Authors: D FernándezGarcía M MuñozTorres P MezquitaRaya M de la Higuera G Alonso R ReyesGarcía A Sebastian Ochoa M E RuizRequena J Dios Luna F EscobarJiménez
Publish Date: 2014/03/27
Volume: 31, Issue: 5, Pages: 416-421
Abstract
Previous in vitro studies suggest that the antiresorptive effect of raloxifene might be mediated by changes in several cytokines involved in the bone remodeling process In this context the osteoprotegerin OPGreceptor activator of NFκB ligand RANKL system is considered a key component in the osteoclastogenesis regulation The aim of this study was to determine the effects of raloxifene treatment on serum concentrations of OPG receptor RANKL and its relationship with biochemica markers of bone turnover and bone mineral density BMD in previously untreated women with postmenopausal osteoporosis We selected 47 postmenopausal women mean age 63±7 yr with densitometric criteria of osteoporosis We determined at baseline 3 6 and 12 months anthropometric parameters biochemical markers of bone turnover serum levels of 25OH D serum levels of OPG and RANKL BMD dualenergy xray absorptiometry in lumbar spine LS femoral neck and total hip was measured at baseline and 12 months after raloxifene 60 mg/day treatment Serum levels of OPG decreased in the 3rd and 6th month of treatment p0001 and returned to basal levels in the 12th month There was a significant decrease of RANKL levels and OPG/RANKL ratio after 1 yr of raloxifene treatment In addition BMD in LS increased significantly 25 in the 12th month of treatment p=0031 Finally the biochemical markers of bone turnover total alkaline phosphatase bone alkaline phosphatase osteocalcin tartrateresistant acid phosphatase urine crosslinked carboxiterminal telopeptide of type I collagen decreased significantly from the 3rd month of treatment In conclusion our results support the hypothesis that raloxifene may inhibit osteoclast activity at least partly modulating the OPGRANKL system
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