Journal of The Royal Society, Interface macrophages and lymphocytes in the loosening of total joint prostheses

摘要

This review considers the causes of loosening of prosthetic joint replacement paying attentionnto the biological mechanisms rather than other effects that are physical, such as componentnfracture and other failure related to mechanical problems. Infection accounts fornapproximately 1.5 per cent of joint loosening and when it occurs it is a cause of seriousnconcern to the surgeon. The loosening of prosthetic joints in the absence of infection is by farnthe most common reason for revision surgery and is known as aseptic loosening. While thisnmay be multifactorial in terms of causation, and non-biological factors may contributensignificantly in a particular individual, a significant part is undoubtedly played by thengeneration of wear debris, mainly from the bearing surfaces of the joint, and the cellularnreaction to this in the implant bed. Phagocytic cells (macrophages and multinucleated giantncells) are the ones that remove foreign material from the tissues, and the ways in which thesencells function in the interface between implant and bone are described. Mediators producednlocally include numerous cytokines, enzymes and integrins. There is evidence for interactionsnbetween macrophages and locally recruited lymphocytes, which may or may not give rise tonan immunologically mediated process.nSensitization of individuals having metal implants in place has been shown by positive skinntests or blood lymphocyte transformation tests and in these cases has been accompanied bynloosening and failure of the replacement joint. The question remains as to whether thisnprocess is also present in a proportion of individuals with aseptic loosening in the absence ofnclearly defined clinical evidence of sensitization.nNumerous studies performed by the author’s group and, latterly, by others suggest that thencellular reactions detected in the tissues in cases of aseptic loosening are indeed those ofncontact sensitization. There is good evidence to show that a type IV cell-mediated immunenreaction is taking place, with TH1 cell involvement and active antigen presentation. Thenextent to which sensitization is present in individual cases of aseptic loosening remains ansubject for further work and this needs all the sophisticated molecular methods now availablento modern biology to be applied in appropriate prospective clinical studies coupled withnexperimental models in vitro and in vivo. Immunological processes may play a morenimportant part in joint loosening than previously considered.