Arthritis & Rheumatism, Volume 62,
November 2010 Abstract Supplement

Abstracts of the American College of
Rheumatology/Association of Rheumatology Health Professionals
Annual Scientific Meeting
Atlanta, Georgia November 6-11, 2010.


Do Patients with Rheumatoid Arthritis Exhibit Differential Cellular Responses to Implant Wear Debris and Do the Implant Failure Mechanisms Differ from Non-RA Patients?

Vasudevan5,  Anant, DiCarlo3,  Edward F., Wright2,  Timothy, Chen2,  Dan, Goldring1,  Steven R., Mandl4,  Lisa A.

Chief Scientific Officer, Hospital for Special Surgery
Department of Biomechanics, Hospital for Special Surgery
Department of Pathology and Laboratory Medicine, Hospital for Special Surgery
Hospital for Special Surgery, New York, NY
Yale School of Medicine, New York, NY

Background:

Peri-implant osteolysis is the major reason total elbow replacements (TER) fail. Osteolysis is caused by implant wear debris, and evidence exists that patients with rheumatoid arthritis (RA) may respond differently to foreign material compared to patients without RA. This study was performed to determine whether TER patients with RA exhibit differential cellular responses to implant wear debris compared to TER patients without inflammatory joint disease.

Materials and Methods:

Thirty-eight patients who had their first TER revision for osteolysis were reviewed. All had similar prosthetic devices removed between 1996 and 2008. Twenty-five had RA, and thirteen had no autoimmune disease. Histopathology, clinical data, and gross wear of the removed prostheses were evaluated and compared in RA and non-RA patients.

Results:

Structural evaluation of the retrieved prostheses showed increased material loss was significantly associated with the generation of more, large polyethylene particles (p-value < 0.01) and a trend towards more metal particles (p-value = 0.05). The amount of wear debris in the tissue was similar regardless of underlying diagnosis (p-value > 0.65). In the presence of large particulate polyethylene debris, RA patients not on anti-TNF therapy showed a trend towards more plasma cell infiltration within lymphocytic aggregates in the periprosthetic tissue compared with non-RA patients (p-value = 0.07). This difference was attenuated in RA patients who had received anti-TNF therapy (p-value = 1.0). Among patients with high levels of plasma cells within lymphocytic aggregates, non-RA and RA patients on anti-TNF inhibitors showed similar perivascular patterns of lymphocytic aggregation, whereas RA patients not on anti-TNF inhibitors showed no perivascular aggregates (p-value = 0.01).

Conclusion:

RA patients exhibit a distinct pattern of cellular response to implant wear debris when compared with non-RA patients, which was not due to differences in the type or amount of particulate debris. The increased number of plasma cells within lymphoid aggregates indicates that RA patients mount an adaptive immune response to implant wear particles, which is mitigated by anti-TNF therapy. These observations provide insights into the pathogenic link between the innate and adaptive immune systems in RA and have implications for future approaches to treating osteolysis in RA patients.

To cite this abstract, please use the following information:
Vasudevan, Anant, DiCarlo, Edward F., Wright, Timothy, Chen, Dan, Goldring, Steven R., Mandl, Lisa A.; Do Patients with Rheumatoid Arthritis Exhibit Differential Cellular Responses to Implant Wear Debris and Do the Implant Failure Mechanisms Differ from Non-RA Patients? [abstract]. Arthritis Rheum 2010;62 Suppl 10 :1080
DOI: 10.1002/art.28847

Abstract Supplement

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