Bone metabolism in inflammatory bowel diseases 1.

ABSTRACT

Inflammatory Bowel Disease encompasses Crohns Disease, which is capable of affecting the entire GI tract, although usually favors the ileocolonic and perianal areas, and Ulcerative Colitis, which is limited to the colon. The pathophysiology is not fully understood but is thought to be caused by a complex interplay among gut microbiota, dysregulation of the hosts immune system, genetic susceptibility and environmental factors. Osteopenia and osteoporosis are considered to be extraintestinal manifestations of inflammatory bowel disease. Osteoporosis is usually diagnosed by dual-energy X-ray absortiometry. Early interventions to treat active CD and preventative treatment strategies to reduce excessive bone loss might prevent long term consequences of bone loss, including fractures. The immune response in IBD includes increased production of variety of proinflammatory cytokines such as IL1β, TNFα, IL6 a IL1 from T cells and macrophages. These have both direct and indirect effects on bone turnover. Vitamin D is vital in mantenance of bone strenght, mineralisation and fracture prevention. Vitamin Ds physiological importance has also been implicated in a number of inflammatory diseases, mainly asthma, atherosclerosis and autoimmune disease.