We report the first use of synchrotron xray spectroscopy to characterize and compare the chemical form and distribution of metals found in tissues surrounding patients with metal-on-metal hip replacements that failed with (Ultima hips) or without (current generation, large diameter hips) corrosion. The commonest clinical category of failure of metal-on-metal (MOM) hip replacements is “unexplained” and commonly involved a soft tissue inflammatory response. The mechanism of failure of the Ultima MOM total hip replacement includes severe corrosion of the metal stem and was severe enough to be removed from clinical use. Corrosion is not a feature that we have found in the currently used MOM bearings. To better understand the biological response to MOM wear debris we hypothesized that tissue from failed hips with implant corrosion contained a different type of metal species when compared to those without corrosion.Summary
Introduction
Metal-on-metal (MOM) hip resurfacings release chromium and cobalt wear debris into the surrounding joint. The hip tissue taken from failed MOM hips shows specific histological features including a subsurface band-like infiltrate of macrophages with particulate inclusions, perivascular lymphocytic infiltrate and fibrin exudation. This tissue response has been called Aseptic Lymphocytic Vasculitis Associated Lesion (ALVAL). There is a recognised carcinogenic potential associated with hexavalent chromium and epidemiological data from first generation MOM arthroplasties may suggest an increased incidence of haematological malignancy. The ALVAL type reaction includes a marked proliferation of lymphocytes in the perivascular space and thorough investigation of this lymphocytic response is warranted. This study aims to further characterise the lymphocytic infiltrate using immunohistochemistry and to test clonality using polymerase chain reaction (PCR). Tissues from revised all cause failed MOM hip arthroplasties (n=77) were collected and analysed initially using routine H&E staining. Those that met the diagnostic criteria of ALVAL described above (n=34) were further stained with a panel of immunohistochemical markers (CD3, CD4, CD8 (T-cell markers) and CD20 (B-cell marker)). 10 representative ALVAL cases were selected and sent for gene rearrangement studies using PCR to determine whether the lymphocytes were polyclonal or monoclonal in nature. The analysis of the lymphocytic aggregates in ALVAL, showed a mixed population of B and T cells. Within the aggregates, there was a predominance of B cells (CD20) over T cells (CD3). Of the 10 cases which were analysed by PCR, 7 were suitable for interpretation. None of these cases showed evidence of monoclonal lymphocyte proliferation. The carcinogenic potential of wear debris from MOM hips, particularly affecting the haematopoietic system should be investigated. This study has shown a predominantly B-lymphocyte response in tissues surrounding MOM hips which is polyclonal. Although the numbers are small, the study suggests an immune mediated response in MOM hip tissue and excludes a neoplastic proliferation. However, long term follow up of patients with MOM hips may be prudent.