CAJ | 학술논문

背景：雌激素通过成骨细胞、破骨细胞、细胞分泌的因子，以及多条骨代谢调控途径参与了骨关节炎骨代谢的调控。 　　目的：综合阐述雌激素及雌激素相关化合物在关节保护、骨与软骨细胞的修复、滑膜炎症的抑制等方面对骨关节炎的作用。 　　方法：作者检索1992至2014年PubMed、Embase、Elseveir数据库文献。检索词为：“Osteoarthritis， Estrogens，Matrix Metal oproteinases，Interleukins，Tumor Necrosis Factor-alpha”。按照事先制定的标准逐一评价纳入研究的文献，提取有效资料进行综合分析。 　　结果与结论：雌激素可通过增加成骨细胞中骨保护素和核因子κB受体活化因子配体的表达，抑制破骨性骨吸收，防止骨关节炎的发生和进展。雌激素能上调抗破骨细胞的细胞因子，而下调亲破骨细胞的细胞因子，通过Wnt与骨形态发生蛋白信号系统也参与骨关节炎患者骨代谢的调控。雌激素可以通过下丘脑-垂体-肾上腺轴的作用促进肾上腺皮质分泌糖皮质激素，从而间接抑制基质金属蛋白酶类的产生，对关节软骨起到保护作用。外源性雌激素通过抑制骨的吸收可能会有助于延缓骨关节炎的发展。雌激素和雌激素相关的化合物在骨关节炎进展的后期阶段可能会抑制滑膜炎症和炎症递质导致的软骨流失。
배경：자격소통과성골세포、파골세포、세포분비적인자，이급다조골대사조공도경삼여료골관절염골대사적조공。 　　목적：종합천술자격소급자격소상관화합물재관절보호、골여연골세포적수복、활막염증적억제등방면대골관절염적작용。 　　방법：작자검색1992지2014년PubMed、Embase、Elseveir수거고문헌。검색사위：“Osteoarthritis， Estrogens，Matrix Metal oproteinases，Interleukins，Tumor Necrosis Factor-alpha”。안조사선제정적표준축일평개납입연구적문헌，제취유효자료진행종합분석。 　　결과여결론：자격소가통과증가성골세포중골보호소화핵인자κB수체활화인자배체적표체，억제파골성골흡수，방지골관절염적발생화진전。자격소능상조항파골세포적세포인자，이하조친파골세포적세포인자，통과Wnt여골형태발생단백신호계통야삼여골관절염환자골대사적조공。자격소가이통과하구뇌-수체-신상선축적작용촉진신상선피질분비당피질격소，종이간접억제기질금속단백매류적산생，대관절연골기도보호작용。외원성자격소통과억제골적흡수가능회유조우연완골관절염적발전。자격소화자격소상관적화합물재골관절염진전적후기계단가능회억제활막염증화염증체질도치적연골류실。
BACKGROUND:The bone metabolism of osteoarthritis is regulated by estrogen with osteoblasts, osteoclasts and cytokines, as wel as a number of regulatory pathways. OBJECTIVE:To describe the role of estrogen and estrogen-related compounds for joint protection, repair of bone and cartilage cells, and inhibition of synovitis in osteoarthritis. METHODS:Author researched PubMed, Embase, Elseveir database from 1992 to 2014, with the key words of“osteoarthritis, estrogens, matrix metal oproteinases, interleukins, tumor necrosis factor-alpha”. After the quality of the included studies was evaluation, valid data were extracted and analyzed. RESULTS AND CONCLUSION:Estrogen can increase the expression of osteoprotegerin and nuclear factor-κB factor ligands in osteoblasts, inhibit bone resorption, prevent the onset and progression of osteoarthritis. Estrogen upregulates anti-osteoclast cytokines, downregulates pro-osteoclast factors, and contribute to regulate bone metabolism of osteoarthritis patients through bone morphogenetic protein and Wnt signaling. Estrogen promotes the adrenal cortex secretion of glucocorticoids and indirectly inhibits the production of matrix metal oproteinases by the hypothalamus-hypophysis-adrenal gland axis. Exogenous estrogen inhibits bone resorption, which may help to delay the development of osteoarthritis. Estrogen and estrogen-related compounds may inhibit the cartilage loss caused by synovitis and inflammatory factors in the late stage of osteoarthritis.