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首页> 外文期刊>Journal of oral rehabilitation >Increased chemokine RANTES in synovial fluid and its role in early-stage degenerative temporomandibular joint disease
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Increased chemokine RANTES in synovial fluid and its role in early-stage degenerative temporomandibular joint disease

机译:在滑液中的趋化因子增加在滑液中及其在早期退行性颞下颌关节疾病中的作用

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Background Degenerative joint disease (DJD) of the temporomandibular joints (TMJs) in adolescents and young adults is closely associated with disc displacement without reduction (DDw/oR). Objective This study aimed to determine the pathogenesis of early-stage TMJ DJD induced by DDw/oR. Methods 31 female subjects aged 12-30 years were enrolled, comprising 12 patients with DDw/oR without DJD, 13 with DDw/oR and early-stage DJD, and 6 healthy volunteers. The synovial fluid samples of the subjects were screened for 27 inflammatory-related cytokines using multiple cytokine array. Significantly increased cytokines and a key regulator of osteoclastogenesis "receptor activator of nuclear factor-kappa B ligand" (RANKL) were further determined by sandwich immunoassay. These factors were also assessed for the possible pathophysiologic actions on RAW264.7 cell proliferation, migration, osteoclastogenesis and bone-resorbing activity using Cell Counting Kit-8, Transwell system, tartrate-resistant acid phosphatase staining and osteo assay plates. Results Macrophage-derived inflammatory protein-1 beta (MIP-1 beta) and regulated upon activation normal T cell expressed and secreted (RANTES) were found to vary significantly in relation to the controls. In contrast to an unchanged concentration of RANKL, a strong increase in the level of RANTES was detected in subjects with DDw/oR and early-stage DJD. MIP-1 beta concentrations were only elevated in subjects with DDw/oR without DJD. Functionally, both MIP-1 beta and RANTES could enhance macrophage migration in a concentration-dependent manner, while only RANTES exhibited a promoting effect on osteoclast formation and bone-resorbing activity. Conclusions Chemokine RANTES was significantly upregulated and might be a key regulator of osteoclastogenesis contributing to DDw/oR-induced early-stage TMJ DJD.
机译:背景青少年颞下颌关节退行性关节病(DJD)与未复位椎间盘移位(DDw/oR)密切相关。目的探讨DDw/oR诱发早期颞下颌关节DJD的发病机制。方法31例12~30岁女性受试者,包括12例DDw/或非DJD患者、13例DDw/或早期DJD患者和6名健康志愿者。使用多种细胞因子阵列对受试者的滑液样本进行27种炎症相关细胞因子筛选。通过三明治免疫分析进一步确定细胞因子显著增加和破骨细胞生成的关键调节因子“核因子-κB配体受体激活剂”(RANKL)。还评估了这些因素对RAW264可能的病理生理作用。7.使用细胞计数试剂盒-8、Transwell系统、抗酒石酸酸性磷酸酶染色和骨测定板检测细胞增殖、迁移、破骨细胞生成和骨吸收活性。结果巨噬细胞源性炎性蛋白-1β(MIP-1β)和活化后调节的正常T细胞表达和分泌(RANTES)与对照组相比存在显著差异。与RANKL浓度不变相比,DDw/oR和早期DJD患者的RANTES水平显著升高。MIP-1β浓度仅在有DDw/或无DJD的受试者中升高。在功能上,MIP-1β和RANTES均能以浓度依赖性方式促进巨噬细胞迁移,而只有RANTES对破骨细胞的形成和骨吸收活性有促进作用。结论趋化因子RANTES显著上调,可能是DDw/oR诱导的早期TMJ-DJD破骨细胞发生的关键调节因子。

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