R Crawford1, N A Athanasou. 1. Department of Surgery, Nuffield Orthopaedic Centre, Oxford, UK.
Abstract
AIMS: Hip joint disease associated with progressive amyloid deposition in uraemic patients receiving chronic haemodialysis treatment often requires treatment by joint arthroplasty. The aim of this study was to determine whether beta 2-microglobulin amyloid deposition occurred in the periprosthetic tissues of arthroplasties that had undergone aseptic loosening and required a revision procedure. METHODS AND RESULTS: Sections of the pseudocapsule, acetabular and femoral pseudomembrane surrounding failed total hip replacements of five uraemic patients known to have beta 2-microglobulin amyloid deposits at the time of primary joint replacement were examined for the presence of beta 2-microglobulin amyloid deposition by Congo red staining and immunohistochemical staining for beta 2-microglobulin and other amyloid proteins. Clinical and radiological features of each case, including postoperative history and extent of osteolysis, were also noted. In all cases evidence of beta 2-microglobulin amyloid deposits were found in one or more of the above periprosthetic tissues. In three of these cases amyloid deposition was extensive. CONCLUSIONS: This study shows that beta 2-microglobulin amyloid deposition occurs in revision arthroplasty tissues. Accelerated loosening of the prosthesis is known to occur in uraemic patients and it is possible that beta 2-microglobulin amyloid deposition may contribute to early arthroplasty failure in uraemic patients who remain on haemodialysis treatment.
AIMS: Hip joint disease associated with progressive amyloid deposition in uraemic patients receiving chronic haemodialysis treatment often requires treatment by joint arthroplasty. The aim of this study was to determine whether beta 2-microglobulin amyloid deposition occurred in the periprosthetic tissues of arthroplasties that had undergone aseptic loosening and required a revision procedure. METHODS AND RESULTS: Sections of the pseudocapsule, acetabular and femoral pseudomembrane surrounding failed total hip replacements of five uraemic patients known to have beta 2-microglobulin amyloid deposits at the time of primary joint replacement were examined for the presence of beta 2-microglobulin amyloid deposition by Congo red staining and immunohistochemical staining for beta 2-microglobulin and other amyloid proteins. Clinical and radiological features of each case, including postoperative history and extent of osteolysis, were also noted. In all cases evidence of beta 2-microglobulin amyloid deposits were found in one or more of the above periprosthetic tissues. In three of these cases amyloid deposition was extensive. CONCLUSIONS: This study shows that beta 2-microglobulin amyloid deposition occurs in revision arthroplasty tissues. Accelerated loosening of the prosthesis is known to occur in uraemic patients and it is possible that beta 2-microglobulin amyloid deposition may contribute to early arthroplasty failure in uraemic patients who remain on haemodialysis treatment.