Postgrad Med J 76:479-483 doi:10.1136/pmj.76.898.479
  • Review

Pathophysiology of chronic bacterial osteomyelitis. Why do antibiotics fail so often?

  1. J Ciampolini,
  2. K G Harding
  1. Wound Healing Research Unit, University of Wales College of Medicine, Cardiff, UK
  1. Mr J Ciampolini, Princess Elizabeth Orthopaedic Centre, Exeter, Devon EX2 5DW, UK
  • Received 19 March 1999
  • Accepted 5 July 1999


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.