Browsing by Author "Cristafovici, Nicoleta"
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- The role of vitamin K in osteoporosisPublication . Cristafovici, Nicoleta; Simes, Dina; Viegas, Carla Alexandra São BentoAccording to the World Health Organization (WHO), osteoporosis is a “progressive systemic skeletal disease characterized by low bone mass and microarchitectural deterioration of bone tissue, with a consequent increase in bone fragility and susceptibility to fracture." The consequences of these fractures can be serious, sometimes life-threatening; the economic costs of treating fractures are also considerable. Alternative methods of treating osteoporosis have been researched in recent decades, and vitamin K (VK) has been found to be a viable therapeutic. This dissertation investigates scientific evidence on the role of VK in osteoporosis. VK is a fat-soluble vitamin required for blood clotting. VK has two main structures: vitamin K1 (VK1) and vitamin K2 (VK2). Different absorption rates, tissue distribution, and bioavailability reflect structural differences between VK1 and VK2. Although they have structural differences, both function as co-factor for the γ-glutamyl carboxylase enzyme (GGCX) in the conversion of glutamic acid (Glu) residues into γ-carboxyglutamic acid (Gla) residues in vitamin K-dependent proteins (VKDPs), involved in hepatic and extrahepatic activity. VKDPs involved in bone metabolism include osteocalcin (OC), matrix G1a protein (MGP), Gla Rich Protein (GRP), Growth Arrest Specific Protein 6 (Gas6), and protein S. OC is the most abundant VKDP in bone. During bone mineralization, osteoblasts produce OC, which binds to calcium ions and hydroxyapatite crystals to modulate bone size and structure. According to studies, VK2, especially menaquinone-7, has more positive results than VK1 in terms of improving bone mineral density (BMD) and decreasing the risk of fractures. In addition, VK2 suppresses IKB phosphorylation and reduces NF-κB activation, resulting in a decrease in the generation of pro-inflammatory cytokines implicated in osteoporosis physiopathology. VK2 also acts as a ligand for the steroid and xenobiotic receptor (SXR) or pregnane X receptor (PXR), increasing the transcription of genes for extracellular matrix proteins to preserve bone structure.
