Wang J H, Rogers G R, Allardyce R A, Gillespie W J
Department of Orthopaedic Surgery, Christchurch School of Medicine, New Zealand.
Chin Med J (Engl). 1990 Apr;103(4):326-30.
Rapid, extensive loss of infected bone implies abnormal localized inflammatory cell activity. We have demonstrated, using a live bone Ca-45 release model, that polymorphonuclear leukocytes degrade bone in a dose dependent manner. Staphylococcus aureus-stimulated blood mononuclear leukocytes release soluble products in vitro that enhance that process. Despite the usually accepted roles of osteoclasts and their blood-borne monocytic precursors in normal bone remodelling, these results indicate that considerable early pathological infected bone loss may be attributable to inflammatory polymorphonuclear leukocytes.
受感染骨骼的快速、广泛丧失意味着局部炎症细胞活动异常。我们使用活骨钙-45释放模型证明，多形核白细胞以剂量依赖的方式降解骨骼。金黄色葡萄球菌刺激的血液单核白细胞在体外释放可溶性产物，从而增强这一过程。尽管破骨细胞及其血源单核细胞前体在正常骨重塑中具有通常公认的作用，但这些结果表明，早期相当一部分病理性感染性骨丢失可能归因于炎症性多形核白细胞。
