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The effect of etanercept on osteoclast precursor frequency and enhancing bone marrow oedema in patients with psoriatic arthritis

¹ Department of Allergy, Immunology and Rheumatology, University of Rochester, New York, USA
² Department of Orthopedics, University of Rochester, New York, USA
³ Virtual Scopics, Rochester, New York, USA
⁴ Department of Radiology, University of Rochester, New York, USA
⁵ Department of Biostatistics, University of Rochester, New York, USA
⁶ Clinical Immunology Research Center, Allergy, Immunology & Rheumatology Research Division, University of Rochester Medical Center, New York, USA

Correspondence to:
A P Anandarajah, Clinical Immunology Research Center, 601 Elmwood Avenue, Box 695, Rochester, New York 14642; allen_anandarajah{at}urmc.rochester.edu

Objective: The frequency of osteoclast precursors (OCPF) and the presence of bone marrow oedema (BMO) are potential response biomarkers in psoriatic arthritis (PsA). Previous studies suggest a central role for tumour necrosis factor (TNF) in the formation of osteoclast precursors. To better understand this association, the effect of etanercept on OCPF and BMO was analysed in PsA patients with erosive arthritis.

Methods: A total of 20 PsA patients with active erosive PsA were enrolled. Etanercept was administered twice weekly for 24 weeks. OCPF was measured and clinical assessments were performed at baseline, 2, 12 and 24 weeks. Gadolinium enhanced MR images were obtained at baseline and 24 weeks.

Results: Significant improvements in joint score (p<0.001), HAQ scores (p<0.001) and SF-36 parameters were observed after 6 months of therapy with etanercept compared to baseline. The median OCPF decreased from 24.5 to 9 (p = 0.04) and to 7 (p = 0.006) after 3 months and 6 months of treatment, respectively. MR images were available for 13 patients. The BMO volume decreased in 47 and increased in 31 sites at 6 months. No correlation was noted between OCPF, BMO and clinical parameters.

Conclusion: The rapid decline in OCPF and overall improvement in BMO after anti-TNF therapy provides one mechanism to explain the anti-erosive effects of TNF blockade in PsA. Persistence of BMO after etanercept treatment, despite a marked clinical response, was unexpected, and suggests ongoing subchondral inflammation or altered remodelling in PsA bone.