Mineralization of Bone: An Active or Passive Process?

Schinke, Thorsten; Amling, Michael

doi:10.1002/9783527619443.ch45

Cited by 6 publications

(7 citation statements)

References 88 publications

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“…The Na ϩ , K ϩ , and Mg 2ϩ ions can play a role in the onset of calcification, because several ion substitutions have been described regarding hydroxyapatite [Ca 10 (PO 4 ) 6 (OH) 2 ]: Mg 2ϩ , Sr 2ϩ , Pb 2ϩ , or Na ϩ for Ca 2ϩ ; carbonate or arsenate for phosphate; and F Ϫ or Cl Ϫ for OH Ϫ (10). 4D) during calciumphosphate deposition, which concurs with previous calcification studies (28) and with some works showing that hydroxy- apatite is synthesized from brushite or octacalcium by adding calcium and hydroxyl ions (3,16). 3C).…”

Section: Discussionsupporting

confidence: 89%

“…For example, one of the key questions that is still unclear refers to whether calcification is an actively promoted phenomenon or an actively inhibited phenomenon (27,28). In this work we are studying whether calcium phosphate deposition (CPD) during vascular calcification is a passive or a cell-mediated mechanism.…”

mentioning

confidence: 99%

“…For example, one of the key questions that is still unclear refers to whether calcification is an actively promoted phenomenon or an actively inhibited phenomenon (27,28). For example, one of the key questions that is still unclear refers to whether calcification is an actively promoted phenomenon or an actively inhibited phenomenon (27,28).…”

mentioning

confidence: 99%

“…For example, one of the key questions that is still unclear refers to whether calcification is an actively promoted phenomenon or an actively inhibited phenomenon (27,28). Regarding the latter possibility, calcification could occur as a consequence of the absence (bone) or loss (VC) of calcification inhibitors, and therefore calcium phosphate deposition (CPD) occurs as a passive phenomenon (28). Calcification is therefore an active process.…”

mentioning

confidence: 99%

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Role of calcium-phosphate deposition in vascular smooth muscle cell calcification

Villa‐Bellosta

Millán

Sorribas

2011

American Journal of Physiology-Cell Physiology

146

149

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In this work we are studying whether calcium phosphate deposition (CPD) during vascular calcification is a passive or a cell-mediated mechanism. Passive CPD was studied in fixed vascular smooth muscle cells (VSMC), which calcify faster than live cells in the presence of 1.8 mM Ca²(+) and 2 mM P(i). CPD seems to be a cell-independent process that depends on the concentration of calcium, phosphate, and hydroxyl ions, but not on Ca × P(i) concentration products, given that deposition is obtained with 2 × 2 and 4 × 1 Ca × P(i) mM² but not with 2 × 1 or 1 × 4 Ca × P(i) mM². Incubation with 4 mM P(i) without CPD (i.e., plus 1 mM Ca) does not induce osteogene expression. Increased expression of bone markers such as Bmp2 and Cbfa1 is only observed concomitantly with CPD. Hydroxyapatite is the only crystalline phase in both lysed and live cells. Lysed cell deposits are highly crystalline, whereas live cell deposits still contain large amounts of amorphous calcium. High-resolution transmission electron microscopy revealed a nanostructure of rounded crystallites of 5-10 nm oriented at random in lysed cells, which is compatible with spontaneous precipitation. The nanostructure in live cells consisted of long fiber crystals, 10-nm thick, embedded in an amorphous matrix. This structure indicates an active role of cells in the process of hydroxyapatite crystallization. In conclusion, our data suggest that CPD is a passive phenomenon, which triggers the osteogenic changes that are involved in the formation of a well organized, calcified crystalline structure.

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Section: Discussionsupporting

confidence: 89%

mentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Role of calcium-phosphate deposition in vascular smooth muscle cell calcification

Villa‐Bellosta

Millán

Sorribas

2011

American Journal of Physiology-Cell Physiology

146

149

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“…70 Many of the hormonal and physiological abnormalities associated with diabetes can promote intimal calcification including oxidative stress, endothelial dysfunction, alternations in mineral metabolism, increased inflammatory cytokine production, and release of osteoprogenitor cells from the marrow into the circulation. Below we briefly discuss some of these mechanisms as they relate to the development of vascular calcification in patients with diabetes (Figure 6).…”

Section: Major Mechanisms Of Vascular Calcificationmentioning

confidence: 99%

Pathology of Human Coronary and Carotid Artery Atherosclerosis and Vascular Calcification in Diabetes Mellitus

Yahagi

Kolodgie

Lutter

et al. 2017

ATVB

402

315

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The continuing increase in the prevalence of diabetes in the general population is predicted to result in a higher incidence of cardiovascular disease. Although the mechanisms of diabetes associated progression of atherosclerosis are not fully understood, at clinical and pathological level, there is an appreciation of increased disease burden and higher levels of arterial calcification in these subjects. Plaques within the coronary arteries of patients with diabetes generally exhibit larger necrotic cores and significantly greater inflammation consisting mainly of macrophages and T lymphocytes relative to patients without diabetes. Moreover, there is a higher incidence of healed plaque ruptures and positive remodeling in hearts from subjects with type 1 diabetes (T1D) and type 2 diabetes (T2D), suggesting a more active atherogenic process. Lesion calcification in the coronary, carotid and other arterial beds is also more extensive. While the role of coronary artery calcification in identifying cardiovascular disease and predicting its outcome is undeniable, our understanding of how key hormonal and physiological alterations associated with diabetes such as insulin resistance and hyperglycemia influence the process of vascular calcification continues to grow. Important drivers of atherosclerotic calcification in diabetes include oxidative stress, endothelial dysfunction, alterations in mineral metabolism, increased inflammatory cytokine production, and release of osteoprogenitor cells from the marrow into the circulation. Our review will focus on the pathophysiology of T1D- and T2D-associated vascular disease with particular focus on coronary and carotid atherosclerotic calcification.

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Effect of the crosslink functionality on the mechanical properties of crosslinked 1,2,3‐triazole polymers as potential binders for rocket propellants

Song

Wang

Gyanda

et al. 2010

J of Applied Polymer Sci

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ABSTRACT:The mechanical properties of crosslinked polymers depend on their structural features, one of which is the functionality of the crosslinks in a polymer network. To study the effect of crosslink functionality (U) on the mechanical properties of 1,2,3-triazole polymers for potential application as rocket propellant binders, crosslinkers with different U's (3, 4, 6, 16, 32, and 64) were used in the polymerization. As the percentage of acetylenic groups provided by crosslinker was kept constant and the functionality of the crosslinker increased, the resulting polymer showed a higher modulus but a lower strain. Compared to traditional polyurethane binders, 1,2,3-triazole polymers showed comparable mechanical properties, although the stress and modulus tended to be lower and the strain capability tended to be greater for the triazole-linked rubbers.

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Mineralization of Bone: An Active or Passive Process?

Cited by 6 publications

References 88 publications

Role of calcium-phosphate deposition in vascular smooth muscle cell calcification

Role of calcium-phosphate deposition in vascular smooth muscle cell calcification

Pathology of Human Coronary and Carotid Artery Atherosclerosis and Vascular Calcification in Diabetes Mellitus

Effect of the crosslink functionality on the mechanical properties of crosslinked 1,2,3‐triazole polymers as potential binders for rocket propellants

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