Αρχειοθήκη ιστολογίου

Αλέξανδρος Γ. Σφακιανάκης
ΩτοΡινοΛαρυγγολόγος
Αναπαύσεως 5
Άγιος Νικόλαος Κρήτη 72100
2841026182
6032607174

Τετάρτη 23 Νοεμβρίου 2016

The nature of collagen in oral submucous fibrosis: A systematic review of the literature

VV Kamath

Saudi Journal of Oral Sciences 2014 1(2):57-64

Background: The nature of collagen in the oral potentially malignant disorder of oral submucous fibrosis (OSF) has always been a subject of interest to researchers studying the condition. The type, constitution, and morphology of the collagen has been studied to understand the pathogenesis of the disorder. Aim: The present review attempts to collate literature to assess the changes reported on the nature of collagen in OSF. Materials and Methods: A systematic analysis of literature based on the PRISMA protocol was carried out on studies that analyzed the nature of collagen in OSF. A total of 30 articles were found acceptable for analysis. The reported literature was categorized into histological, immuno-histochemistry (IHC), electron microscopic (EM)/scanning electron microscopic (SEM), biochemical, culture, and genetic studies. Results: Light microscopic studies revealed increased collagen with compaction and condensation as the disease advanced. Polarising microscopy revealed presence of greenish yellow (type I) thick fibers replacing the yellowish orange (type III) thin fibers in the submucosa. Fibrosis originated in the submucosa and subsequently involved the lamina propria as the disease advanced. EM/SEM investigations revealed frayed ends, degeneration of collagen cores. Increased expression of collagen antibodies and total collagen content were observed in IHC and biochemical studies, respectively. Cultured fibroblasts from OSF tend to produce more collagen in comparison to normal fibroblasts indicating a phenotypic change. Increased expression and upregulation of collagen genes were consistent in OSF cases. Conclusion: The collagen deposition in OSF is biochemically normal but quantitatively more. Fibroblast phenotypic change, upregulation of collagen genes, and selective remodeling due to decreased degradation seem to contribute to the increased fibrosis in the disorder.

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