Osteoprotegerin, s-RANKL, and selected interleukins in the pathology of bone metabolism in patients with Crohn’s disease

Krela‐Kaźmierczak, Iwona; Wysocka, Ewa; Szymczak, Aleksandra; Eder, Piotr; Michalak, Michał; Łykowska‐Szuber, Liliana; Stawczyk‐Eder, Kamila; Klimczak, Katarzyna; Linke, Krzysztof; Horst‐Sikorska, Wanda

doi:10.5114/pg.2015.52589

Cited by 8 publications

(8 citation statements)

References 15 publications

(21 reference statements)

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“…Krela-Kaźmierczak I. et al showed that low OPG levels may be associated with osteoporosis in UC. Nevertheless, in CD patients increased RANKL levels were observed [ 20 , 21 ]. 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.…”

Section: Introductionmentioning

confidence: 99%

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%

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

et al. 2020

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“…Interestingly, smoking might affect patients with CD and UC in different ways; it seems to protect against UC, whereas, on the other hand, it increases the risk of CD development [ 29 ]. As already mentioned, the RANK–RANKL–OPG pathway is considered a key element of osteoporosis pathogenesis among patients suffering from IBD [ 30 ]. Generally, inflammation and increased pro-inflammatory cytokines (i.e., IL-6, IL-1, IL-17, and TNF-α) affect RANKL production in IBD patients, thereby promoting osteoclastogenesis and bone resorption [ 28 , 31 ].…”

Section: Inflammatory Bowel Disease (Ibd)mentioning

confidence: 99%

Bone Fragility in Gastrointestinal Disorders

Merlotti

Mingiano

Valenti

et al. 2022

IJMS

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Osteoporosis is a common systemic disease of the skeleton, characterized by compromised bone mass and strength, consequently leading to an increased risk of fragility fractures. In women, the disease mainly occurs due to the menopausal fall in estrogen levels, leading to an imbalance between bone resorption and bone formation and, consequently, to bone loss and bone fragility. Moreover, osteoporosis may affect men and may occur as a sequela to different diseases or even to their treatments. Despite their wide prevalence in the general population, the skeletal implications of many gastrointestinal diseases have been poorly investigated and their potential contribution to bone fragility is often underestimated in clinical practice. However, proper functioning of the gastrointestinal system appears essential for the skeleton, allowing correct absorption of calcium, vitamins, or other nutrients relevant to bone, preserving the gastrointestinal barrier function, and maintaining an optimal endocrine-metabolic balance, so that it is very likely that most chronic diseases of the gastrointestinal tract, and even gastrointestinal dysbiosis, may have profound implications for bone health. In this manuscript, we provide an updated and critical revision of the role of major gastrointestinal disorders in the pathogenesis of osteoporosis and fragility fractures.

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“…Stanisławowski et al [ 19 ] reported that patients with UC have higher local expression of serum OPG mRNA and protein than healthy participants[ 19 ]. Krela-Kaźmierczak et al [ 20 ] reported an increase in the OPG/RANKL ratio in CD patients[ 20 ]. According to a recent study, elevated osteocyte tumor necrosis factor (TNF)-α, interleukin (IL)-6, RANKL, and OPG correspond to higher osteoclast surfaces and a lower bone formation rate in an IBD model induced with dextran sodium sulfate[ 21 ].…”

Section: Introductionmentioning

confidence: 99%

Jianpi Qingchang Bushen decoction improves inflammatory response and metabolic bone disorder in inflammatory bowel disease-induced bone loss

Zhang¹,

Chen²,

Zhang³

et al. 2022

WJG

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BACKGROUND Bone loss and osteoporosis are commonly described as extra-intestinal manifestations of inflammatory bowel disease (IBD). Jianpi Qingchang Bushen decoction (JQBD) is a prescription used in clinical practice. However, further studies are needed to determine whether JQBD regulates the receptor activator of nuclear factor kappa B (NF-κB) (RANK)/receptor activator of NF-κB ligand (RANKL)/ osteoprotegerin (OPG) pathways and could play a role in treating IBD-induced bone loss. AIM To evaluate the therapeutic effect of JQBD in IBD-induced bone loss and explore the underlying mechanisms. METHODS An IBD-induced bone loss model was constructed by feeding 12 6-to-8-wk-old interleukin-10 (IL-10)-knockout mice with piroxicam for 10 d. The mice were randomly divided into model and JQBD groups. We used wild-type mice as a control. The JQBD group was administered the JQBD suspension for 2 wk by gavage, while the control and model groups were given normal saline at the corresponding time points. All mice were killed after the intervention. The effect of JQBD on body weight, disease activity index (DAI), and colon length was analyzed. Histopathological examination, colon ultrastructure observation, and micro-computed tomographic scanning of the lumbar vertebrae were performed. The gene expression of NF-κB, tumor necrosis factor-α (TNF-α), IL-1β, IL-6, and IL-8 in the colon was evaluated by real-time polymerase chain reaction. Colon samples were assessed by Western blot for the expression of RANKL, OPG, RANK, and NF-κB proteins. RESULTS The model group lost body weight, had a shorter colon, and showed a dramatic increase in DAI score, whereas JQBD had protective and therapeutic effects. Treatment with JQBD significantly improved inflammatory cell infiltration and reduced crypt abscess and ulcer formation. Three-dimensional imaging of the vertebral centrum in the model group revealed a lower bone mass, loose trabeculae, and “rod-shaped” changes in the structure compared to the control group and JQBD groups. The bone volume/total volume ratio and bone mineral density were significantly lower in the model group than in the control group. JQBD intervention downregulated the NF-κB, TNF-α, IL-1β, IL-6, and IL-8 mRNA expression levels. The RANKL and OPG protein levels were also improved. CONCLUSION JQBD reduces inflammation of the colonic mucosa and inhibits activation of the RANK/ RANKL/OPG signaling pathway, thereby reducing osteoclast activation and bone resorption and improving bone metabolism.

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Osteoprotegerin, s-RANKL, and selected interleukins in the pathology of bone metabolism in patients with Crohn’s disease

Cited by 8 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

Bone Fragility in Gastrointestinal Disorders

Jianpi Qingchang Bushen decoction improves inflammatory response and metabolic bone disorder in inflammatory bowel disease-induced bone loss

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