1,25(OH)2D3 Induces a Mineralization Defect and Loss of Bone Mineral Density in Genetic Hypercalciuric Stone-Forming Rats

Ng, Amy; Frick, Kevin K.; Krieger, Nancy S.; Asplin, John R.; Cohen-McFarlane, Madison; Culbertson, Christopher D.; Kyker-Snowman, Kelly; Grynpas, Marc D.; Bushinsky, David A.

doi:10.1007/s00223-014-9838-7

Cited by 15 publications

(8 citation statements)

References 49 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Rats in the LPS group underwent intraperitoneal anesthesia using 2% pentobarbital sodium salt (30 mg/kg, P3761; Sigma‐Aldrich) before 10 μL Escherichia coli LPS (2 mg/mL, L2880; Sigma) was bilaterally injected into the gingival sulcus between the first molar (M1) and the second molar (M2) in the left and right maxillary regions; injection was performed every 2 days . Animals in the LPS + Cal group were subjected to similar LPS injections as those in the LPS group but received calcitriol intervention (oral gavage with water; 0.2 μg/kg d) along with the LPS injection . Calcitriol was purchased from Shanghai Roche Pharmaceuticals Ltd., China.…”

Section: Methodsmentioning

confidence: 99%

“…25 Animals in the LPS + Cal group were subjected to similar LPS injections as those in the LPS group but received calcitriol intervention (oral gavage with water; 0.2 μg/kg d) along with the LPS injection. [26][27][28] Calcitriol was purchased from Shanghai Roche Pharmaceuticals Ltd., China. Rats in the control group were injected with saline and did not receive calcitriol.…”

Section: Animal Treatment and Experimental Groupsmentioning

confidence: 99%

See 1 more Smart Citation

Calcitriol suppresses lipopolysaccharide‐induced alveolar bone damage in rats by regulating T helper cell subset polarization

Wang

et al. 2019

J of Periodontal Research

View full text Add to dashboard Cite

Background Although the immunomodulatory properties of calcitriol in bone metabolism have been documented for decades, its therapeutic role in the management of periodontitis remains largely unexplored. In this study, we hypothesized that calcitriol suppresses lipopolysaccharide (LPS)‐induced alveolar bone loss by regulating T helper (Th) cell subset polarization. Methods To test this hypothesis, we determined the effect of calcitriol intervention on the development of LPS‐induced periodontitis in rats in terms of bone loss (micro‐CT analysis), local inflammatory infiltration levels, the number of osteoclasts (hematoxylin and eosin staining) and the level of osteoclastogenesis (tartrate‐resistant acid phosphatase method). Furthermore, immunohistochemistry was used to assess the expression levels of the receptor activator of NF‐κB ligand (RANKL) and osteoprotegerin (OPG) as well as the cytokine levels of interferon‐γ (IFN‐γ), interleukin‐4 (IL‐4), IL‐17, and IL‐10 throughout the LPS‐injected region. Finally, the polarization potential of Th cells in peripheral blood was analyzed using flow cytometry. Results Calcitriol intervention decreased alveolar bone loss in response to LPS injection and inflammatory cell infiltration. Analysis of osteoclast number and RANKL and OPG expression showed that bone resorption activity was largely suppressed in response to calcitriol administration, along with decreased IL‐17 levels but increased IL‐4 and IL‐10 levels in periodontal tissues (the LPS‐injected region). Similarly, the percentages of Th2 and Treg cells in peripheral blood increased, but the percentages of Th1 and Th17 cells decreased in rats receiving calcitriol. Conclusion Our findings suggest that calcitriol can be used to inhibit bone loss in experimental periodontitis, likely via the regulation of local and systemic Th cell polarization.

show abstract

Section: Methodsmentioning

confidence: 99%

Section: Animal Treatment and Experimental Groupsmentioning

confidence: 99%

Calcitriol suppresses lipopolysaccharide‐induced alveolar bone damage in rats by regulating T helper cell subset polarization

Wang

et al. 2019

J of Periodontal Research

View full text Add to dashboard Cite

show abstract

“…On the one hand, calcitriol and VDR stimulation may protect against bone mass loss by enhancing calcium digestive absorption. On the other hand, it has been evidenced that VDR activation may result in increased bone resorption (20,21). As a consequence, vitamin D administration is accompanied by increased calcium intakes to avoid bone demineralization.…”

Section: Discussionmentioning

confidence: 99%

Calcium and vitamin D have a synergistic role in a rat model of kidney stone disease

Letavernier

Verrier

Goussard

et al. 2016

Kidney International

View full text Add to dashboard Cite

“…To determine whether the effects of calcitriol on the development of rats would persist after the drug withdrawal, after 3 weeks of calcitriol administration, the rats of group C were withdrawn from drug treatment and kept for another week followed by execution at the fourth week. The high dose of 1,25(OH) 2 D 3 was utilized as it elicits a maximal physiologic response in normal rats (Ng et al 2014;Yao et al 2005). The rats were given only PBS as control (same quantity and frequency with the VD group) and sacrificed at the indicated time points corresponding to their respective experimental groups.…”

Section: Animal and Tissue Preparationmentioning

confidence: 99%

Histochemical examination of the effects of high-dose 1,25(OH)2D3 on bone remodeling in young growing rats

Sun

Wang

et al. 2016

J Mol Hist

View full text Add to dashboard Cite

Vitamin D has an anabolic effect on bone developmental processes and is involved in maintaining skeletal integrity. In recent years, pediatric cases of vitamin D intoxication have attracted attention. Therefore, the aim of this study was to investigate the influence of long-term administration of physiologically-high-dose calcitriol (1,25(OH)2D3) on bone remodeling in young developing rats. Neonatal rats received once-daily subcutaneous injection of calcitriol (250 ng/kg body weight), or PBS only as a control, for 3 weeks. At 1, 2 and 4 weeks' post-administration, rats were sacrificed and fixed by transcardial perfusion with 4 % paraformaldehyde, following which tibiae were extracted for histochemical analysis. Compared with the control group, the number of tartrate-resistant acid phosphatase- and Cathepsin K-positive osteoclasts were significantly increased, and the expression of alkaline phosphatase in osteoblasts was decreased in trabecular bone of rats administered high-dose 1,25(OH)2D3, leading to decreased trabecular bone volume. In addition, the expression of receptor activator of nuclear factor kappa-B ligand (RANKL) was increased, while that of osteoprotegerin was weaker in osteoblasts in the experimental group compared with the control group. Moreover, there was weaker immunoreactivity for EphrinB2 in osteoclasts and EphB4 in osteoblasts of trabecular bone in the experimental group compared with the control group. These findings suggest that long-term use of physiologically-high dose calcitriol may result in bone loss through RANKL/RANK/osteoprotegerin and EphrinB2-EphB4 signaling pathways, and that these negative effects could continue after drug withdrawal. Therefore, optimal limits for vitamin D administration need to be established for children and adolescents.

show abstract

1,25(OH)2D3 Induces a Mineralization Defect and Loss of Bone Mineral Density in Genetic Hypercalciuric Stone-Forming Rats

Cited by 15 publications

References 49 publications

Calcitriol suppresses lipopolysaccharide‐induced alveolar bone damage in rats by regulating T helper cell subset polarization

Calcitriol suppresses lipopolysaccharide‐induced alveolar bone damage in rats by regulating T helper cell subset polarization

Calcium and vitamin D have a synergistic role in a rat model of kidney stone disease

Histochemical examination of the effects of high-dose 1,25(OH)2D3 on bone remodeling in young growing rats

Contact Info

Product

Resources

About