Bone alterations in inflammatory bowel diseases

Sgambato, D.; Gimigliano, Francesca; Musis, Cristiana De; Moretti, Antimo; Toro, Giuseppe; Ferrante, Emanuele; Miranda, Agnese; Mauro, Domenico De; Romano, Lorenzo; Iolascon, Giovanni; Romano, Marco

doi:10.12998/wjcc.v7.i15.1908

Cited by 45 publications

(42 citation statements)

References 115 publications

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“…Inflammatory bowel diseases (IBD), including Crohn’s Disease (CD) and Ulcerative Colitis (UC), are chronic conditions, the aetiology of which is not entirely known. Possible risk factors comprise genetic predisposition, immunological disorders, and environmental conditions [ 1 ]. Furthermore, the chronic character of these diseases causes extra-intestinal complications such as osteoporosis, which is manifested by low bone mineral density, resulting in an increased risk of fractures [ 2 ].…”

Section: Introductionmentioning

confidence: 99%

“…In the course of IBD, pro-inflammatory molecules TNF-α, IL-1β, IL-6, and IL-17 levels are elevated and lead to increased bone resorption, causing a decrease in bone mineral density [ 4 ]. In fact, low bone mineral density, osteopenia and osteoporosis were found in 22–77%, 32–36%, and 7–15% of IBD patients, respectively [ 1 ]. Additionally, low BMD is observed more frequently in CD than UC patients [ 5 ].…”

Section: Introductionmentioning

confidence: 99%

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Nutrients in the Prevention of Osteoporosis in Patients with Inflammatory Bowel Diseases

et al. 2020

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The chronic character of inflammatory bowel diseases, such as Crohn’s disease and ulcerative colitis, results in various complications. One of them is osteoporosis, manifested by low bone mineral density, which leads to an increased risk of fractures. The aetiology of low bone mineral density is multifactorial and includes both diet and nutritional status. Calcium and vitamin D are the most often discussed nutrients with regard to bone mineral density. Moreover, vitamins A, K, C, B12; folic acid; calcium; phosphorus; magnesium; sodium; zinc; copper; and selenium are also involved in the formation of bone mass. Patients suffering from inflammatory bowel diseases frequently consume inadequate amounts of the aforementioned minerals and vitamins or their absorption is disturbed, resulting innutritional deficiency and an increased risk of osteoporosis. Thus, nutritional guidelines for inflammatory bowel disease patients should comprise information concerning the prevention of osteoporosis.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Nutrients in the Prevention of Osteoporosis in Patients with Inflammatory Bowel Diseases

et al. 2020

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“…Specific nutritional challenges exist in many children and adolescents post‐transplantation; interventions for these must be individualized based on the underlying disorder and specific nutritional laboratory abnormalities. Specific interventions for less common nutritional problems in this population are detailed in other references 23,24 . This section provides recommendations for general measures to promote bone health in all children and adolescents post–solid organ transplantation (Table 3).…”

Section: General Measures For Promoting Bone Health For All Children mentioning

confidence: 99%

Promoting bone health in children and adolescents following solid organ transplantation

Kusumi

Shaikhkhalil

Patel

et al. 2020

Pediatric Transplantation

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Solid organ transplantation in children and adolescents provides many benefits through improving critical organ function, including better growth, development, cardiovascular status, and quality of life. Unfortunately, bone status may be adversely affected even when overall status is improving, due to issues with pre-existing bone disease as well as medications and nutritional challenges inherent post-transplantation. For all children and adolescents, bone status entering adulthood is a critical determinant of bone health through adulthood. The overall health and bone status of transplant recipients benefits from attention to regular physical activity, good nutrition, adequate calcium, phosphorous, magnesium and vitamin D intake and avoidance/minimization of soda, extra sodium, and obesity. Many immunosuppressive agents, especially glucocorticoids, can adversely affect bone function and development. Minimizing exposure to "bone-toxic" medications is an important part of promoting bone health in children post-transplantation. Existing guidelines detail how regular monitoring of bone status and biochemical markers can help detect bone abnormalities early and facilitate valuable bone-directed interventions. Attention to calcium and vitamin D supplementation, as well as tapering and withdrawing glucocorticoids as early as possible after transplant, can provide best bone outcomes for these children. Dual-energy X-ray absorptiometry can be useful to detect abnormal bone mass and fracture risk in this population and newer bone assessment methods are being evaluated in children at risk for poor bone outcomes. Newer bone therapies being explored in adults with transplants, particularly bisphosphonates and the RANKL inhibitor denosumab, may offer promise for children with low bone mass post-transplantation.

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“…8 Other factors, such as malabsorption of essential nutrients like calcium and vitamin D and longterm use of glucocorticoids (GCs), contribute to bone loss in IBD patients. 9,10 Despite significant advances in uncovering the pathogenesis of IBD, the precise mechanisms underlying IBD-associated bone loss have not been fully elucidated.…”

Section: Introductionmentioning

confidence: 99%

Skeletal Phenotype and Mechanisms of Bone Loss inWinnieMice as a Model for Inflammatory Bowel Disease

Saedi

Hassan

et al. 2020

Preprint

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ObjectiveWe aimed to investigate the skeletal phenotype of Winnie mouse model of spontaneous chronic colitis, which carries a mutation in the Muc2 gene and closely replicates IBD symptoms and pathophysiology. These mice have a high level of gut-derived serotonin (GDS), a potent osteoblastogenesis inhibitor. We explored the underlying mechanisms of bone loss associated with chronic intestinal inflammation.DesignWinnie male and female mice prior to colitis onset (6 weeks old) and progression (14 and 24 weeks) were compared to age- and sex-matched C57BL/6 controls. We assessed bone quality (static and dynamic histomorphometry, micro-CT, 3-point bending), intestinal inflammation (lipocalin-2), GDS levels, serum levels of calcium, phosphorus and vitamin D, ex vivo bone marrow analysis and molecular mechanisms inhibiting osteoblastogenesis.ResultsSignificant deterioration in trabecular and cortical microarchitecture, reductions in bone formation, mineral apposition rate, bone volume, osteoid volume and bone strength were observed in Winnie mice compared to C57BL/6 controls. Decreased osteoblast and increased osteoclast numbers were prominent in Winnie mice. We report for the first time that elevated GDS cross-talks with molecular pathways to inhibit bone formation in Winnie mice. Increased expression of 5-HTR1B and FOXO1 mRNAs, dissociation of FOXO1/CREB1 complex and association of FOXO1 with ATF4, promoting the transcriptional activity of FOXO1, results in suppression of osteoblast proliferation in Winnie mice compared to controls.ConclusionThese findings open avenues for the development of targeted therapies for IBD-related bone loss.Significance of this studyWhat is already known on this subject?- Osteoporosis is a common extraintestinal manifestation of inflammatory bowel disease (IBD).- Currently available treatments are not effective for IBD-associated bone loss.- The mechanisms of bone loss are poorly understood. A major limitation has been the lack of an appropriate animal model for IBD-associated bone loss.What are the new findings?- We report for the first-time the skeletal phenotype in Winnie mouse model of IBD- This study presents a novel mechanism of IBD-associated bone loss, involving elevated gut-derived serotonin crosstalk with molecular pathways inhibiting bone formation.How might it impact on clinical practice in the foreseeable future- These findings open avenues for the development of targeted therapies for IBD-related bone loss.

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Bone alterations in inflammatory bowel diseases

Cited by 45 publications

References 115 publications

Nutrients in the Prevention of Osteoporosis in Patients with Inflammatory Bowel Diseases

Nutrients in the Prevention of Osteoporosis in Patients with Inflammatory Bowel Diseases

Promoting bone health in children and adolescents following solid organ transplantation

Skeletal Phenotype and Mechanisms of Bone Loss inWinnieMice as a Model for Inflammatory Bowel Disease

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