Abstract
ObjectivesRheumatoid arthritis (RA) and ankylosing spondylitis (AS) have been associated with generalized and localized bone loss. We conducted a comprehensive study using imaging (dual-energy X-ray absorptiometry, DXA) and laboratory biomarkers in order to determine bone health and to study the effects of anti-tumor necrosis factor (TNF) biologics in RA and AS.Patients and methodsThirty-six RA and 17 AS patients undergoing 1-year etanercept (ETN) or certolizumab-pegol (CZP) therapy were studied. Bone density was assessed by DXA at baseline and after 12 months. Serum C-reactive protein (CRP), calcium, phosphate, parathyroid hormone (PTH), vitamin D3, osteocalcin, procollagen type I N-propeptide (P1NP), C-terminal telopeptide (βCTX), osteoprotegerin, sclerostin (SOST), Dickkopf-1 (DKK-1), soluble receptor activator nuclear kappa B ligand (sRANKL), and cathepsin K (cathK) levels were determined at baseline and after 6 and 12 months.ResultsTNF-α inhibition was clinically effective. Anti-TNF-α halted further bone loss over 1 year. In general, anti-TNF therapy significantly increased P1NP, SOST levels, and the P1NP/βCTX ratios, while decreased DKK-1 and CathK production at different time points in most patient subsets. In the full cohort and in RA, baseline and/or 12-month bone mineral density (BMD) at multiple sites exerted inverse relationships with CRP and βCTX, and positive correlation with SOST. In AS, L2-4 BMD after 1-year biologic therapy inversely correlated with baseline βCTX, while femoral neck BMD rather showed inverse correlations with CRP.ConclusionsAnti-TNF therapy slowed down generalized bone loss, in association with clinical improvements, in both diseases. TNF blockade may enhance bone formation and suppress joint destruction. Anti-TNF therapy may act inversely on DKK-1 and SOST. Independent predictors of BMD were SOST and βCTX in RA, whilst CRP in AS.Key Points• One-year anti-TNF therapy halted generalized bone loss in association with clinical improvement in arthritides.• Anti-TNF therapy may inversely act on DKK-1 and SOST.• Independent predictors of BMD were SOST and βCTX in RA, while CRP in AS.
Highlights
Rheumatoid arthritis (RA) and ankylosing spondylitis (AS) have been associated with osteoporosis, as well as localized inflammatory bone resorption and/or formation [1, 2]
RA and AS have been associated with secondary osteoporosis and increased fracture risk [1, 2]
Biological therapy may affect the production of bone markers in RA and AS [12]
Summary
Rheumatoid arthritis (RA) and ankylosing spondylitis (AS) have been associated with osteoporosis, as well as localized inflammatory bone resorption and/or formation [1, 2]. Low bone mineral density (BMD) and increased fracture risk have been observed in two-third of these patients [1, 2]. The RANK-RANKL system is highly involved in inflammatory bone resorption [3, 4]. Clin Rheumatol (2020) 39:167–175 factor α (TNF-α) induces bone loss via the stimulation of RANKL [1, 3,4,5]. Osteoprotegerin (OPG), a decoy receptor of RANKL, influences bone erosions in arthritides [8]. A low OPG/RANKL ratio has been associated with increased radiographic damage in RA [9, 10]. TNF-α inhibitors inhibited bone destruction and reduced radiological progression in RA [11,12,13]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
