Contributions of human tissue analysis to understanding the mechanisms of loosening and osteolysis in total hip replacement

Abstract

Aseptic loosening and osteolysis are the most frequent late complications of total hip arthroplasty (THA) leading to revision of the prosthesis. This review aims to demonstrate how histopathological studies contribute to our understanding of the mechanisms of aseptic loosening/osteolysis development. Only studies analysing periprosthetic tissues retrieved from failed implants in humans were included. Data from 101 studies (5532 patients with failure of THA implants) published in English or German between 1974 and 2013 were included. "Control" samples were reported in 45 of the 101 studies. The most frequently examined tissues were the bone-implant interface membrane and pseudosynovial tissues. Histopathological studies contribute importantly to determination of key cell populations underlying the biological mechanisms of aseptic loosening and osteolysis. The studies demonstrated the key molecules of the host response at the protein level (chemokines, cytokines, nitric oxide metabolites, metalloproteinases). However, these studies also have important limitations. Tissues harvested at revision surgery reflect specifically end-stage failure and may not adequately reveal the evolution of pathophysiological events that lead to prosthetic loosening and osteolysis. One possible solution is to examine tissues harvested from stable total hip arthroplasties that have been revised at various time periods due to dislocation or periprosthetic fracture in multicenter studies.

Keywords: Aseptic loosening; Immunostaining; Osteolysis; Tissue analysis; Total hip.

Fig. 1

Flowchart of the methodology of the study.

Fig. 2

Cell types identified by immunostains.

Fig. 3

Studies focused on cytokines produced by harvested tissues.

Fig. 4

(A) Hyperplasia of synovial membrane, fibroproliferative changes in subsynovial stroma, reactive neovascularization; hematoxylin and eosin (H&E); ×1000. (B) “Neovascularization” in the synovial membrane; H&E; ×200. (C) Highly vascularized synovial membrane; CD34-positive vessels; ×1000. (D) Fibroproliferative changes with fibrinoid degeneration of connective tissue; H&E; ×1000. (E) Synovial-like cells containing metallic debris; H&E; ×1000. (F) Nodular hyperplasia with reactive changes; vimentin-positive mesenchymal cells; v200. (G) Reactive changes with macrophages containing granules of exogenous material; CD68; ×600. (H) Lymphocytic infiltration typical for chronic inflammatory changes around an implant; H&E; ×1000. (I) Bone covered by osteoblasts and osteoclasts with multiple nuclei; HE; ×200. A scale bar of 50 or 100 µm is included in each particular figure. Sources of figures: (A–H) Department of Pathology, University Hospital Ostrava, Czech Republic; (I) Department of Pathology, Faculty of Medicine and Dentistry, University Hospital, Palacky University Olomouc, Czech Republic.

Fig. 4

(A) Hyperplasia of synovial membrane, fibroproliferative changes in subsynovial stroma, reactive neovascularization; hematoxylin and eosin (H&E); ×1000. (B) “Neovascularization” in the synovial membrane; H&E; ×200. (C) Highly vascularized synovial membrane; CD34-positive vessels; ×1000. (D) Fibroproliferative changes with fibrinoid degeneration of connective tissue; H&E; ×1000. (E) Synovial-like cells containing metallic debris; H&E; ×1000. (F) Nodular hyperplasia with reactive changes; vimentin-positive mesenchymal cells; v200. (G) Reactive changes with macrophages containing granules of exogenous material; CD68; ×600. (H) Lymphocytic infiltration typical for chronic inflammatory changes around an implant; H&E; ×1000. (I) Bone covered by osteoblasts and osteoclasts with multiple nuclei; HE; ×200. A scale bar of 50 or 100 µm is included in each particular figure. Sources of figures: (A–H) Department of Pathology, University Hospital Ostrava, Czech Republic; (I) Department of Pathology, Faculty of Medicine and Dentistry, University Hospital, Palacky University Olomouc, Czech Republic.