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Review
. 2019 Aug 6;7(15):1908-1925.
doi: 10.12998/wjcc.v7.i15.1908.

Bone alterations in inflammatory bowel diseases

Dolores Sgambato  1 , Francesca Gimigliano  2 , Cristiana De Musis  1 , Antimo Moretti  3 , Giuseppe Toro  3 , Emanuele Ferrante  1 , Agnese Miranda  1 , Domenico De Mauro  1 , Lorenzo Romano  4 , Giovanni Iolascon  3 , Marco Romano  5
Affiliations
Review

Bone alterations in inflammatory bowel diseases

Dolores Sgambato et al. World J Clin Cases. .

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.

Keywords: Bone alterations; Bone mineral density; Crohn’s disease; Inflammatory bowel diseases; Osteopenia; Osteoporosis; Ulcerative colitis.

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Conflict of interest statement

Conflict-of-interest statement: No potential conflicts of interest. No financial support.

Figures

Figure 1
Figure 1
Modulation of osteoclast differentiation by serum TNF-α and anti-TNF-α treatment. A: TNF-α influences osteoclast precursor differentiation and bone resorption activity inducing RANKL expression on osteoblast cells and preventing the binding of OPG; B: Anti-TNF-α treatment reduces RANKL expression resulting in decrease of osteoclast differentiation and bone resorption.
Figure 2
Figure 2
Gut-bone immune signaling: interplay between different factors which may affect bone metabolism in patients with inflammatory bowel diseases.
Figure 3
Figure 3
Diagramatic representation of the pathogenic mechanisms involved in alteration of bone mineral density in inflammatory bowel diseases.
See this image and copyright information in PMC

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