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Osteoporosis in IBD has long been attributed to impaired bone formation caused by malabsorption and consequent vitamin D and calcium deficiency or to long-term steroid therapy. However, systemic bone loss is not restricted to chronic inflammatory conditions of the intestine such as IBD or coeliac disease, but is also found in non-intestinal chronic inflammatory conditions including rheumatoid arthritis, ankylosing spondylitis and psoriatric arthritis.1 In a groundbreaking paper in 1999, rheumatologists started to shed light on the process of inflammation-induced bone loss.2 In this work by Kong and colleagues, the initial evidence indicated that T cells affect maturation of osteoclasts, the primary bone-resorbing cells. They showed in an arthritis model that systemically activated T cells are sufficient to induce receptor activator of NF-κB ligand (RANKL), which binds to its corresponding receptor RANK on osteoclast precursor cells, which ultimately induces their differentiation into osteoclasts. Hence, this work suggested a novel role for T cells in bone pathology. In the same year, the osteoclastogenic function of interleukin (IL)-17, at this time a newly discovered T-cell-derived cytokine, was first described. It was shown that IL-17 induces RANKL expression by osteoblasts, which further promotes osteoclast maturation. The presence of high levels of IL-17 in the synovial fluid of patients with rheumatoid arthritis led the authors to conclude that IL-17 is a crucial cytokine for osteoclastogenic bone resorption in …
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