Immunohistochemical evaluation of interface membranes from failed cemented and uncemented acetabular components.
Aseptic loosening of acetabular components is a primary factor compromising the long-term outcome of cemented and cementless total hip replacement. It is unknown whether the pathogenesis of the loosening process is identical for both types of fixation. The specific aim of this study was to determine whether there is a difference in the cellular and cytokine profiles of interface membranes removed from between the implant and the host bone from failed cemented (n = 5) and failed cementless acetabulae (n = 5). Routine histology and immunohistochemical evaluations were completed on each tissue specimen. The monoclonal antibodies used included those specific for cell types (macrophages, fibroblasts, T lymphocytes) and for cytokines (IL-1beta, IL-6, TNF-alpha). The patients were all revised for loosening. The time to revision was significantly longer for the cemented group (16.6 yr; 13-21 range) than for the cementless group (8.9 yr; 4-13 range). In all cases, slides from each group stained positively for each of the cell types and cytokines evaluated. Immunohistochemical analyses indicated a predominance of macrophages and ubiquitous staining for the cytokines IL-1beta and TNF-alpha within the membranes of both patient groups. The intensities of cytokine staining were similar for both patient groups. More regions of fibroblastic connective tissue were observed surrounding failed cementless components as compared to those of the cemented group. The clinical ramification of our findings is that, despite differences in the cellular composition of the periprosthetic membranes, the membranes from failed cemented and cementless implants contain cytokines, which have been shown to be capable of modulating the inflammatory response. These inflammatory mediators are likely to play a significant role in the development of osteolysis and prosthetic loosening.
Jones
L C
LC
Division of Arthritis Surgery, Department of Orthopaedic Surgery, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. lcj@welchlink.welch.jhu.edu
Frondoza
C
C
Hungerford
D S
DS
D000077:Acetabulum / Q000378:metabolism / Q000473:pathology*; D019644:Arthroplasty, Replacement, Hip; D001843:Bone Cements; D016207:Cytokines / Q000378:metabolism; D006801:Humans; D007150:Immunohistochemistry; D007375:Interleukin-1 / Q000096:biosynthesis; D015850:Interleukin-6 / Q000096:biosynthesis; D008264:Macrophages / Q000276:immunology; D008566:Membranes / Q000378:metabolism / Q000473:pathology; D011475:Prosthesis Failure; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis
D001843:Bone Cements; D016207:Cytokines; D007375:Interleukin-1; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha