- oral submucous fibrosis -- transforming growth factor‐β1 -- alpha‐smooth muscle actin; Dentistry -- Periodicals; Mouth -- Diseases -- Periodicals; Mouth Diseases -- Periodicals; Tooth Diseases -- Periodicals; 617.6
• DOI: 10.1111/jicd.12473
• Languages: English
• ISSNs: 2041-1618

Abstract

Abstract: Aim: The aim of the present study was to correlate the immunoexpression of alpha‐smooth muscle actin (α‐SMA) for myofibroblasts with the serum levels of transforming growth factor‐β1 (TGF‐β1) in oral submucous fibrosis (OSMF). Methods: A total of 100 cases of histopathologically confirmed OSMF were assessed for α‐SMA expression. Clinical data, such as age, sex, mouth opening, and habit history, were obtained for each case. Serum TGF‐β1 levels were recorded in 73 patients with the help of enzymelinked immunosorbent assay technique. Results: The staining index of α‐SMA increased concomitantly with higher myofibroblast count in the increasing histopathological grades of OSMF ( P ≤ .05). Serum TGF‐β1 levels were highest in the intermediate grades of OSMF. Clinical parameters, such as mouth opening, cheek flexibility, and tongue protrusion, showed a direct correlation with increasing clinical grades of OSMF. Conclusions: The progressive increase in myofibroblasts from early to advanced stages suggests their potential use as markers for evaluating the severity of OSMF. Additionally, as myofibroblasts are responsible for producing a variety of factors that are involved in the fibrotic processes; they could be the key link in the pathogenesis of OSMF. Interruption of their development, recruitment, or activation could provide a unique therapeutic target for future treatment options in patients with OSMF.