Abstract
BackgroundGlucocorticoids (GC) modulate several regulators involved in the pathogenesis of bone changes in rheumatoid arthritis (RA). Trabecular bone score (TBS) allows the indirect assessment of bone quality. The aim of this study was to investigate the effects of GC on TBS and serum levels of bone turnover regulators in patients with recent-onset RA.Materials and methodsForty-seven subjects with recent-onset RA (< 6 months) were classified in two groups, low (lGC) and high (hGC) glucocorticoids, according to glucocorticoid dose regimens. Bone mineral density (BMD), TBS, and circulating Dickkopf-1 (Dkk1), sclerostin, osteoprotegerin (OPG), and RANK-L were evaluated at baseline and 6 and 12 months.ResultsBMD significantly declined after 12 months with no significant difference between the lGC and hGC group, whereas TBS decreased in the hGC group only. Circulating OPG decreased during the follow-up period, the reduction being significantly greater in hGC group; conversely, sclerostin and RANK-L serum increased, in a significantly greater extent in the hGC group. TBS inversely correlated with sclerostin, RANK-L, and Dkk1 circulating levels whereas directly correlated with OPG circulating levels. GC cumulative dose showed an inverse relationship with BMD in both the hGC and lGC groups; TBS values showed an inverse relationship with GC cumulative dose in the hGC group only. GC cumulative dose was associated to higher sclerostin and lower OPG serum levels. TBS did not correlate with disease activity whereas BMD was inversely related to disease activity.ConclusionsIn early RA, GC exposure contributes to the reduction of BMD and affects bone quality depending on dose regimens. TBS could be a useful tool to evaluate the negative effect of GC on bone microarchitecture.Trial registrationThis study was ancillary to a parallel-group observational prospective study which was approved by the medical local ethics committee (protocol number DDG 334/19-06-2019).
Highlights
Glucocorticoids (GC) modulate several regulators involved in the pathogenesis of bone changes in rheumatoid arthritis (RA)
bone mineral density (BMD) significantly declined after 12 months with no significant difference between the low glucocorticoid (lGC) and high glucocorticoid (hGC) group, whereas Trabecular bone score (TBS) decreased in the hGC group only
In early RA, GC exposure contributes to the reduction of BMD and affects bone quality depending on dose regimens
Summary
Glucocorticoids (GC) modulate several regulators involved in the pathogenesis of bone changes in rheumatoid arthritis (RA). Rheumatoid arthritis (RA) is a chronic systemic inflammatory disease mainly involving the synovial joints, and it is characterized by both local bone loss, represented by juxta-articular osteoporosis and erosions, and systemic bone loss, represented by generalized osteoporosis [1]. The physiopathology of osteoporosis in RA is very complex; systemic inflammation and glucocorticoid (GC) treatment are two major determinants of generalized bone loss; inflammatory cytokines, such as TNFα, IL6, and IL1 are associated to enhanced osteoclast activity, mainly mediated by receptor activator of nuclear factor kappa-Β ligand (RANKL), while GC-induced bone loss is related to both inhibition of bone formation mediated by the inhibitory effects on Wnt signaling and to an increase of bone resorption associated to the dysregulation of RANKL/osteoprotegerin (OPG) system [2]. BMD only partially represents bone strength, which results from both bone density and bone quality; in patients treated with GC, osteoporotic fractures occur with higher BMD values compared to untreated patients [4]
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