The osteogenic properties of the interface membrane at the site of orthopedic implants: the impact of underlying joint disease.

Osseointegration at the site of orthopedic implants is dependent on the recruitment, attachment, and differentiation of osteogenic cells. Data concerning the effect of a patient's underlying joint disease on the modulation of the cellular activity and the long-term survival of joint prostheses is limited. In this study, immunocytochemistry was used to investigate the osteogenic cell phenotype within the bone-implant interface fibrous membrane in 60 patients with different underlying joint disease. Tissue specimens were removed during revision operations performed at variable times following implantation. The results provided histological evidence of the presence of fibrocartilage tissue and calcified bone within the interface. TGF-beta, metalloproteinases (MMP1 and MMP2) and their inhibitors (TIMP1 and TIMP2) were immunolocalized within fibroblasts, chondrocytes, and osteoblasts throughout the interface, indicating that signals modulating the osteogenic cell phenotype at these sites are highly regulated. Finally, the study identified a significant difference in the histological changes elicited by implant particulate debris in patients of different diagnostic categories. Such observations imply that the activity of the original joint disorder could augment specific cellular activation/immune signals that subsequently affect the degree of the local inflammatory responses to implant wear particles. The negative balance between the rate of bone growth and resorption around the prosthetic joint is central to the pathogenesis of aseptic loosening of implants.