Via practica 11/2008

SECONDARY OSTEOPOROSIS BY INFLAMMATION BOWEL DISEASE

Low bone mineral density is a frequent and serious complication by patients with inflammatory bowel disease (IBD). IBD comprising Crohn´s disease and ulcerative colitis is associated with increased risk of osteoporosis and bone fractures. Character of metabolic bone disease depends on origin, duration, seriousness a treatment of IBD. The cause of bone disease is multifactorial an has a few common characteristics: malabsorption, calcium malabsorption, vitamin D deficiency, hypogonadism, secondary hyperparathyreosis, low body weight, reduced physical activity, smoking and alcohol excess. Cytokines (i.e. interleukin 1, tumor necrosis factor, interleukin-6) play an important role in the pathogenesis of IBD. IL-6 contributes to differentiation of osteocytes into osteoclasts. These osteoclasts are then activated in the bone by IL-1 a TNF resulting in an increase in bone resorption. The evolution of knowledge regarding receptor for activated factor of nuclear factor κB (RANK), its legend RANKL, and osteoprotegerin (OPG), which serves as a decoy receptor has enhanced the understanding of osteoporosis. Early diagnostics and treatment lower the risk of fractures, which are most serious complication of osteoporosis.

Keywords: secondary osteoporosis, inflammatory bowel disease (IBD), Crohn´s disease, ulcerative collitis