Changes of OPG and RANKL concentrations in Crohnʼs disease after infliximab therapy

Miheller, Pál; Műzes, Györgyi; Rácz, Kàroly; Blázovits, A.; Lakatos, László; Herszényi, László; Tulassay, Zsolt

doi:10.1002/ibd.20234

Cited by 58 publications

(13 citation statements)

References 34 publications

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“…The role of TNF-␣ in mediating bone loss is supported by several clinical studies in which IBD patients were treated with infliximab, and markers of bone remodeling were assessed. In these studies, improvements in bone metabolism were observed in the infliximab-treated patients (1,22,43). However, this does not prove that TNF-␣ is the direct cause because TNF-␣ has multiorgan effects.…”

Section: Discussionmentioning

confidence: 92%

Intestinal inflammation without weight loss decreases bone density and growth

Irwin

Raehtz

Parameswaran

et al. 2016

American Journal of Physiology-Regulatory, Integrative and Comp

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Increasing evidence indicates a strong link between intestinal health and bone health. For example, inflammatory bowel disease can cause systemic inflammation, weight loss, and extra-intestinal manifestations, such as decreased bone growth and density. However, the effects of moderate intestinal inflammation without weight loss on bone health have never been directly examined; yet this condition is relevant not only to IBD but to conditions of increased intestinal permeability and inflammation, as seen with ingestion of high-fat diets, intestinal dysbiosis, irritable bowel syndrome, metabolic syndrome, and food allergies. Here, we induced moderate intestinal inflammation without weight loss in young male mice by treating with a low dose of dextran sodium sulfate (1%) for 15 days. The mice displayed systemic changes marked by significant bone loss and a redistribution of fat from subcutaneous to visceral fat pad stores. Bone loss was caused by reduced osteoblast activity, characterized by decreased expression of osteoblast markers (runx2, osteocalcin), histomorphometry, and dynamic measures of bone formation. In addition, we observed a reduction in growth plate thickness and hypertrophic chondrocyte matrix components (collagen X). Correlation analyses indicate a link between gut inflammation and disease score, but more importantly, we observed that bone density measures negatively correlated with intestinal disease score, as well as colon and bone TNF-α levels. These studies demonstrate that colitis-induced bone loss is not dependent upon weight loss and support a role for inflammation in the link between gut and bone health, an important area for future therapeutic development.

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Section: Discussionmentioning

confidence: 92%

Intestinal inflammation without weight loss decreases bone density and growth

Irwin

Raehtz

Parameswaran

et al. 2016

American Journal of Physiology-Regulatory, Integrative and Comp

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“…Finally, administration of anti-TNFs has been associated with improved bone mineral density in CD. Long-term maintenance therapy improves bone density and IFX improves bone mineral metabolism in CD [40,41]. …”

Section: Osteoporosis and Osteopeniamentioning

confidence: 99%

Treatment of Extraintestinal Manifestations in Inflammatory Bowel Disease

Lakatos

Lakatos²,

Kiss

et al. 2012

Digestion

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Inflammatory bowel disease (IBD) is a systemic disease associated with a large number of extraintestinal manifestations (EIM). EIM are present in 15–20% of patients with ulcerative colitis and in 20–40% of patients with Crohn’s disease. The management of EIM is best provided by a multidisciplinary team, which includes specialists in the affected organ systems with training in the treatment of IBD. Therapeutic strategy is often empirical. This is explained by the paucity of randomized-controlled studies for the specific treatment of EIM in IBD and by the fact that treatment models are based on extrapolation from patients with similar conditions but without IBD. For most EIM, the mainstay of therapy is the treatment of the underlying active IBD. However, some EIM such as axial arthritis, pyoderma gangrenosum, uveitis and primary sclerosing cholangitis run a clinical course independent of IBD activity and need specific therapy (e.g. TNF antagonists in ankylosing spondylitis and skin manifestations). This review summarizes the conventional and novel (e.g. anti-TNF) treatment modalities, and the therapeutic implications for the management of extraintestinal symptoms in IBD, in order to assist clinicians in optimizing treatment strategies for IBD patients with EIM.

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“…Accelerated bone resorption - so-called uncoupling - is responsible for low bone mass in CD [32]. It has been demonstrated that serum markers for bone formation and bone resorption are higher in CD than HC [33].…”

Section: Discussionmentioning

confidence: 99%

Low bone mass in microscopic colitis

et al. 2011

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BackgroundMicroscopic colitis presents with similar symptoms to classic inflammatory bowel diseases. Osteoporosis is a common complication of Crohn's disease but there are no data concerning bone metabolism in microscopic colitis.AimsThe aim of the present study was to evaluate bone density and metabolism in patients with microscopic colitis.MethodsFourteen patients microscopic colitis were included in the study, and 28 healthy persons and 28 age and gender matched Crohn's disease patients were enrolled as controls. Bone mineral density was measured using dual x-ray absorptiometry at the lumbar spine, femoral neck and the radius. Serum bone formation and bone resorption markers (osteocalcin and beta-crosslaps, respectively) were measured using immunoassays.ResultsLow bone mass was measured in 57.14% patients with microscopic colitis. Bone mineral density at the femoral neck in patients suffering from microscopic colitis and Crohn's disease was lower than in healthy controls (0.852 ± 0.165 and 0.807 ± 0.136 vs. 1.056 ± 0.126 g/cm2; p < 0.01). Bone mineral density at the non-dominant radius was decreased in microscopic colitis patients (0.565 ± 0.093 vs. 0.667 ± 0.072 g/cm2; p < 0.05) but unaffected in Crohn's disease patients (0.672 ± 0.056 g/cm2). Mean beta-crosslaps concentration was higher in microscopic colitis and Crohn's disease patients than controls (417.714 ± 250.37 and 466.071 ± 249.96 vs. 264.75 ± 138.65 pg/ml; p < 0.05). A negative correlation between beta-crosslaps concentration and the femoral and radius t-scores was evident in microscopic colitis patients.ConclusionsLow bone mass is frequent in microscopic colitis, and alterations to bone metabolism are similar to those present in Crohn's disease. Therefore, microscopic colitis-associated osteopenia could be a significant problem in such patients.

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Changes of OPG and RANKL concentrations in Crohnʼs disease after infliximab therapy

Cited by 58 publications

References 34 publications

Intestinal inflammation without weight loss decreases bone density and growth

Intestinal inflammation without weight loss decreases bone density and growth

Treatment of Extraintestinal Manifestations in Inflammatory Bowel Disease

Low bone mass in microscopic colitis

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