Mortality risk is increased after low-trauma osteoporotic fractures
There are surprisingly few data on long-term mortality following osteoporotic fracture and even fewer following subsequent fracture. This study [1] examined long-term mortality risk in women and men following all osteoporotic fractures and assessed the association of subsequent fracture with that risk. This was achieved through a prospective cohort from the Dubbo Osteoporosis Epidemiology Study of community-dwelling women and men aged 60 years and older from Dubbo, Australia, who sustained a fracture between April 1989 and May 2007. Main outcome measures were age- and sex-specific standardized mortality ratios (SMRs) compared with the overall Dubbo population for hip, vertebral, major, and minor fractures.
Oral Vitamin D dose-dependently prevent nonvertebral fractures
Antifracture efficacy with supplemental vitamin D has been questioned by recent trials. For that reason, the authors of a recent study [1] performed a meta-analysis on the efficacy of oral supplemental vitamin D in preventing nonvertebral and hip fractures among older individuals (> 65 years). They included 12 double-blind randomized controlled trials (RCTs) for nonvertebral fractures (n=42 279) and 8 RCTs for hip fractures (n=40 886) comparing oral vitamin D, with or without calcium, with calcium or placebo. To incorporate adherence to treatment, they multiplied the dose by the percentage of adherence to estimate the mean received dose (dose x adherence) for each trial.
MEPE is a new bone renal hormone and vascularization modulator
MEPE (Matrix Extracellular PhosphoglycoprotEin) is a protein secreted by osteoblasts and osteocytes. Its synthesis is increased in several phosphate and bone-mineral metabolic disorders such as hypophosphatemic rickets and oncogenic hypophosphatemic osteomalacia. Under normal circumstances, MEPE is cleaved to release a peptide which acts as an inhibitor of bone mineralization. MEPE may be a substrate for an enzyme called PHEX, and PHEX may prevent proteolysis of MEPE and release of the peptide which inhibits bone mineralization. In patients with X-linked hypophosphatemic rickets (XLH) and in mice with the Hyp mutation, PHEX is mutated and therefore cannot bind to MEPE. This results in the release of MEPE into the circulation, thereby causing hypophosphatemia and renal Pi wasting. To elucidate the causative role of MEPE in these disorders, the authors of a recent study [1] created a murine model overexpressing MEPE protein in bone.
Bril: a novel bone-specific modulator of mineralization
In the course of attempting to define the bone “secretome,” a gene encoding a small membrane protein novel to osteoblasts was identified. Although previously identified in silico as ifitm5, no functional studies had been undertaken on this gene. A recent study [1] characterized the expression patterns and localization of this gene in vitro and in vivo and assessed its role in matrix mineralization in vitro.
 Download here the slide set presented by Prof. Friedlander, on Thursday, November 10th. |
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