Abstract
Temporomandibular joint osteoarthrosis (TMJOA) is characterised by chronic inflammatory changes, with subsequent gradual loss of joint cartilage. NF-κB is a crucial transcription factor in the course of inflammatory and immune responses, which are involved in OA pathology activated by proinflammatory cytokines. Genistein is known to have anti-inflammation and modulation of metabolic pathways through repression of the NF-κB signaling pathway in inflammatory disease. But so far, studies on the effects of genistein on TMJOA are very limited. So, the purpose of this study is to investigate the protective effect of genistein against experimentally induced condylar cartilage degradation through downregulating NF-κB expression in created osteoarthritis rats in vivo. Male SD rats were created as temporomandibular joint osteoarthritis models and administered through oral gavage with low and high dosage genistein (30 mg/kg and 180 mg/kg, respectively) daily for 4 weeks. The morphological changes of the condylar cartilage were studied with HE and Masson staining. The expressions of p65 and inflammatory cytokines (IL-1β and TNFα) were detected using immunohistochemistry and real-time PCR. The results showed that experimentally created osteoarthritis reduced the condylar cartilage thickness of rats and increased the gene expression of cytokines (IL-1β and TNFα) and positive cells of p65. Genistein treatment had positive effects on the condylar cartilage renovation, while high dose genistein treatment had more significant effects on the reversing of OA changes and reduction of the expression of p65 and inflammatory cytokines (IL-1β and TNFα). The results indicated that high dose genistein treatment had obvious therapeutic effects on condyle cartilage damages of OA rats. The mechanism may be that genistein suppresses the NF-κB expression activated by inflammatory cytokines.
Highlights
Temporomandibular joint osteoarthrosis (TMJOA), which is characterised by chronic inflammatory changes, with subsequent gradual loss of joint cartilage, mostly occurred in condyle [1,2,3]
Some studies showed that IL-1β and tumor necrosis factor-α (TNF-α) contributed to the pathogenesis of osteoarthrosis and induced the inflammation and destruction of the joints [7,8]
Many studies reported that synovial fluids of OA joints showed higher concentration of TNFα than that of normal joints [7, 24, 27], while high TNFα expression was detected in local arthritic tissues, which was related to the autoimmune reaction and can cause aggressive cartilage destruction of joints by suppressing the synthesis of the cartilage matrix [24]. e present result showed that the expression of TNF-α was higher in OA rats than that of normal rats, which had the same tendency with IL-1β
Summary
Temporomandibular joint osteoarthrosis (TMJOA), which is characterised by chronic inflammatory changes, with subsequent gradual loss of joint cartilage, mostly occurred in condyle [1,2,3]. Some study has demonstrated that genistein has a bone-protective effect in rat models of osteoporosis in knee joints [19]. E modified Mankin scores system was used to evaluate the structural changes of the condyle cartilage in the four groups.
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