Vitamin D Control of Osteoblast Function and Bone Extracellular Matrix Mineralization

Yen

J Cellular Molecular Medi

et al. 2015

Designed sockets prepared on the mandibles of nine Beagle dogs were divided into three groups: Calcitriol +Alloplast, Alloplast and Empty. Five of the nine dogs received Vit.D3 and calcium supplement (Vit.D/Ca group), while the other four dogs without supplements were assigned to Non-Vit.D/Ca group. After 4 weeks, the extent of vertical ridge resorption (VRR), bone density (density), new bone formation (NBF) and implant stability quotient (ISQ) were measured. Following systemic Vit.D/Ca administration, the Empty subgroup showed significant differences from the Calcitriol + Alloplast subgroup on variants NBF/Density/VRR and the Alloplast subgroup on items NBF/Density/ISQ/VRR. Alternatively, the Calcitriol + Alloplast subgroup revealed higher values of NBF/Density/ISQ (P < 0.001) and a lower VRR value (P = 0.001) than the Alloplast subgroup. Although there were no significant differences in NBF (P = 0.349), density (P = 0.796), ISQ (P = 0.577) and VRR (0.979) comparisons on alloplast treatment between the Vit.D/Ca and Non-Vit.D/Ca groups, local application with Calcitriol + Alloplast demonstrated better NBF/Density/ISQ (P = 0.02 to <0.001) effects than which of Alloplast subgroups. Consequently, the results showed that both systemic and local vitamin D3 treatment might accelerate bone regeneration in dogs. Within the using dose, systemic vitamin D3 treatment displayed a superior stimulating effect than local vitamin D3 application did.

“…The benefit of local calcitriol application on bone regeneration in this observation may be rationalized partially by previous in vitro studies 16,18,19.…”

Section: Discussionmentioning

confidence: 65%

Section: Introductionmentioning

confidence: 66%

Association of vitamin D₃ with alveolar bone regeneration in dogs

Yen

J Cellular Molecular Medi

et al. 2015

“…During the final extracellular matrix formation step, some osteoblasts get embedded in osteoid as osteocytes [6]. 1,25(OH) 2 D 3 promotes differentiation of human BMSCs into osteoblasts, inhibits cell proliferation, and stimulates mineralisation in both human and mouse osteoblast cells [7–10]. Some of these effects are mediated through LRP5 and the Wnt signalling pathway [11,12], and the stimulation of mineralisation is partly secondary to an increase in osteoblastic alkaline phosphatase (ALP) activity [13].…”

Section: Introductionmentioning

confidence: 99%

“…Some of these effects are mediated through LRP5 and the Wnt signalling pathway [11,12], and the stimulation of mineralisation is partly secondary to an increase in osteoblastic alkaline phosphatase (ALP) activity [13]. The 1α,25-hydroxylated metabolites induce the expression of osteoblast signature genes, including collagen type-I ( col1a ), osteocalcin ( ocn ), osteopontin ( opn ), osteoprotegerin ( opg ), receptor activator of nuclear factor kappa-B ligand ( rankl ), vdr [10,14]. Thus, formation of COL1a and non-collagenous proteins, such as OCN and OPN, are stimulated by 1,25(OH) 2 D 3 , and osteoclastogenesis is inhibited by an increase in OPG, which binds RANKL and prevents its interaction with RANK on osteoclast precursors [8].…”

Section: Introductionmentioning

confidence: 99%

25-Hydroxy- and 1α,25-Dihydroxycholecalciferol Have Greater Potencies than 25-Hydroxy- and 1α,25-Dihydroxyergocalciferol in Modulating Cultured Human and Mouse Osteoblast Activities

et al. 2016

Despite differences in the phamacokinetics of 25-hydroxycholecalciferol (25(OH)D3) and 25-hydroxyergocalciferol (25(OH)D2) in man, the effects of these and their 1α-hydroxylated forms (1,25(OH)2D3 and 1,25(OH)2D2) on cellular activity of vitamin D-responsive cells have hardly been compared. We studied differences in the effects of these metabolites on cell number, gene transcription, protein expression and mineralisation of cultured human bone marrow-derived stromal cells (hBMSC) and rapidly mineralising mouse 2T3 osteoblasts. 50–1000 nM 25(OH) and 0.05–10 nM 1,25(OH)2 metabolites were used. At high concentrations, 25(OH)D2/D3 and 1,25(OH)2D2/D3 suppressed cell number in both human and mouse cells. The suppression was greater with cholecalciferol (D3) metabolites than with those of ergocalciferol (D2). In both cell types, 25(OH)D2 and 25(OH)D3 increased the expression of osteopontin, osteocalcin, collagen-1, receptor activator of nuclear factor kappa-B ligand, vitamin D receptor, CYP24A1 and CYP27B1 genes. Whereas there was little or no difference between the effects of 25(OH)D2 and 25(OH)D3 in hBMSCs, differences were observed in the magnitude of the effects of these metabolites on the expression of most studied genes in 2T3 cells. Alkaline phosphatase (ALP) activity was increased by 25(OH)D2/D3 and 1,25(OH)2D2/D3 in hBMSC and 2T3 cells, and the increase was greater with the D3 metabolites at high concentrations. In hBMSCs, mineralisation was also increased by 25(OH)D2/D3 and 1,25(OH)2D2/D3 at high concentrations, with D3 metabolites exerting a greater influence. In 2T3 cells, the effects of these compounds on mineralisation were stimulatory at low concentrations and inhibitory when high concentrations were used. The suppression at high concentrations was greater with the D3 metabolites. These findings suggest that there are differences in the effects of 25-hydroxy and 1α,25(OH)2 metabolites of D3 and D2 on human preosteoblasts and mouse osteoblasts, with the D3 metabolites being more potent in suppressing cell number, increasing ALP activity and influencing mineralisation.

“…Addition of dexamethasone to differentiation medium is not always justifi ed because of stimulation of adipogenic differentiation on AT MSC culture [2], while the role of 1,25-dihydroxyvitamin D 3 as differentiation inductor and regulator of mineralization is well documented [11,14].…”

mentioning

confidence: 99%

Tissue Engineering Construct on the Basis of Multipotent Stromal Adipose Tissue Cells and Osteomatrix for Regeneration of the Bone Tissue

Бухарова

Arutyunyan

Shustrov³

et al. 2011

Bull Exp Biol Med

We developed a new method of creation of tissue engineering constructs for regeneration of the bone tissue based on the principle of free distribution of cells in a fibrin clot within a scaffold. The tissue engineering construct includes multipotent stromal adipose tissue cells committed in osteogenic lineage, platelet-rich plasma, and resorbed material on the basis of xenogeneic bone collagen. The culture of bone progenitor cells was characterized by the main markers of osteoblastic differon. The material meets all requirements for materials intended for tissue engineering. An innovative high-technological tissue engineering product for clinical application is prepared.