Immunohistochemical panel of degenerated articular discs from patients with temporomandibular joint osteoarthritis
Bruno Viezzer Fernandes, João Armando Brancher, Arieli Carini Michels, Seigo Nagashima, Aline Cristina Batista Rodrigues Johann, Marianna Bóia-Ferreira, Delson João da Costa, Nelson Luís Barbosa Rebellato, Leandro Eduardo Klüppel, Rafaela Scariot, João Cézar Zielak
Abstract
Abstract Background Temporomandibular joint osteoarthritis (TMJOA) is a progressive degenerative disease caused by imbalance between anabolic and catabolic stimuli. Objective The aim of this study was to evaluate histopathological changes, collagen degeneration and the expression of eleven TMJOA biomarkers in articular discs. Methods Specimens were obtained from eight female patients submitted to discectomy. Discs were divided into anterior band (AB), intermediate zone (IZ) and posterior band (PB) for computerised histomorphometric analyses. Each was assigned a histopathological degeneration score (HDS). Collagen degeneration was assessed with Picrosirius‐polarisation method. Biomarkers were evaluated through immunohistochemistry, including IGF‐1, OPG, VEGF, TNF‐α, FGF‐23, IHH, MMP‐3, MMP‐9, TGF‐β 1 , BMP‐2 and WNT‐3. Image processing software was used to calculate average immature collagen ratios and immunostained areas. Spearman rank tests were applied to verify correlations, with significance level of 0.05. Results The HDS showed negative correlation with expression of VEGF in IZ and PB ( P < .05) and positive with TNF‐α in AB ( P < .01). Collagen degeneration correlated with TGF‐β 1 ( P < .05), BMP‐2 ( P < .01) and IHH ( P < .05) immunostained areas in the IZ; TGF‐β 1, BMP‐2 and IHH expression correlated among each other in AB and IZ ( P < .05). Conclusion Angiogenesis and tissue fragmentation may result from aberrant physiologic responses mediated by VEGF and TNF‐α, compromising TMJ discs during OA progression. The expression of TGF‐β 1, BMP‐2 and IHH could be related to collagen degeneration in displaced discs and may participate in TMJOA pathogenesis.