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Osteoporosis in SpA — SCE Rheumatology MCQ

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ModerateSpondyloarthropathyOsteoporosis in SpASCE Rheumatology

A 58-year-old postmenopausal woman has a 10-year history of HLA-B27-positive radiographic axial spondyloarthritis. She has persistent inflammatory disease activity and reduced weight-bearing activity because of pain and stiffness. She has never received systemic glucocorticoids, and her serum calcium and 25-hydroxyvitamin D are normal. Hip DXA shows a T-score of −2.6, while spinal radiographs demonstrate syndesmophytes. Which disease-related mechanism best explains her low bone mineral density?

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Correct answer: B — Cytokine-driven RANK–RANKL osteoclast activation, compounded by reduced mechanical loading

The correct answer is B. Axial SpA can produce systemic and local trabecular bone loss despite simultaneous syndesmophyte formation. TNF, IL-17 and other inflammatory mediators promote RANK–RANKL-dependent osteoclast differentiation and activation; impaired mobility and reduced weight-bearing provide an additional loss of mechanical stimulus. Syndesmophytes therefore do not indicate preserved systemic bone strength and may artefactually increase lumbar-spine DXA measurements, making hip DXA more reliable. Vitamin D deficiency and systemic glucocorticoids can worsen osteoporosis when present, but neither is required and both are excluded here. Reduced loading alone is also incomplete because inflammatory osteoclast activation is a central disease-related mechanism. HLA-B27 supports the axSpA diagnosis but is not itself the direct explanation for osteoporosis.

Reference: Nakamura A, Towheed T. Pathogenesis, assessment, and management of bone loss in axial spondyloarthritis. Seminars in Arthritis and Rheumatism. 2024;64:152345. https://pubmed.ncbi.nlm.nih.gov/38103486/