Osteoporosis as a risk in inflammatory bowel disease

The association between inflammatory bowel disease (IBD) and metabolic bone disease has been known for some decades. When dual-energy X-ray absorptiometry (DXA) became available the number and the size of studies on this subject increased. The reported prevalence of decreased bone mass varies from 2.7-77% depending on patient selection, method of bone density measurement and definitions used. Osteoporosis is defined as a systemic skeletal disease characterized by low bone mass and microarchitectural deterioration of bone tissue, with an increase in bone fragility and fracture risk. Osteopenia is the preclinical condition of osteoporosis. The pathogenesis of bone loss in IBD is probably multifactorial and involves maldigestion and malabsorption with other influential factors, such as vitamin D deficiency and calcium deficiency, sex hormone deficiency, smoking, disease activity and corticosteroid use. In several studies, bone mineral density in patients with Crohn's disease has been found to be similar to bone mineral density in patients with ulcerative colitis, but others have indicated that low bone mineral density is preferentially a feature of Crohn's disease. In Crohn's disease more risk factors for the pathogenesis of bone loss are present than in ulcerative colitis. The use of corticosteroids and the disease process in IBD are thought to have a central role in the negative effects on bone metabolism. Many studies support the negative effect of corticosteroids on bone mineral density, but data are also controversial. Corticosteroids are effective in the treatment of IBD; however, they cause a negative calcium balance, reduce bone formation, increase bone resorption and suppress the gonadal steroid production. Furthermore, it has been demonstrated that proinflammatory cytokines directly influence osteoblast and osteoclast function. Osteoblast and osteoclast function can be measured by biochemical markers of bone turnover such as bone-specific alkaline phosphatase, osteocalcin, deoxypyridinoline and collagen type 1 C-terminal crosslinks. With these methods some studies have found no significant changes, while others have found a disturbed remodelling due to impaired bone formation, increased bone resorption, or both. In three out of five longitudinal studies of bone loss in IBD the rate of bone loss is higher than the expected age-related bone loss. Clinical risk factors are inadequate predictors of actual bone mass in the individual patient and there seems to be an individual susceptibility for steroids. Therefore, the threshold for measuring bone mineral density should be low and such measurement ought to be performed in every patient in whom long-term corticosteroid therapy can be expected. Recently, the first series of children with Crohn's disease who developed fractures have been reported. However, there are only a few studies on prevention and treatment of osteopenia and osteoporosis in IBD available. Supplementation of calcium and vitamin D in corticosteroid-treated patients should become a basic therapy. There are no studies available on treatment with bisphosphonates in IBD, which is the treatment of choice in steroid-induced osteoporosis. Locally applied corticosteroids such as budesonide might have less negative effect on bone metabolism than prednisolone. This is currently being examined in a large controlled study on bone mineral density, bone metabolism and vertebral fracture rate in patients with Crohn's disease.