Inflammatory bowel diseases as secondary causes of osteoporosis

Abstract

Inflammatory bowel disease (IBD), comprising Crohn's disease and ulcerative colitis, is associated with an increased risk of osteoporosis and bone fractures. Initial studies suggested very high rates of osteoporosis in IBD, but more recent studies have suggested that bone mineral density (BMD) is often normal in patients with IBD and typically changes little over time. Nonetheless, IBD is associated with an increased risk of fractures. Doctors managing patients with IBD must consider a variety of risk factors, not just BMD measurements, in assessing fracture risk. Advances have been made in exploring the pathogenesis of osteoporosis in IBD. The evolution of knowledge regarding receptor for activated factor of nuclear factor kappaB (RANK), its ligand RANKL, and osteoprotegerin (OPG), which serves as a decoy receptor, has enhanced the understanding of both osteoporosis and T-cell immunobiology. Recent clinical studies in patients with IBD have revealed that serum OPG levels may be elevated and inflamed intestinal tissue secretes increased amounts of OPG. It is suspected that OPG levels are elevated as a counterregulatory response to low BMD, as serum OPG levels in IBD have been found to be inversely associated with BMD. Finally, in animal models of IBD, exogenous OPG has reversed both the osteopenia and the enterocolitis, suggesting that it may have a therapeutic role in human IBD.