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Bone Alterations in Inflammatory Bowel Diseases

Abstract

Inflammatory bowel diseases (IBDs) are characterized by a multifactorial partially unknown etiology that involves genetic, immunological and environmental factors. Up to 50% of IBD patients experience at least one extraintestinal manifestation; among them is the involvement of bone density which is referred to as metabolic bone disease (MBD), including osteopenia and osteoporosis. Bone alterations in IBDs population appear to have a multifactorial etiology: Decreased physical activity, inflammation-related bone resorption, multiple intestinal resections, dietary malabsorption of minerals and vitamin D deficiency, genetic factors, gut-bone immune signaling interaction, steroid treatment, microbiota and pathogenic micro-organisms interaction, and dietary malabsorption of minerals, that, all together or individually, may contribute to the alteration of bone mineral density. This review aims to summarize the prevalence and pathophysiology of metabolic bone alterations in IBD subjects outlining the main risk factors of bone fragility. We also want to underline the role of the screening and prophylaxis of bone alterations in Crohn's disease and ulcerative colitis patients and the importance of treating appropriately MBD.

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References
1.
Takahashi N, Udagawa N, Suda T . A new member of tumor necrosis factor ligand family, ODF/OPGL/TRANCE/RANKL, regulates osteoclast differentiation and function. Biochem Biophys Res Commun. 1999; 256(3):449-55. DOI: 10.1006/bbrc.1999.0252. View

2.
von Tirpitz C, Pischulti G, Klaus J, Rieber A, Bruckel J, Bohm B . [Pathological bone density in chronic inflammatory bowel diseases--prevalence and risk factors]. Z Gastroenterol. 1999; 37(1):5-12. View

3.
Tsuboi M, Kawakami A, Nakashima T, Matsuoka N, Urayama S, Kawabe Y . Tumor necrosis factor-alpha and interleukin-1beta increase the Fas-mediated apoptosis of human osteoblasts. J Lab Clin Med. 1999; 134(3):222-31. DOI: 10.1016/s0022-2143(99)90201-9. View

4.
Hofbauer L, Gori F, Riggs B, Lacey D, Dunstan C, Spelsberg T . Stimulation of osteoprotegerin ligand and inhibition of osteoprotegerin production by glucocorticoids in human osteoblastic lineage cells: potential paracrine mechanisms of glucocorticoid-induced osteoporosis. Endocrinology. 1999; 140(10):4382-9. DOI: 10.1210/endo.140.10.7034. View

5.
Scott E, Gaywood I, Scott B . Guidelines for osteoporosis in coeliac disease and inflammatory bowel disease. British Society of Gastroenterology. Gut. 2000; 46 Suppl 1:i1-8. PMC: 1766735. DOI: 10.1136/gut.46.suppl_1.i1. View