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The Wnt pathways are regulated by multiple families of secreted antagonists or modulators, including secreted frizzled related proteins (s FRP) and dickkopfs (DKK) as well as Wnt inhibitory factor-1 (WIF1).In bone, s FRP3 and WIF1 have been shown to influence both canonical and noncanonical activation by preventing Wnt from binding to its receptors [10–13] whereas DKK1 antagonizes the canonical Wnt pathway by inhibiting Wnt co-receptors, including low-density lipoprotein receptor–related proteins 5 and 6, which are intrinsically involved in regulation of bone remodeling and angiogenesis [9, 14, 15].Participants had no medical conditions that were likely to influence 5-year survival, and exclusion criteria at baseline (1998) included current use of bone active agents as hormone replacement therapy.In the 5 years of the randomized controlled trial, participants were given 1.2 g of elements of calcium as calcium carbonate on daily basis or a similar placebo.

Emerging evidence suggests that AAC is an actively regulated process with important clinical implications [6].Because this was completed prior to the advent of the clinical trials registry, the trial was retrospectively registered in the Australian New Zealand Clinical Trials Registry ACTRN12615000750583.All participants were similar in terms of disease burden and pharmaceutical consumption to the general populations of this age, but they were more likely to be from higher socio-economic groups.We tested the hypothesis that low Wnt antagonist levels of Dickkopf-1 (DKK1), secreted frizzled related protein 3 (s FRP3), and Wnt inhibitory factor 1 (WIF1) are associated with severe AAC (AAC24 score Severe AAC was present in 146 women (19%).Lower levels of DKK1, but not WIF1 and s FRP3, were associated with higher odds of severe AAC.