Details

Autor(en) / Beteiligte

• Cafferata, Emilio A.
• Monasterio, Gustavo
• Castillo, Francisca
• Carvajal, Paola
• Flores, Guillermo
• Díaz, Walter
• Fuentes, Aler D.
• Vernal, Rolando

Titel

Overexpression of MMPs, cytokines, and RANKL/OPG in temporomandibular joint osteoarthritis and their association with joint pain, mouth opening, and bone degeneration: A preliminary report

Ist Teil von

• Oral diseases, 2021-05, Vol.27 (4), p.970-980

Ort / Verlag

Denmark: Wiley Subscription Services, Inc

Erscheinungsjahr

2021

Link zum Volltext

Quelle

Wiley Online Library Journals Frontfile Complete

Beschreibungen/Notizen

• Objective This study aimed to determine the expression of distinct matrix metalloproteinases, cytokines, and bone resorptive factors in temporomandibular joint osteoarthritis (TMJ‐OA) patients and their association with joint pain, mouth opening, and subchondral bone degeneration. Materials and methods Twelve patients affected with TMJ‐OA (n = 5), disk displacement without reduction (DDWoR) (n = 3), or disk displacement with reduction (DDWR) (n = 4) were selected. Joint pain was quantified by using visual analog scale, mouth opening was quantified at the maximum pain‐free aperture, and bone degeneration was quantified using joint imaging. Synovial fluid samples were collected and immediately processed for cell and synovial fluid recovering. From cells, the MMP‐1, MMP‐2, MMP‐8, MMP‐13, IL‐6, IL‐23, and TNF‐α expression was quantified by qPCR. From synovial fluid, the RANKL and OPG levels were quantified by ELISA. Results Higher levels of MMP‐1, MMP‐8, MMP‐13, IL‐6, IL‐23, TNF‐α, and RANKL/OPG ratio were detected in TMJ‐OA compared with DDWoR and DDWR patients (p < .05). Joint pain significantly correlated with TNF‐α levels (r = .975, p = .029). Besides, imaging signs of bone degeneration significantly correlated with RANKL/OPG ratio (r = .949, p = .042). Conversely, mouth opening did not correlate with any of the analyzed mediators. Conclusion During TMJ‐OA, a pathological response characterized by the overexpression of TNF‐α and RANKL/OPG could be involved in joint pain and subchondral bone degeneration.