Seasonal changes in mineralization are related to Vitamin D deficiency
A seasonal variation in osteoid surfaces and calcification fronts was noted several decades ago in bone biopsies from hip fracture patients and attributed to vitamin D status. It was suggested at that time that mild vitamin D deficiency might cause osteoporosis from malabsorption of calcium and more severe deficiency might cause osteomalacia. In order to further explore this hypothesis, Need et al. [1] examined bone biopsies, calcium absorption data, and serum vitamin D metabolites in 121 ambulant patients with osteoporosis.
A subunit of v-ATPase controls osteoclast fusion and bone formation
Matrix-producing osteoblasts and bone-resorbing osteoclasts maintain bone homeostasis. Osteoclasts are multinucleated, giant cells of hematopoietic origin formed by the fusion of mononuclear preosteoclasts derived from myeloid cells. Fusion-mediated giant cell formation is critical for osteoclast maturation; without it, bone resorption is inefficient. One gene predominantly expressed in osteoclasts is the d2 isoform of vacuolar (H+) ATPase (v-ATPase) V0 domain (Atp6v0d2). What is the function of this protein?
Alcohol consumption and bone density: could be worse
Hip fractures are common causes of morbidity and mortality in older adults, with a lifetime cost for hip fractures which is a major burden in public health. Two of the most important proximal factors leading to hip fracture are low bone density (osteopenia or osteoporosis) and falls. Alcohol consumption may influence each of these factors. Although alcohol use has been associated with an increased risk for falls, leading to injury or death in a variety of populations, this relation among older adults has not been established.
Osteocalcin: a skeleton key to metabolism
A link between energy metabolism and bone has long been suspected but poorly defined. Obesity protects against osteoporosis, and maturity-onset (type 2) diabetes is associated with increased bone mineral density and fewer fractures. A direct link was made with the discovery that the adipocyte-derived hormone leptin acts on the osteoblasts to inhibit bone formation through hypothalamic and sympathetic nervous system relays. Working on the hypothesis that endocrine regulation requires feedback control, the same investigators complete a previously unknown endocrine circuit with their discovery [1] that the skeleton is a ductless gland, whose osteoblasts secrete osteocalcin, a protein that profoundly influences insulin production and sensitivity and fat metabolism.
 Download here the slide set presented by Prof. Friedlander, on Thursday, November 10th. |
Latest news
