Bone marrow Th17 TNF{alpha} cells induce osteoclast differentiation and link bone destruction to IBD

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-B ligand (RANKL), which binds to its corresponding receptor RANK on osteoclast precursor cells, which ultimately induces their differentiation into osteoclasts. Hence, this work...
Source: Gut - Category: Gastroenterology Authors: Tags: Commentary Source Type: research