Expression of tenascin-C in aseptic loosening of total hip replacement

Abstract

Objective: To assess if the bonding interlayer between the implant and bone in aseptic loosening of total hip replacement (THR) is qualitatively deteriorated by excessive accumulation of anti-adhesive glycoprotein, tenascin-C.

Methods: Alkaline phosphatase-anti-alkaline phosphatase (APAAP) method was used for immunohistochemical staining of tenascin-C in interface tissue and control synovial tissue.

Results: Tenascin-C was found to be a major component of the extracellular matrix at a hitherto unrecognised site, namely the synovial membrane-like interface tissue between implant and bone in aseptic loosening of THR. The overall tenascin-C staining (median score 4.0) was greatly increased in aseptic loosening compared with synovial membrane (median score 2.0; p < 0.001) and fibrous capsule (median score 2.0; p < 0.001) from primary THR operations. Topological analysis disclosed that tenascin-C was also found at the critical implant-interface and interface-bone surfaces.

Conclusion: Local tenascin-C expression is increased as a result of a chronic foreign body type reaction associated with excessive cytokine production and tissue injury mediated by microtrauma and neutral endoproteinases. This qualitative and topological deterioration of the bonding interlayer by an increase of anti-adhesive tenascin-C expression may inadvertantly contribute to loosening.

Figure 1

Immunoreactivity for tenascin-C in the synovial membrane-like interface tissue from aseptic loosening of THR and control synovial samples (APAAP staining, original magnification × 250). (A) Immunoreactivity for tenascin-C in the synovial membrane-like interface tissue. Tenascin-C staining was very strong in the synovial lining-like layer (arrows) of interface tissue. This sample/ section also contains intervening matrix, which does not stain for tenascin. (B)Tenascin-C was detected in all fields/extracellular matrix of the synovial membrane-like interface tissue in this revision THR patient. Particularly strong staining was found in the synovial lining-like layer (larger arrows). Heavy deposits of debris (see (C) for verification) were found embedded in the tissue (small arrows). (C) Same section as in (B) photographed with polarised light shows that there were many birefringent polyethylene particles embedded in the tissue (some are marked with arrows). (D) Fibroblasts and their pericellular matrix (arrows) showed usually intense tenascin expression in the synovial membrane-like interface tissue samples, whereas the extracellular collagenous matrix did not stain as strongly (the white intervening areas). Note, that fibroblasts send long and slender extensions, which pass between the collagenous fibres of the connective tissue and would be difficult to identify without tenascin-C staining. (E) Same section as in (D) photographed with polarised light shows polyethylene deposits (some are marked with small arrows). (F) Very weak tenascin-C staining in the control synovial sample from osteoarthritis. (G) For staining control the specific primary IgG_2a antibody were replaced with monoclonal IgG with an irrelevant specificity (Aspergillus niger glucose oxidase), but of the same subtype and concentration as the specific primary antibody. Comparison with the (A) confirms the specificity of the staining.

Figure 2

Histological examination of the interface tissue samples with different staining scores (haematoxylin and eosin staining, original magnification × 250). (A) Macrophage-like cells accumulation in a synovial membrane-like interface tissue sample with high staining score (staining score = 4). (B) Matrix fibrosis in the interface tissue sample with lower staining score (staining score = 3).