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THU0184 Repair of Bone Erosion in Rheumatoid Arthritis by Denosumab: An HR-pQCT Study
  1. J. Yue1,
  2. J.F. Griffith2,
  3. L. Shi1,
  4. D.F. Wang3,
  5. J. Shen4,
  6. P. Wong1,
  7. E.K. Li1,
  8. T.Y. Zhu5,
  9. L. Qin6,
  10. L.-S. Tam1
  1. 1Department of Medicine & Therapeutics, The Prince of Wales Hospital, The Chinese University of Hong Kong, Hongkong
  2. 2Department of Imaging and Interventional Radiology, The Prince of Wales Hospital, The Chinese University of Hong Kong, Hong Kong
  3. 3Department of Imaging and Interventional Radiology, The Prince of Wales Hospital, The Chinese University of Hong Kong, Hong Kong, Hongkong
  4. 4Department of Medicine & Therapeutics
  5. 5Bone Quality and Health Center of the Department of Orthopedics & Traumatology, The Prince of Wales Hospital, The Chinese University of Hong Kong, Hong Kong
  6. 6Department of Orthopedics & Traumatology, The Prince of Wales Hospital, The Chinese University of Hong Kong, Hongkong, Hong Kong

Abstract

Background Blockade of receptor activator of nuclear factor kappa B ligand (RANKL), using denosumab retards bone damage in RA. Whether RANKL blockade allows repair of existing bone erosions is so far unclear.

Objectives To compare the reparative effect of denosumab and alendronate on erosions in female RA patients with low bone mass using HR-pQCT.

Methods This is a post-hoc analysis of a randomized-controlled trial. 40 patients with bone erosions were randomized in a 1:1 ratio to receive either subcutaneous denosumab (60mg) once or oral alendronate (70mg) weekly for 6 months. The size of individual bone erosions and the presence and degree of marginal osteosclerosis around the second metacarpophalangeal joint of the non-dominant hand were measured both semi-quantitatively and quantitatively at baseline, 3- and 6-months.

Results At baseline, the mean (±SD) width, depth and volume of the bone erosion were similar for both groups (Table). At 6 months, erosion size significantly decreased in the denosumab group, and significantly increased in the alendronate group. The between group differences in all size criteria were statistically significant at 6 months (all p<0.01). The degree of marginal osteosclerosis was similar between both groups at baseline. At 6-month, more than half of the patients (57.1%) in the alendronate group showed no osteosclerosis (grade 0). In contrast, most patients (80.9%) in the denosumab group showed osteosclerosis (grade 1 or 2). Mean (±SD) pixel attenuation of the erosion margin was similar between both groups at baseline. Mean pixel attenuation was significantly increased at 6 months in the denosumab group though unchanged in the alendronate group. Between group differences for change in mean pixel attenuation between baseline and 6 months were also significant (p<0.05).

Conclusions Bone erosions in RA patients treated with denosumab show evidence of limited repair in contrast to bone erosions in patients treated with alendronate, indicating a favourable impact of RANKL inhibitor on the local bone remodeling.

Disclosure of Interest None declared

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