Effect of modification of hydroxyapatite/collagen composites with sodium citrate, phosphoserine, phosphoserine/RGD-peptide and calcium carbonate on bone remodelling

Schneiders, Wolfgang; Reinstorf, Antje; Pompe, W.; Grass, R.; Biewener, A.; Holch, M.; Zwipp, H.; Rammelt, Stefan

doi:10.1016/j.bone.2006.11.019

Cited by 80 publications

(89 citation statements)

References 32 publications

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“…The results of enhanced differentiation of MC3T3-E1 cells and in vivo new bone formation induced by phosphoserine are in agreement with other studies reporting enhanced bone healing with phosphoserinemodified CaP cements (Mai et al 2008;Schneiders et al 2007;Vater et al 2010). However, collagen composition in bone cements seems to be a prerequisite for exerting in vivo bone healing promoting effect of phosphoserine.…”

Section: New Bone Formation In Rabbit Calvarial Defectssupporting

confidence: 94%

“…CaP-based bone cements have been modified by adding phosphoserine to achieve favorable bone healing by harmonizing the bioresorption of bone cements with simultaneous new bone substitution (Offer et al 2011;Reinstorf et al 2004;Schneiders et al 2007;Vater et al 2010). Phosphoserine modification improves the mechanical properties of bone cements which resulted in a rise of compressive strength and more closely packed hydroxyapatite crystals (Reinstorf et al 2004).…”

Section: Introductionmentioning

confidence: 99%

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MC3T3-E1 cell differentiation and in vivo bone formation induced by phosphoserine

et al. 2011

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Bone formation induced by phosphoserine was investigated in vitro and in vivo using MC3T3-E1 cells and a rabbit calvarial osseous defect model. MC3T3-E1 cells supplemented by phosphoserine displayed two-fold higher alkaline phosphatase activity and mineralization nodule formation, and calvarial defects treated with phosphoserine showed statistically significant new bone formation compared with the control (P < 0.05).

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Section: New Bone Formation In Rabbit Calvarial Defectssupporting

confidence: 94%

Section: Introductionmentioning

confidence: 99%

MC3T3-E1 cell differentiation and in vivo bone formation induced by phosphoserine

et al. 2011

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“…Indeed, it has been shown in vitro that hydroxyapatite forms thinner nanocrystals in the presence of citrate (30)(31)(32). In vivo, addition of citrate to calcium phosphate biocement for bone implants improves biocompatibility (32,33), and various citrate nutritional supplements appear to prevent the onset of osteoporosis (34), presumably by stabilizing the apatite crystals.…”

Section: Resultsmentioning

confidence: 99%

Strongly bound citrate stabilizes the apatite nanocrystals in bone

Rawal

Schmidt‐Rohr

2010

Proc. Natl. Acad. Sci. U.S.A.

472

495

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Nanocrystals of apatitic calcium phosphate impart the organicinorganic nanocomposite in bone with favorable mechanical properties. So far, the factors preventing crystal growth beyond the favorable thickness of ca. 3 nm have not been identified. Here we show that the apatite surfaces are studded with strongly bound citrate molecules, whose signals have been identified unambiguously by multinuclear magnetic resonance (NMR) analysis. NMR reveals that bound citrate accounts for 5.5 wt% of the organic matter in bone and covers apatite at a density of about 1 molecule per ð2 nmÞ 2 , with its three carboxylate groups at distances of 0.3 to 0.45 nm from the apatite surface. Bound citrate is highly conserved, being found in fish, avian, and mammalian bone, which indicates its critical role in interfering with crystal thickening and stabilizing the apatite nanocrystals in bone.T he load-bearing material in bone is a fascinating organicinorganic nanocomposite whose stiffness is provided by thin nanocrystals of carbonated apatite, a calcium phosphate, imbedded in an organic matrix consisting mostly of collagen, a fibrous protein (1-5). The small (ca. 3-nm) thickness of the apatite nanocrystals is favorable for mechanical properties, likely preventing crack propagation (6). While the size and shape of the nanocrystals have been studied extensively (4, 5), the mechanism stabilizing them at a thickness corresponding to only about four unit cells has not been elucidated. A better understanding of the factors controlling the nanocrystals in bone is desirable for prevention and treatment of bone diseases such as osteoporosis, which causes millions of fractures each year (7), and for more efficient synthesis of biomimetic nanocomposites (8, 9). In vitro experiments have shown that carboxylate-rich proteins such as osteocalcin and osteopontin (7) can affect hydroxyapatite crystal formation and growth (10, 11). These observations might suggest that such proteins limit nanocrystal thickening (12); however, these proteins are not sufficiently abundant in vivo to bind to all the nanocrystal surfaces at high enough area concentration; possibly, they control the length of the nanocrystals (7).Here we show instead that the surfaces of the apatite crystals in bone are studded with strongly bound citrate molecules, at a density of ca. 1∕ð2 nmÞ 2 , using advanced solid-state nuclear magnetic resonance (NMR) as a unique tool for probing buried interfaces. Citrate is quite abundant in bone (ca. 1 wt%, or 5 wt% of the organic components) (13,14). Before 1975, citrate in bone was studied by simple wet-chemical methods and thought to regulate bone demineralization (14). However, citrate is no longer even mentioned in most of the prominent literature on the bone nanocomposite published during the last thirty years (1)(2)(3)(4)(5)(15)(16)(17)(18). We now highlight the importance of citrate in bone by demonstrating that it is not a dissolved calcium-solubilizing agent but a strongly bound, integral part of the nanocomposite. Structurally, citrate s...

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“…Zn can also change protein structure leading to inhibition of specific metabolic enzymes, thereby causing growth inhibition [18]. Another possible reason for inhibition by B TSC could be explained by the mechanism of action of TSC, which is known to chelate Ca [42], which in this case slows the setting reaction in these cements [39]. However, regarding bacterial inhibition, TSC may be binding any Ca being used by the bacteria for metabolism.…”

Section: Resultsmentioning

confidence: 99%

Comparison of antibacterial properties of commercial bone cements and fillers with a zinc-based glass polyalkenoate cement

2010

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Effect of modification of hydroxyapatite/collagen composites with sodium citrate, phosphoserine, phosphoserine/RGD-peptide and calcium carbonate on bone remodelling

Cited by 80 publications

References 32 publications

MC3T3-E1 cell differentiation and in vivo bone formation induced by phosphoserine

MC3T3-E1 cell differentiation and in vivo bone formation induced by phosphoserine

Strongly bound citrate stabilizes the apatite nanocrystals in bone

Comparison of antibacterial properties of commercial bone cements and fillers with a zinc-based glass polyalkenoate cement

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