Osteopontin stimulates matrix metalloproteinase expression through the nuclear factor-κB signaling pathway in rat temporomandibular joint and condylar chondrocytes.

BACKGROUND: To examine the possible regulatory mechanisms of osteopontin (OPN) and the nuclear factor-κB (NF-κB) signaling pathway in the temporomandibular joint (TMJ) of rats subjected to chronic sleep deprivation (CSD).

METHODS: Rats were subjected to CSD using the modified multiple platform method. The histomorphology of the TMJ was observed by hematoxylin-eosin staining. OPN and NF-κB/p65 expression were detected by immunohistochemical and immunofluorescence staining together with western blotting. The condylar chondrocytes were isolated from the rat TMJ and treated with recombinant OPN (r-OPN) before detection for the expression of NF-κB/p65 and matrix metalloproteinases (MMPs). Western blotting and reverse transcription-polymerase chain reaction were performed to determine the expression of MMP-1, MMP-3, MMP-9, and MMP-13 in the TMJ and chondrocytes respectively.

RESULTS: There was a statistically significant difference in OPN and NF-κB/p65 expression between the CSD group and control (CON) group. OPN and NF-κB/p65 expression was increased in the CSD group as compared with in the CON group. NF-κB/p65 expression was significantly increased by r-OPN treatment in the chondrocytes. Furthermore, MMP-1, MMP-3, MMP-9, and MMP-13 production was also remarkably elevated in the CSD group as well as in the chondrocytes. Treatment with 1 μg/ml r-OPN for 48 h led to the highest production of inflammatory cytokines in chondrocytes.

CONCLUSIONS: CSD causes pathological alterations in the TMJ. OPN treatment activates the NF-κB signaling pathway and stimulates MMPs in the TMJ and condylar chondrocytes through NF-κB signaling pathway. Chondrocytes treated with 1 μg/ml r-OPN for 48 h produced the highest level of inflammatory cytokines.