Abstract
Vitamin K is a cofactor of γ-glutamyl carboxylase, which plays an important role in the activation of γ-carboxyglutamate (gla)-containing proteins that negatively regulate calcification. Thus, vitamin K status might be associated with osteoarthritis (OA), in which cartilage calcification plays a role in the pathogenesis of the disease. This review collates the evidence on the relationship between vitamin K status (circulating or dietary intake level of vitamin K, or circulating uncarboxylated gla proteins) and OA from human observational studies and clinical trial, to examine its potential as an agent in preventing OA. The current literature generally agrees that a sufficient level of vitamin K is associated with a lower risk of OA and pathological joint features. However, evidence from clinical trials is limited. Mechanistic study shows that vitamin K activates matrix gla proteins that inhibit bone morphogenetic protein-mediated cartilage calcification. Gla-rich proteins also inhibit inflammatory cascade in monocytic cell lines, but this function might be independent of vitamin K-carboxylation. Although the current data are insufficient to establish the optimal dose of vitamin K to prevent OA, ensuring sufficient dietary intake seems to protect the elderly from OA.
Highlights
Osteoarthritis (OA) is a debilitating disease of the movable joints commonly experienced by the elderly
It is tempting to speculate that vitamin K, a dietary component, can influence cartilage calcification through carboxylation of Matrix gamma-carboxyglutamic acid (gla) protein (MGP), and prevent the occurrence of OA
In the Multicenter Osteoarthritis Study (MOST) involving 1180 subjects, subclinical vitamin K deficiency at baseline was associated with incident radiographic knee OA and cartilage lesion but not osteophytes
Summary
Osteoarthritis (OA) is a debilitating disease of the movable joints commonly experienced by the elderly. Numerous preventive agents for OA are available in the market, such as glucosamine sulfate, chondroitin sulfate, curcumin, and avocado soybean unsaponifiables but their efficacy remains elusive [6,7,8]. Dietary components, such as vitamin D, vitamin E, polyphenols, have been reported to retard the progression of OA [9,10,11,12]. It is tempting to speculate that vitamin K, a dietary component, can influence cartilage calcification through carboxylation of MGP, and prevent the occurrence of OA. Human studies were presented and discussed according to the strength of evidence, followed by a discourse on the mechanism of action of vitamin K in preventing OA
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