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Aseptic loosening of total joint replacements: mechanisms underlying osteolysis and potential therapies

机译:无菌性全关节置换术的松动:骨溶解和潜在疗法的潜在机制

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摘要

Total joint replacement, although considered an excellent surgical procedure, can be complicated by osteolysis induced by implant particles and subsequent aseptic loosening of the implant. The pathogenesis of implant-associated osteolysis includes inflammatory and osteolytic processes. The sustained chronic inflammatory response initiated by particulate debris at the implant-bone interface is manifested by recruitment of a wide array of cell types. These cells include macrophages, fibroblasts, giant cells, neutrophils, lymphocytes, and – most importantly – osteoclasts, which are the principal bone resorbing cells. The 'cellular response' entails secretion of osteoclastogenic and inflammatory cytokines that favor exacerbated osteoclast activity and enhanced osteolysis. An appreciation of the complex network that leads to these cellular and inflammatory responses will form a foundation on which to develop therapeutic interventions to combat inflammatory periprosthetic bone loss.
机译:全关节置换尽管被认为是一种极好的外科手术方法,但由于植入物颗粒引起的骨溶解以及随后的植入物无菌性松动而变得复杂。植入物相关性骨溶解的发病机制包括炎症和溶骨过程。植入物-骨界面处的微粒碎片引发的持续性慢性炎症反应可通过募集多种细胞类型来体现。这些细胞包括巨噬细胞,成纤维细胞,巨细胞,嗜中性粒细胞,淋巴细胞,最重要的是破骨细胞,它们是主要的骨吸收细胞。 “细胞反应”需要分泌破骨细胞和炎性细胞因子,从而加剧破骨细胞活性并增强溶骨作用。对导致这些细胞和炎性反应的复杂网络的认识将为发展治疗性措施以对抗炎性假体周围骨质流失奠定基础。

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