Cemented versus cementless hip arthroplasty A review of prosthetic biocompatibility

Abstract

The fibrous interface tissue between hip prostheses and surrounding bone is often morphologically and functionally synovial-like. The fibroblast is the major cell type; but also giant cells and macrophages are present, and their numbers are increased in the occasional adverse-type host reaction to the prosthesis. Adverse lytic reactions are often associated with methylmethacrylate debris, whereas in cementless cases, polyethylene and metallic (titanium) wear debris seem to cause adverse reactions. Osteoblasts, osteoclasts, and mesenchymal collagenase secreted by fibroblasts and macrophages play an important role in the process of prosthetic loosening. Methylmethacrylate is immunologically relatively inert, while it induces inflammatory mononuclear-cell migration. Both cemented and cementless prostheses cause a foreign-body type host response, including adaptive and reactive processes. This response includes the formation of fibroblast-like B-type lining cells, which are able to synthesize and secrete hyaluronate. Material surfaces of hip arthroplasty components also provide a unique environmental niche to which staphylococcal strains adhere and colonize. Antibiotic resistance is related to the material colonized rather than to the presence of an exopolysaccharide barrier; organisms bound to polyethylene and methylmethacrylate are more resistant than organisms that are bound to stainless steel. An understanding of prosthetic biocompatibility requires an appreciation of tissue cell, bacterial cell and host defense-system response to biomaterials. The site of implantation is a stage on which the “players” (bacteria, host cells, and organic moieties) interact and compete, and before which the host is a “responsive audience.”