Abstract
BackgroundA number of studies have examined the association between the polymorphisms of the low-density lipoprotein receptor-related protein 5 gene (LRP5), but previous results have been inconclusive. Thus we performed a meta-analysis of studies on the association between the LRP5 polymorphisms and bone mineral density (BMD) to assess their pooled effects.MethodsPublished literature from PubMed, EMBASE and ISI web of science were searched for eligible publications. Weighted mean difference (WMD) and 95% confidence interval (CI) was calculated using fixed- or random-effects model.ResultsA total of 19 studies with 25773 subjects were considered in this meta-analysis. Of them, 17 examined the association between the A1330V polymorphism and BMD, 8 were focused on the V667M polymorphism, and 2 analyzed the Q89R polymorphism. Individuals with the A1330V AA genotype showed significantly higher BMD than those with the AV/VV genotypes [at lumbar spine (LS): WMD = 0.02g/cm2, 95% CI = 0.01-0.03, P < 10-4; at femur neck (FN): WMD = 0.01g/cm2, 95% CI = 0.00-0.02, P = 0.01] or VV genotype (at LS: WMD = 0.02g/cm2, 95% CI = 0.01-0.04, P = 0.01). Significant associations were also detected in the analysis for V667M (VV vs. VM/MM: WMD at LS = 0.02g/cm2, 95% CI = 0.02-0.03, P < 10-5; WMD at FN = 0.01g/cm2, 95% CI = 0.01-0.02, P = 0.0002). As for Q89R, subjects with the QQ genotype tended to have higher BMD than those with the QR/RR genotypes at FN (WMD = 0.03g/cm2, 95% CI = 0.01-0.05, P = 0.005).ConclusionThis meta-analysis demonstrated that the LRP5 polymorphisms may be modestly associated with BMD of LS and FN.
Highlights
Osteoporosis is a common disease characterized by low bone mass, microarchitectural deterioration of bone tissue and enhanced bone fragility which leads to an increased incidence of fracture
It has been reported that loss-of-function mutations of the lipoprotein receptor-related protein 5 gene (LRP5) gene cause osteoporosis-pseudoglioma (OPPG), an autosomal recessive disease characterized by low bone mass and childhood fractures [15], whereas the LRP5 G171V mutation is associated with autosomal dominant high bone mass (HBM) traits [16,17,18]
Egger’s test was performed to access the publication bias of the literatures, and no publication bias was detected for the associations of the LRP5 polymorphisms with bone mineral density (BMD) phenotypes. In this meta-analysis, we investigated the association of the LRP5 A1330V, V667M and Q89R polymorphisms with BMD
Summary
Osteoporosis is a common disease characterized by low bone mass, microarchitectural deterioration of bone tissue and enhanced bone fragility which leads to an increased incidence of fracture. LRP5 cooperates with members of the frizzled family of sevenpass transmembrane receptors to bind Wnt proteins, and forms a functional ligand-receptor complex that activates the Wnt-βcatenin pathway [12,13,14]. Transgenic and knock-out mouse models mimic the human phenotypes of high and low bone mass, respectively [19] In addition to these mutations, a number of polymorphisms have been described in the LRP5 gene. A number of studies have examined the association between the polymorphisms of the low-density lipoprotein receptor-related protein 5 gene (LRP5), but previous results have been inconclusive. We performed a meta-analysis of studies on the association between the LRP5 polymorphisms and bone mineral density (BMD) to assess their pooled effects. Conclusion: This meta-analysis demonstrated that the LRP5 polymorphisms may be modestly associated with BMD of LS and FN
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