Recent studies found a clear association between long-term oral (or intravenous) anticoagulant treatment (OAC) and reducedbone quality due to reduction of active osteocalcin. OAC might lead to an increased incidence of fracture, reducedbone mineral density or content, osteopenia, and increased serum levels of undercarboxylated osteocalcin.
In humans, the percentage of the circulating osteocalcin that is not γ-carboxylated (percent ucOC) is used as a biomarker of vitamin K status. In contrast, when ucOC is not corrected for total osteocalcin, the interpretation of this measure is confounded by osteoblastic activity, independent of vitamin K.
Oral anticoagulants are putative riskfactors for osteoporosis, but observational cross-sectional studies describing their effects on bone mineral density have reported conflicting results, prospective studies are not available, and randomized trials are not feasible.