假体周围骨溶解：遗传学、机制和潜在的治疗干预。
Periprosthetic osteolysis: genetics, mechanisms and potential therapeutic interventions.
机构信息
Department of Orthopaedic Surgery, University of British Columbia, Vancouver, BC.
出版信息
Can J Surg. 2012 Dec;55(6):408-17. doi: 10.1503/cjs.003711.
Abstract
Aseptic loosening and periprosthetic osteolysis occur as a result of the biological response to particulate wear debris and are one of the leading causes of arthroplasty failure. Periprosthetic osteolysis originates from chronic inflammatory responses triggered by implant-derived particulate debris, which cause recruitment of cells, including macrophages, fibroblasts, lymphocytes and osteoclasts. These cells secrete proinflammatory and osteoclastogenic cytokines, exacerbating the inflammatory response. In addition to their direct activation by phagocytosis, there are contributing autocrine and paracrine effects that create a complex milieu within the periprosthetic space, which ultimately governs the development of osteolysis. Chronic cell activation may upset the delicate balance between bone formation and bone resorption leading to periprosthetic osteolysis. This article summarizes the genetic mechanisms underlying periprosthetic loosening and identifies potential therapeutic agents.
摘要
无菌性松动和假体周围骨溶解是对颗粒性磨损碎片的生物反应的结果，也是导致关节置换失败的主要原因之一。假体周围骨溶解源于由植入物衍生的颗粒性碎片引发的慢性炎症反应，这些碎片会招募包括巨噬细胞、成纤维细胞、淋巴细胞和破骨细胞在内的细胞。这些细胞分泌促炎和破骨细胞生成细胞因子，从而加剧炎症反应。除了通过吞噬作用的直接激活外，还有促进自分泌和旁分泌的作用，这些作用在假体周围空间内创造了一个复杂的环境，最终控制着骨溶解的发展。慢性细胞激活可能会破坏骨形成和骨吸收之间的微妙平衡，导致假体周围骨溶解。本文总结了假体周围松动的遗传机制，并确定了潜在的治疗药物。
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