Ciampolini J, Harding K G
Wound Healing Research Unit, University of Wales College of Medicine, Cardiff, UK.
Postgrad Med J. 2000 Aug;76(898):479-83. doi: 10.1136/pmj.76.898.479.
In this review the pathophysiology of chronic bacterial osteomyelitis is summarised, focusing on how bacteria succeed so often in overcoming both host defence mechanisms and antibiotic agents. Bacteria adhere to bone matrix and orthopaedic implants via receptors to fibronectin and to other structural proteins. They subsequently elude host defences and antibiotics by "hiding" intracellularly, by developing a slimy coat, or by acquiring a very slow metabolic rate. The presence of an orthopaedic implant also causes a local polymorphonuclear cell defect, with decreased ability to kill phagocytosed bacteria. Osteolysis is determined locally by the interaction of bacterial surface components with immune system cells and subsequent cytokine production. The increasing development of antibiotic resistance by Staphylococcus aureus and S epidermidis will probably make conservative treatment even less successful than it is now. A close interaction between orthopaedic surgeons and physicians, with combined medical and operative treatment, is to be commended.
在本综述中,总结了慢性细菌性骨髓炎的病理生理学,重点关注细菌如何常常成功克服宿主防御机制和抗生素。细菌通过与纤连蛋白及其他结构蛋白的受体黏附于骨基质和骨科植入物。随后,它们通过在细胞内“隐藏”、形成黏液层或获得非常缓慢的代谢率来躲避宿主防御和抗生素。骨科植入物的存在还会导致局部多形核细胞缺陷,降低杀死吞噬细菌的能力。骨溶解是由细菌表面成分与免疫系统细胞的相互作用以及随后的细胞因子产生在局部决定的。金黄色葡萄球菌和表皮葡萄球菌对抗生素耐药性的不断发展可能会使保守治疗比目前更不成功。值得称赞的是骨科外科医生和内科医生之间密切合作,采用联合药物和手术治疗。