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 absorptiom etry (DXA) became available the number and the size of studies on this subj ect increased. The reported prevalence of decreased bone mass varies from 2 .7-77% depending on patient selection, method of bone density measurement a nd definitions used. Osteoporosis is defined as a systemic skeletal disease characterized by low bone mass and microarchitectural deterioration of bon e 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 malabsorpt ion with other influential factors, such as vitamin D deficiency and calciu m deficiency, sex hormone deficiency, smoking, disease activity and cortico steroid use. In several studies, bone mineral density in patients with Croh n's disease has been found to be similar to bone mineral density in patient s 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 ulc erative colitis. The use of corticosteroids and the disease process in IBD are thought to have a central role in the negative effects on bone metaboli sm. Many studies support the negative effect of corticosteroids on bone min eral density, but data are also controversial. Corticosteroids are effectiv e in the treatment of IBD; however, they cause a negative calcium balance, reduce bone formation, increase bone resorption and suppress the gonadal st eroid production. Furthermore, it has been demonstrated that proinflammator y cytokines directly influence osteoblast and osteoclast function. Osteobla st and osteoclast function can be measured by biochemical markers of bone t urnover such as bone-specific alkaline phosphatase, osteocalcin, deoxypyrid inoline and collagen type 1 C-terminal crosslinks. With these methods some studies have found no significant changes, while others have found a distur bed 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. Clinic al risk factors are inadequate predictors of actual bone mass in the indivi dual patient and there seems to be an individual susceptibility for steroid s. Therefore, the threshold for measuring bone mineral density should be lo w 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. H owever, there are only a few studies on prevention and treatment of osteope nia and osteoporosis in IBD available. Supplementation of calcium and vitam in D in corticosteroid-treated patients should become a basic therapy. Ther e 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 fra cture rate in patients with Crohn's disease.