Interleukin 6, osteoprotegerin, sRANKL and bone metabolism in inflammatory bowel diseases

Krela‐Kaźmierczak, Iwona; Szymczak-Tomczak, Aleksandra; Łykowska‐Szuber, Liliana; Wysocka, Ewa; Michalak, Michał; Stawczyk‐Eder, Kamila; Waszak, Katarzyna; Linke, Krzysztof; Eder, Piotr

doi:10.17219/acem/75675

Cited by 15 publications

(16 citation statements)

References 15 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Interleukin 6 can modulate BMD via the OPG/sRANKL system in the femoral neck, which can cause a loss of bone, particularly in the course of CD. Therefore, these studies may contribute to the development and implementation of new secondary osteoporosis therapy in the course of IBD [ 22 ]. It is worth emphasizing the effects of biological therapy employed in IBD on bones.…”

Section: Introductionmentioning

confidence: 99%

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

et al. 2020

Self Cite

View full text Add to dashboard Cite

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.

show abstract

Section: Introductionmentioning

confidence: 99%

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

et al. 2020

Self Cite

View full text Add to dashboard Cite

show abstract

“…IL-6 can affect the early stage of osteoclasts, stimulate the proliferation and division of osteoclast precursors, increase the number of osteoclasts, and promote the formation of osteoclast pits. It can also increase the release of collagenase to promote matrix degradation and affect osteoblast activity [16].…”

Section: Discussionmentioning

confidence: 99%

Association of pro-inflammatory cytokines with QCT-measured bone mineral density and its gender difference in a Chinese population — a pilot study

Zeng

Gong

et al. 2019

Endokrynologia Polska

View full text Add to dashboard Cite

Introduction: The primary objective of this study was to explore the association of pro-inflammatory cytokines with quantitative computed tomography (QCT)-measured bone mineral density (BMD) and its sexual difference in a Chinese population. Material and methods: In a cross-sectional study, a total of 85 participants aged 48-85 years were recruited and classified into three groups: normal bone mass with BMD > 120 mg/cm 3 , osteopaenia with BMD 80-120 mg/cm 3 , and osteoporosis with BMD < 80 mg/cm 3. ANOVA analysis and multivariable ordinal logistic regression was used to estimate the associations of interest. Results: The proportions of osteoporosis, osteopaenia, and normal BMD were 29.41% (25), 37.65% (32), and 32.94% (28), respectively. Males had the highest proportion of osteopaenia while females had osteoporosis (p < 0.01). In contrast with the null findings in males, significant statistical difference was observed in females. Compared to the normal BMD, the OR for increasing IL-6 level of decreasing BMD groups (osteoporosis and/or osteopaenia) was 9.50 (95% CI: 1.44-62.80). TNF-a and IL-17 tended to show an increased risk (OR > 1) but did not reach significance. Current OR result cannot confirm these relationships of IL-1b, and ORs of PAI-1 and MCP-1 are too close to 1 to determine the practical meaning. Conclusions: IL-6 is an obviously independent risk factor of QCT-measured osteoporosis in Chinese females. Sex hormones and fat-related factors are important confounders in the research of osteoimmunology.

show abstract

“…Several cytokines are known to be chronically elevated in the serum of individuals with IBD, such as TNF-α, IL-1β, and IL-6 inhibit osteoblast function (responsible for bone formation) and promote osteoclastogenesis (responsible for bone resorption) [ 16 , 17 , 18 ]. TNF-α appears to be the master regulator of bone loss in IBD as it promotes expression of receptor activator of nuclear factor κB ligand (RANKL) from osteogenic cells and independently interacts with RANKL as a potent stimulator of osteoclastogenesis, via the nuclear factor kappa B (NF-κB) signaling pathway [ 19 , 20 ].…”

Section: Pathogenesis Of Musculoskeletal Deficits In Ibdmentioning

confidence: 99%

“…However, this mechanism appears insufficient to reverse RANKL and TNF-α mediated bone resorption, as OPG levels were inversely associated with bone density [ 21 ]. During a disease flare, elevated serum RANKL was observed in CD compared to healthy controls, highlighting the influence of inflammation on the RANKL/OPG pathway in perpetuating bone resorption [ 17 ]. Inflammatory cytokines also adversely affect bone formation in IBD.…”

Section: Pathogenesis Of Musculoskeletal Deficits In Ibdmentioning

confidence: 99%

Pathogenesis of Musculoskeletal Deficits in Children and Adults with Inflammatory Bowel Disease

et al. 2021

View full text Add to dashboard Cite

Musculoskeletal deficits are among the most commonly reported extra-intestinal manifestations and complications of inflammatory bowel disease (IBD), especially in those with Crohn’s disease. The adverse effects of IBD on bone and muscle are multifactorial, including the direct effects of underlying inflammatory disease processes, nutritional deficits, and therapeutic effects. These factors also indirectly impact bone and muscle by interfering with regulatory pathways. Resultantly, individuals with IBD are at increased risk of osteoporosis and sarcopenia and associated musculoskeletal morbidity. In paediatric IBD, these factors may contribute to suboptimal bone and muscle accrual. This review evaluates the main pathogenic factors associated with musculoskeletal deficits in children and adults with IBD and summarises the current literature and understanding of the musculoskeletal phenotype in these patients.

show abstract

Interleukin 6, osteoprotegerin, sRANKL and bone metabolism in inflammatory bowel diseases

Cited by 15 publications

References 15 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

Association of pro-inflammatory cytokines with QCT-measured bone mineral density and its gender difference in a Chinese population — a pilot study

Pathogenesis of Musculoskeletal Deficits in Children and Adults with Inflammatory Bowel Disease

Contact Info

Product

Resources

About