Abstract
Background: Previous studies demonstrated that significant association was found between IL-34 synovial tissue expression and synovitis severity in RA. Furthermore the overexpression of cathepsin K in RA synovia proves that this protease may become a new and highly specific biomarker for RA. Objective: To find out whether serum levels of IL-34 and Cathepsin-K vary in patients with longstanding RA treated with biologic therapy versus early RA patients treated with conventional DMARDS. Also to estimate any association between their baseline serum levels and disease activity, subsequent joint destruction and osteoporosis. Methods: This study included forty one RA patients, 21 as a patient group who started treatment with anti TNFα therapy. Group of controls included 20 RA patients who were treated with DMARDs. Full clinical and laboratory assessment as well as radiological by Van Der Heide Sharp score (SHS) and DEXA T scores were done. Serum IL34 and cathepsin k were assessed by ELISA before and one year after treatment. Results: After one year of therapy, patients group had significant lower serum IL-34 (s.IL-34) level, cathepsin K level CRP, DAS28, DEXA T-score, and SHS. (p<0.01) than baseline values(p<0.01), while no significant change in s.IL-34, cathepsin-K in controls. Baseline sIL34 and cathepsin K were positively correlated with DAS28 and SHS and DEXA T scores (pE‚0.05). There was a significant difference in morning stiffness, DAS28, and serum IL-34 in good responders versus poor responders according to WHO/ILAR response criteria of improvement among patients group. High baseline DAS28 is independent risk factors for radiographic change in RA while high baseline CRP is a risk factor for osteoporosis in RA patients. Conclusion: Serum IL 34 and cathepsin k were strongly linked to disease activity and duration in RA patients and were highly relevant to both localized osteoporosis and generalized osteoporosis. Also, Anti TNFα therapy effectively decrease both biomarkers regardless drug type, with amelioration of clinical, laboratory and radiological parameters of RA patients.
Highlights
Rheumatoid arthritis (RA) is an autoimmune chronic inflammatory disease characterized by inflammatory infiltration of the synovium and synovial hyperplasia, leading to cartilage degradation and bone destruction which may be manifested as erosions, localized juxtaarticular bone loss, or generalized bone loss [1]
There was a significant difference in morning stiffness, DAS28, and serum IL-34 in good responders versus poor responders according to World Health Organization (WHO)/ILAR response criteria of improvement among patients group
Serum IL 34 and cathepsin k were strongly linked to disease activity and duration in RA patients and were highly relevant to both localized osteoporosis and generalized osteoporosis
Summary
Rheumatoid arthritis (RA) is an autoimmune chronic inflammatory disease characterized by inflammatory infiltration of the synovium and synovial hyperplasia, leading to cartilage degradation and bone destruction which may be manifested as erosions, localized juxtaarticular bone loss, or generalized bone loss [1]. Osteoclasts (OCs) differentiate from the monocyte/macrophage lineage of hematopoietic myeloid progenitors and its differentiation correlates with the severity of the inflammatory condition. Imbalance between osteoblast and osteoclast activities due to inflammatory cytokines pannus interface, periarticular and generalized bone loss in RA pathophysiology [5]. Tumor necrosis factor alpha (TNF−α) is mediating mobilization of osteoclast precursors (OCPs) from bone marrow into the inflamed joint. It stimulates fibroblast-like synovial cells (FLS) to increase cytokines production, which accelerates OC activation in the inflamed synovium of RA [6].
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