ABSTRACT
PURPOSE: To evaluate the relationships between the apoptosis induced by nitric oxide (NO), aseptic loosening and osteolysis, which are the most serious causes of failure after total hip arthroplasty. MATERIALS AND METHODS: Apoptosis of the inflammatory cells of interface tissues from 18 patients who underwent revision hip arthroplasty was identified by Terminal Deoxyribonucleotidyl Transferase-Mediated dUTP Nick End Labeling (TUNEL). The reaction to immunostaining of inducible nitric oxide synthase (iNOS), p53, Bax, Bcl2, and Ki-67 were evaluated. Six joint capsules obtained from six patients of femoral neck fracture were studied as controls. RESULTS: Sixteen (89%) of 18 interface tissues were positive for iNOS, p53, and Bax monoclonal antibody and twelve (67%) for Bcl2 and Ki-67 monoclonal antibody. All tissues were positive for TUNEL. In the control group of six joint capsules, only one (17%) was positive for iNOS and Bax, and three (50%) were positive for TUNEL. The incidences of apoptotic signals at the interfacial tissue of aseptic loosening and osteolysis were significantly greater than those of the control. CONCLUSION: The current study suggested that the apoptosis of inflammatory cells, due to oxidative stress by NO, might be involved in the development of implant loosening and osteolysis after total hip arthroplasty. This information might be crucial for the treatment and prevention of periprosthetic osteolysis and subsequent loosening.
