Abstract
Backgrounds. Heme oxygenase-1 (HO-1) has been reported to play a regulatory role in osteoclastogenesis. Bone morphogenetic protein (BMP) pathways induce osteoblastic differentiation and bone remodeling. Aims. To identify serum levels of HO-1, BMP-7, and Runt related-transcription factor 2 (Runx2) in patients with rheumatoid arthritis (RA) and ankylosing spondylitis (AS) and to investigate the relationships between HO-1, BMP-7, Runx2, and other common biomarkers for bone metabolism. Results. Serum levels of HO-1 and BMP-7 were revealed to be significantly higher in patients with RA or AS than in healthy controls (p < 0.01). In RA group, HO-1 was positively correlated with BMP-7, Runx2, and tartrate-resistant acid phosphatase-5b (TRAP-5b) (p < 0.05, resp.), BMP-7 was positively correlated with Runx2 and TRAP-5b (p < 0.05, resp.), and Runx2 was negatively correlated with N-terminal midfragment of osteocalcin (NMID) (p < 0.05). In AS group, we observed identical correlation between HO-1 and BMP-7, but opposite correlations between BMP-7 and TRAP-5b and between Runx2 and NMID, when comparing with the RA cohort. Conclusion. Our findings suggest that HO-1 and BMP-7 are potential biomarkers for bone metabolism in patients with RA and AS. The different correlations between the bone markers point to distinct differences in bone remodeling pathways in the two types of arthritis.
Highlights
Chronic inflammatory arthritis involves both inflammation and, disruption to bone architecture, but the predominant locations and patterns of structural change differ between different types of rheumatic disease [1, 2]
The sexes and median ages in the ankylosing spondylitis (AS) group were similar to the healthy control group, while more females and older ages were found in the Rheumatoid arthritis (RA) group (Table S1)
Heme oxygenase-1 (HO-1) was positively correlated with Bone morphogenetic protein (BMP)-7, Runx2, and tartrate-resistant acid phosphatase-5b (TRAP-5b), BMP-7 was positively correlated with Runx2 and Tartrate-resistant acid phosphatase (TRAP)-5b, and Runx2 was negatively correlated with N-terminal midfragment of osteocalcin (NMID) in patients with RA
Summary
Chronic inflammatory arthritis involves both inflammation and, disruption to bone architecture, but the predominant locations and patterns of structural change differ between different types of rheumatic disease [1, 2]. Rheumatoid arthritis (RA) is characterized by synovitis, interaction of lymphocytes, macrophages, and synovial cells, the production of matrix metalloproteinases and cytokines such as tumor necrosis factor (TNF), interleukin-1 (IL-1), and interleukin-6 (IL-6), leading to excessive erosion of articular cartilage and marginal bone, and defective bone repair [2,3,4,5,6]. To maintain structural integrity of bone, osteoclasts resorb bone and osteoblasts produce osteoid which is subsequently mineralized to new bone [2, 3, 7]. Unbalanced activity between osteoclasts and osteoblasts resulting in dysregulated bone remodeling occurs both in RA and AS [3].
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