Chronic inflammatory bowel diseases (IBD) affect bone metabolism and are frequently associated with decreased bone mineral density (BMD) and increased risk of fractures. Experimental models of IBD and as well as data from pediatric and adult IBD patients do not provide a uniform answer whether the changes in bone metabolism leading to decreased mineral density are the result of decreased bone formation, increased bone desorption, or both. New studies continue to unravel a complex network of interactions leading to the inflammation-associated loss of BMD, and may help direct treatment of IBD toward more bone-sparing strategies. Nutritional interventions (dietary calcium and vitamin D supplementation) are of limited efficacy in IBD patients. Therefore, appreciating the extent of the problem and understanding the pathophysiology of osteopenia and osteoporosis in Crohn's disease and ulcerative colitis are critical for the correct choice of available treatments or the development of new targeted therapies.
|Original language||English (US)|
|Number of pages||11|
|State||Published - Sep 1 2012|
ASJC Scopus subject areas