Lrp5 functions in bone to regulate bone mass
The human skeleton is affected by mutations in low-density lipoprotein receptor-related protein 5 (LRP5). Mutations of this LRP5 lead to dominant high bone mass (HBM) syndrome. To understand how LRP5 influences bone properties, the authors generated transgenic mice with knockin or knockout mutation of the LRP5 gene. Depending on the strain studied, the mutation was specifically localized in the osteocytes, the gut, or the appendicular skeleton.
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Matrix-embedded cells control osteoclast formation
Osteoclast activity is crucial for bone growth during development by resorbing calcified cartilage produced by chondrocytes. Bone-resorbing activity is also important for bone remodeling throughout mammalian life. Osteoclast differentiation is mediated by the cytokine receptor activator of nuclear factor κ-B ligand (RANKL). However, RANKL is expressed by a variety of cell types and it is still unclear which cells are essential sources for RANKL synthesis and thus for osteoclastogenesis.
Bone formation is significantly greater in women on strontium ranelate than in those on alendronate after 6 and 12 months of treatment
Strontium ranelate and alendronate are two effective osteoporosis treatments. Previous studies have shown that strontium ranelate promotes bone formation and inhibits bone resorption, while alendronate is a potent antiresorptive agent. The aim of this study [1] was to compare bone formation activity of both treatments, performing paired bone biopsies in a group of 268 postmenopausal osteoporotic women, each treated by one of these two molecules, for a final period of 12 months.
PTH deletion ameliorates the anomalies of Fgf23-deficient mice by suppressing elevated Vitamin D and calcium levels
Fibroblast Growth Factor 23 (FGF23) is a key regulator of calcium and phosphate homeostasis. Fgf23-deficient mice exhibit an elevated serum level of 1,25 dihydroxyvitamin D (1,25(OH)2D), calcium, phosphate and a decreased PTH level. As PTH is known to increase 1,25(OH)2D and calcium level, the authors of a recent study [1] hypothesized that PTH deletion in a Fgf23 deficient background could supress these vitamin D, ion and PTH abnormal levels, and could ameliorate their negative effects on soft tissue atrophies and skeletal abnormalities.
Influence of adipokines and ghrelin on bone mineral density and fracture risk
Adipose tissue may regulate bone metabolism and be involved in osteoporosis pathophysiology. Adiponectin and leptin are adipokine hormones, synthesized by adipocytes. Leptin plays a particular role in weight and appetite regulation. Adiponectin regulates metabolism and inflammatory pathways. Ghrelin is a growth hormone secretagogue implicated in fat mass and appetite regulation. Epidemiological data have established positive relationships between fat mass and bone mineral density (BMD). Using systematic review and meta-analysis, the authors of this study [1] tested the association and correlation of adipokines (adiponectin, leptin) and ghrelin serum level with bone mineral density and fracture risk.
 Download here the slide set presented by Prof. Friedlander, on Thursday, November 10th. |
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