Animal experiments consistently demonstrated that Vinp treatment significantly attenuated ovariectomy-induced bone loss with a decrease in the osteoclast number and decreases in serum levels of RANKL, TRAP, interleukin-1β, and tumor necrosis factor-alpha, as well as increased serum levels of osteoprotegerin.
Animal experiments consistently demonstrated that Vinp treatment significantly attenuated ovariectomy-induced bone loss with a decrease in the osteoclast number and decreases in serum levels of RANKL, TRAP, interleukin-1β, and tumor necrosis factor-alpha, as well as increased serum levels of osteoprotegerin.
Animal experiments consistently demonstrated that Vinp treatment significantly attenuated ovariectomy-induced bone loss with a decrease in the osteoclast number and decreases in serum levels of RANKL, TRAP, interleukin-1β, and tumor necrosis factor-alpha, as well as increased serum levels of osteoprotegerin.
Thus it remains appealing to find the new residues of IKK-β to influence osteoclasts for alleviating bone loss diseases such as rheumatoid arthritis (RA).
Growth hormone (GH) deficiency and loss of physical activity are common features in traumatic brain injury (TBI) patients that may contribute to bone loss.
In addition, degeneration of cartilage was found from 8 weeks, accompanied by decreased expression of mechanically sensitive TRPV4 and collagen II, and increased expression of MMP-13.<b>Conclusions</b>: This study proved that trochlear dysplasia can be caused by patellar dislocation in growing rabbits, accompanied by significant subchondral bone loss.
In addition, degeneration of cartilage was found from 8 weeks, accompanied by decreased expression of mechanically sensitive TRPV4 and collagen II, and increased expression of MMP-13.<b>Conclusions</b>: This study proved that trochlear dysplasia can be caused by patellar dislocation in growing rabbits, accompanied by significant subchondral bone loss.
Mg deficiency was associated with higher concentrations of PTH and DPD, and significant decrease on both systemic and mandibular BMD, as well as greater severity of alveolar and trabecular bone loss.
The combination significantly improved the lumbar spine and hip BMD and reduced FRAX scores, suggesting that ZOL combined with MTX reduces bone loss and risk of hip fracture in RA patients with secondary osteoporosis.
The combination significantly improved the lumbar spine and hip BMD and reduced FRAX scores, suggesting that ZOL combined with MTX reduces bone loss and risk of hip fracture in RA patients with secondary osteoporosis.
In several studies, it has been shown that elevated concentrations of systemic and local pro-inflammatory cytokines, including tumor necrosis factor alpha (TNF-α), interferon-γ (IFNγ), interleukin (IL)-1β, IL-4, IL-5, IL-6, IL-13, and IL-17, present in IBD patients are potentially detrimental for bone metabolism and may be responsible for bone loss and increased fracture risk.
In several studies, it has been shown that elevated concentrations of systemic and local pro-inflammatory cytokines, including tumor necrosis factor alpha (TNF-α), interferon-γ (IFNγ), interleukin (IL)-1β, IL-4, IL-5, IL-6, IL-13, and IL-17, present in IBD patients are potentially detrimental for bone metabolism and may be responsible for bone loss and increased fracture risk.
In several studies, it has been shown that elevated concentrations of systemic and local pro-inflammatory cytokines, including tumor necrosis factor alpha (TNF-α), interferon-γ (IFNγ), interleukin (IL)-1β, IL-4, IL-5, IL-6, IL-13, and IL-17, present in IBD patients are potentially detrimental for bone metabolism and may be responsible for bone loss and increased fracture risk.
Neutralization of circulating FGF-21 by IP injection of anti-FGF-21 antibody significantly alleviated progressive bone loss in weight-bearing (vertebra, femur and tibia) and non-weight bearing bones (parietal bones) in dKO mice.
Recently reported 15-deoxy-Δ<sup>12,14</sup>-prostaglandin J<sub>2</sub> (15d-PGJ<sub>2</sub>) is an endogenous ligand of peroxisome proliferator-activated receptor-gamma, with an inhibitory activity on bone loss.
Micro-CT, western blotting, quantitative PCR, transmission electron microscopy, and Alizarin Red mineralization staining assays were performed to evaluate bone density, FNDC1 expression and autophagy to determine whether FNDC1 might play a significant role in rutin-inhibited trabecular bone loss in rats.
To determine whether Bmi1 overexpression in mesenchymal stem cells (MSCs) could correct bone loss induced by 1,25(OH)<sub>2</sub> D deficiency, we overexpressed Bmi1 in MSCs using Prx1-driven Bmi1 transgenic mice (Bmi1<sup>Tg</sup> ) mice.
We analyzed the skeletal phenotypes of heterozygous null Cyp27b1 (Cyp27b1<sup>+/-</sup> ) mice and their wild-type (WT) littermates to determine whether haploinsufficiency of Cyp27b1 accelerated bone loss, and to examine potential mechanisms of such loss.