Color stability of bleached tooth enamel brushed with different stain-removing toothpastes.

OBJECTIVE: The effects of four toothpastes on the color stability of in-office bleached tooth specimens were determined. MATERIALS AND METHODS: We evaluated an experimental toothpaste (EXP) and three commercially available toothpastes: Colgate Optic White (OPW), Aquafresh White & Protect (AWP), and Crest 3D White (CDW). OPW, AWP, and CDW contained inorganic abrasives, whereas EXP and AWP contained sodium polyphosphate. Forty-eight randomly selected human-extracted maxillary central incisors were bleached and brushed twice daily over 30 days. We analyzed the final color difference (ΔE*ab, ΔE00 , ΔWID ), arithmetic average surface roughness (Ra) of the enamel measured on days 0 and 30, and scanning electron microscopy images of enamel surfaces and toothpastes. ΔE*ab, ΔE00 , ΔWID , and Ra were analyzed using one-way analysis of variance and Tukey's test (α = 0.05). RESULTS: ΔE*ab and ΔE00 values were significantly lower after toothbrushing with EXP, OPW, and CDW than with AWP. OPW induced the greatest positive ΔWID . Ra was significantly increased by OPW and CDW, but slightly increased by AWP, with cube-like particles, and EXP, with no particle-like structures. CONCLUSIONS: Only EXP stabilized the color of bleached teeth without increasing the enamel surface roughness. Sodium polyphosphate with approximately 10 phosphate groups was effective at removing stains. CLINICAL SIGNIFICANCE: The effect of toothpaste on the color stability of bleached teeth depends on the constituting abrasives and chemical components. Polyphosphoric acid has different stain-removal effects depending on its degree of polymerization. Additionally, although certain types of abrasives may be effective for color stability, they also increase the surface roughness of the enamel.

The anabolic effect of inorganic polyphosphate on chondrocytes is mediated by calcium signalling.

Inorganic polyphosphates (polyP) are polymers composed of phosphate residues linked by energy-rich phosphoanhydride bonds. As polyP can bind calcium, the hypothesis of this study is that polyP enters chondrocytes and exerts its anabolic effect by calcium influx through calcium channels. PolyP treatment of cartilage tissue formed in 3D culture by bovine chondrocytes showed an increase in proteoglycan accumulation but only when calcium was also present at a concentration of 1.5 mM. This anabolic effect could be prevented by treatment with either ethylene glycol-bis(ß-aminoethyl ether)-N,N,N',N'-tetraacetic acid or the calcium channel inhibitors gadolinium and nifedipine. Calcium and polyP cotreatment of chondrocytes in monolayer culture resulted in calcium oscillations that were polyP chain length specific and were inhibited by gadolinium and nifedipine. The calcium influx resulted in increased gene expression of sox9, collagen type II, and aggrecan which was prevented by treatment with either calphostin, an inhibitor of protein kinase C, and W7, an inhibitor of calmodulin; suggesting activation of the protein kinase C-calmodulin pathway. Tracing studies using  4',6-diamidino-2-phenylindole, Mitotracker Red, and/or Fura-AM staining showed that polyP was detected in the nucleus, mitochondria, and intracellular vacuoles suggesting that polyP may also enter the cell. PolyP colocalizes with calcium in mitochondria. This study demonstrates that polyP requires the influx of calcium to regulate chondrocyte matrix production, likely via activating calcium signaling. These findings identify the mechanism regulating the anabolic effect of polyP in chondrocytes which will help in its clinical translation into a therapeutic agent for cartilage repair.

Anti-Obesity Effect of Ginkgo Vinegar, a Fermented Product of Ginkgo Seed Coat, in Mice Fed a High-Fat Diet and 3T3-L1 Preadipocyte Cells.

Ginkgo seed coat is rarely used and is typically discarded, due to its offensive odor and its toxicity. Ginkgo vinegar is a fermented product of ginkgo seed coat, and fermentation removes the bad smell and most of the toxicity. Thus, ginkgo vinegar contains very low concentrations of toxic components. The present study examined the anti-obesity effect of ginkgo vinegar in mice fed a high-fat diet and its inhibition of adipogenesis in 3T3-L1 cells. Ginkgo vinegar suppressed high-fat diet-induced body weight gain and reduced the size of fat cells in mice. Ginkgo vinegar suppressed the expression of C/EBPδ and PPARγ, key proteins in adipogenesis, and inhibited lipid accumulation in 3T3-L1 cells that were induced to become adipocytes. These results suggested that ginkgo vinegar inhibited adipocyte differentiation. On the other hand, a corresponding concentration of acetic acid had significantly less effect on lipid accumulation and virtually no effect on adipogenic gene expression. These results suggested that, similar to Ginkgo biloba extract, ginkgo vinegar might prevent and improve adiposity. Therefore, ginkgo seed coat could be a useful material for medicinal ingredients.

Dual role of inorganic polyphosphate in cardiac myocytes: The importance of polyP chain length for energy metabolism and mPTP activation.

We have previously demonstrated that inorganic polyphosphate (polyP) is a potent activator of the mitochondrial permeability transition pore (mPTP) in cardiac myocytes. PolyP depletion protected against Ca2+-induced mPTP opening, however it did not prevent and even exacerbated cell death during ischemia-reperfusion (I/R). The central goal of this study was to investigate potential molecular mechanisms underlying these dichotomous effects of polyP on mitochondrial function. We utilized a Langendorff-perfused heart model of I/R to monitor changes in polyP size and chain length at baseline, 20 min no-flow ischemia, and 15 min reperfusion. Freshly isolated cardiac myocytes and mitochondria from C57BL/6J (WT) and cyclophilin D knock-out (CypD KO) mice were used to measure polyP uptake, mPTP activity, mitochondrial membrane potential, respiration and ATP generation. We found that I/R induced a significant decrease in polyP chain length. We, therefore, tested, the ability of synthetic polyPs with different chain length to accumulate in mitochondria and induce mPTP. Both short and long chain polyPs accumulated in mitochondria in oligomycin-sensitive manner implicating potential involvement of mitochondrial ATP synthase in polyP transport. Notably, only short-chain polyP activated mPTP in WT myocytes, and this effect was prevented by mPTP inhibitor cyclosprorin A and absent in CypD KO myocytes. To the contrary, long-chain polyP suppressed mPTP activation, and enhanced ADP-linked respiration and ATP production. Our data indicate that 1) effect of polyP on cardiac function strongly depends on polymer chain length; and 2) short-chain polyPs (as increased in ischemia-reperfusion) induce mPTP and mitochondrial uncoupling, while long-chain polyPs contribute to energy generation and cell metabolism.

Inorganic polyphosphate protects against lipopolysaccharide-induced lethality and tissue injury through regulation of macrophage recruitment.

Sepsis is an etiologically complex and often fatal inflammatory process involving a multitude of cytokine signaling pathways. Tumor necrosis factor α (TNFα) acts as a central regulator of the acute-phase inflammatory response by recruiting immune cells, including circulating monocyte/macrophages, to sites of infection or tissue damage. Inorganic polyphosphate (polyP), a linear polymer of orthophosphate residues, has been found in almost all cells and tissues, but its functions in immunity remain largely unknown. In this study, we show that pre- or post-treatment of mice with polyP150 (average chain length of 150 phosphate residues) markedly increases survival from lipopolysaccharide (LPS)-induced shock and inhibits macrophage recruitment to the liver and lungs, resulting in protection against tissue injury. In accord with these in vivo results, pretreatment of cultured peritoneal macrophages with polyP150 inhibited chemotaxis and actin polarization in response to TNFα. PolyP150 also inhibited phosphorylation of stress-activated protein kinases c-Jun N-terminal kinase (JNK) and p38, two downstream signaling molecules of the TNFα cascade, thereby preventing cyclooxygenase-2 gene expression by macrophages. These findings suggest that polyP150 inhibits recruitment of macrophages into organs by regulating the TNFα-JNK/p38 pathway, which may, in turn, protect against multi-organ dysfunction and lethality induced by LPS. Our findings identify polyP regulation as a novel therapeutic target for sepsis.

Multifunctional Biomaterial Coating Based on Bio-Inspired Polyphosphate and Lysozyme Supramolecular Nanofilm.

Current implant materials have widespread clinical applications together with some disadvantages, the majority of which are the ease with which infections are induced and difficulty in exhibiting biocompatibility. For the efficient improvement of their properties, the development of interface multifunctional modification in a simple, universal, and environmently benign approach becomes a critical challenge and has acquired the attention of numerous scientists. In this study, a lysozyme-polyphosphate composite coating was fabricated for titanium(Ti)-based biomaterial to obtain a multifunctional surface. This coating was easily formed by sequentially soaking the substrate in reduced-lysozyme and polyphosphate solution. Such a composite coating has shown predominant antibacterial activity against Gram-negative bacteria ( E. coli) and improved cell adhesion, proliferation, and differentiation, which are much better than those of the pure substrate. This facile modification endows the biomaterial with anti-infective and potential bone-regenerative performance for clinical applications of biomaterial implants.

Simple Silica Column-Based Method to Quantify Inorganic Polyphosphates in Cartilage and Other Tissues.

OBJECTIVE: Inorganic polyphosphates (polyP) play a multitude of roles in mammalian biology. PolyP research is hindered by the lack of a simple and sensitive quantification method. The aim of this study was to develop a robust method for quantifying the low levels of polyP in mammalian tissue such as cartilage, which is rich in macromolecules that interfere with its determination. DESIGN: Native and in vitro formed tissues were digested with proteinase K to release sequestrated polyP. The tissue digest was loaded on to silica spin columns, followed by elution of bound polyP and various treatments were assessed to minimize non-polyP fluorescence. The eluent was then quantified for polyP content using fluorometry based on DAPI (4',6-diamidino-2-phenylindole) fluorescence shift occurring with polyP. RESULTS: Proteinase K pretreatment reduced the inhibitory effect of proteins on polyP recovery. The eluent was contaminated with nucleic acids and glycosaminoglycans, which cause extraneous fluorescence signals. These were then effectively eliminated by nucleases treatment and addition of concentrated Tris buffer. PolyP levels were quantified and recovery ratio determined using samples spiked with a known amount of polyP. This silica spin column method was able to recover at least 80% of initially loaded polyP, and detect as little as 10-10 mol. CONCLUSIONS: This sensitive, reproducible, easy to do method of quantifying polyP will be a useful tool for investigation of polyP biology in mammalian cells and tissues. Although the protocol was developed for mammalian tissues, this method should be able to quantify polyP in most biological sources, including fluid samples such as blood and serum.

Inorganic polyphosphates enhances nucleus pulposus tissue formation in vitro.

Disc degeneration is associated with low back pain for which currently there is no optimal therapy so there is a great need to identify new treatment approaches. Inorganic polyphosphates (polyP) are linear polymers of orthophosphate units varying in chain length and present in many cell types. As polyP has anabolic effects on chondrocytes, we hypothesized that polyP treatment would enhance matrix accumulation by nucleus pulposus (NP) cells. NP cells isolated from bovine caudal discs were grown in 3D culture under normoxic or in select experiments under hypoxic conditions, in the presence or absence of various concentrations and sizes of polyP. Gene expression was determined using RT-PCR. Matrix accumulation was quantified by measuring proteoglycan and collagen contents. DAPI fluorescence shift was used to stain for polyP in tissue. DAPI staining showed polyP present predominantly in the pericellular region of in vitro formed tissue. PolyP treatment enhanced matrix accumulation in a concentration and chain length dependant manner. NP cells exposed to polyP-22 (22 phosphate units length) showed an increase in gene expression of aggrecan, Collagen II, Sox 9, and MMP-13 which was maintained for the 14 days of culture. This suggests that polyP may enhance NP tissue formation in vitro by upregulating the expression of matrix genes. As polyP enhances proteoglycan accumulation even under hypoxic conditions, this raises the possibility that polyP may be a novel treatment to induce NP regeneration. © 2016 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 35:41-50, 2017.

Polyphosphate is a novel cofactor for regulation of complement by a serpin, C1 inhibitor.

The complement system plays a key role in innate immunity, inflammation, and coagulation. The system is delicately balanced by negative regulatory mechanisms that modulate the host response to pathogen invasion and injury. The serpin, C1-esterase inhibitor (C1-INH), is the only known plasma inhibitor of C1s, the initiating serine protease of the classical pathway of complement. Like other serpin-protease partners, C1-INH interaction with C1s is accelerated by polyanions such as heparin. Polyphosphate (polyP) is a naturally occurring polyanion with effects on coagulation and complement. We recently found that polyP binds to C1-INH, prompting us to consider whether polyP acts as a cofactor for C1-INH interactions with its target proteases. We show that polyP dampens C1s-mediated activation of the classical pathway in a polymer length- and concentration-dependent manner by accelerating C1-INH neutralization of C1s cleavage of C4 and C2. PolyP significantly increases the rate of interaction between C1s and C1-INH, to an extent comparable to heparin, with an exosite on the serine protease domain of the enzyme playing a major role in this interaction. In a serum-based cell culture system, polyP significantly suppressed C4d deposition on endothelial cells, generated via the classical and lectin pathways. Moreover, polyP and C1-INH colocalize in activated platelets, suggesting that their interactions are physiologically relevant. In summary, like heparin, polyP is a naturally occurring cofactor for the C1s:C1-INH interaction and thus an important regulator of complement activation. The findings may provide novel insights into mechanisms underlying inflammatory diseases and the development of new therapies.

In situ investigation of mammalian inorganic polyphosphate localization using novel selective fluorescent probes JC-D7 and JC-D8.

Inorganic polyphosphate (polyP) is a polymer composed of many orthophosphates linked together by phosphoanhydride bonds. Recent studies demonstrate that in addition to its important role in the function of microorganisms, polyP plays multiple important roles in the pathological and physiological function of higher eukaryotes, including mammalians. However, due to the dramatically lower abundance of polyP in mammalian cells when comparing to microorganisms, its investigation poses an experimental challenge. Here, we present the identification of novel fluorescent probes that allow for specific labeling of synthetic polyP in vitro as well as endogenous polyP in living cells. These probes demonstrate high selectivity for the labeling of polyP that was not sensitive to a number of ubiquitous organic polyphosphates, notably RNA. Use of these probes allowed us to demonstrate the real time detection of polyP release from lysosomes in live cells. Furthermore, we have been able to detect the increased levels of polyP in cells with Parkinson's disease related mutations.

Ultraphosphate, a potent stain control agent that is effective for both stain removal and prevention of stain deposition.

Polyphosphate is a phosphate polymer which is effective for stain removal and prevention of stain deposition. Ultraphosphate belongs to the polyphosphate group and has a highly branched mesh-like structure. To evaluate stain control ability of ultraphosphate, we used HAP powder, glass-ionomer cement and detached human teeth for models of in vitro stain control experiments. When using HAP powder, the stain removal ability of ultraphosphate was the highest among common chelating agents. In addition, ultraphosphate efficiently removed stain and prevented stain deposition on glass-ionomer cement at 20°C and 37°C. Finally, ultraphosphate removed coffee stain from human teeth surface efficiently and the color difference (ΔE*ab) before and after ultraphosphate treatment was changed dramatically from 59.4 to 8.3. Similarly, the ΔE*ab value of human teeth treated with ultraphosphate before coffee treatment was only 9.9, while the value without ultraphosphate pre-treatment was 21.2. These results indicate that ultraphosphate is a potent agent for stain control.

Morphogenetic study on the maturation of osteoblastic cell as induced by inorganic polyphosphate.

Since inorganic polyphosphates [poly(P)] have an activity to induce bone differenciation in vitro and in vivo, we examined an effect of poly(P) on organelle by light microscopy and electron microscopy in Murine MC3T3-E1 osteoblastic cells. The MC3T3-E1 cells were ultrastructurally observed to possess morphological characteristics of osteoblasts. Cells cultured with poly(P) were strongly stained with an anti-collagen type I antibody but not in those cultured without poly(P). Ultrastructural analysis of cells cultured with poly(P) revealed a well-developed Golgi apparatus, swollen and elongated rough endoplasmic reticulum, large mitochondria and many coated pits. Since MC3T3-E1 cells can be transformed from a resting phase to an active blastic cell phase after supplementation with poly(P), it implies that poly(P) can be an effective material for bone regeneration.

Inorganic polyphosphate adsorbed onto hydroxyapatite for guided bone regeneration: an animal study.

Inorganic polyphosphate (poly(P)) is recognized as a therapeutic agent that promotes fibroblast growth factor and enhances osteogenic differentiation, and in vivo, when adsorbed onto interconnected porous calcium hydroxyapatite (IP-CHA) enhances bone regeneration. The present study focused on the effect of poly(P) adsorbed onto IP-CHA granules (Poly(P)/IP-CHA) in guided bone regeneration (GBR). Dental implants were placed into the edentulous mandibular areas of five Beagle-Labrador hybrid dogs with screw expose on the buccal side, and then bone defects were filled Poly(P)/IP-CHA (test) or IP-CHA (control). After 12 weeks, histological evaluation and histomorphometrical analysis were performed. Newly-bone formation around exposed implant screw was clearly detected in the test-group. The ratio for regenerated bone height in the test group versus the control-group was 85.6±20.2 and 62.6±23.8, respectively, with no significant difference, while, that for bone implant contact was significantly higher (67.9±11.8 and 48.8±14.1, respectively). These findings indicate that Poly(P)/IP-CHA enhances bone regeneration in GBR.

Polyphosphate-mediated inhibition of tartrate-resistant acid phosphatase and suppression of bone resorption of osteoclasts.

Inorganic polyphosphate (poly(P)) has recently been found to play an important role in bone formation. In this study, we found that tartrate-resistant acid phosphatase (TRAP), which is abundantly expressed in osteoclasts, has polyphosphatase activity that degrades poly(P) and yields Pi as well as shorter poly(P) chains. Since the TRAP protein that coprecipitated with anti-TRAP monoclonal antibodies exhibited both polyphosphatase and the original phosphatase activity, poly(P) degradation activity is dependent on TRAP and not on other contaminating enzymes. The ferrous chelator α, α'-bipyridyl, which inhibits the TRAP-mediated production of reactive oxygen species (ROS), had no effect on such poly(P) degradation, suggesting that the degradation is not dependent on ROS. In addition, shorter chain length poly(P) molecules were better substrates than longer chains for TRAP, and poly(P) inhibited the phosphatase activity of TRAP depending on its chain length. The IC50 of poly(P) against the original phosphatase activity of TRAP was 9.8 µM with an average chain length more than 300 phosphate residues, whereas the IC50 of poly(P) with a shorter average chain length of 15 phosphate residues was 8.3 mM. Finally, the pit formation activity of cultured rat osteoclasts differentiated by RANKL and M-CSF were markedly inhibited by poly(P), while no obvious decrease in cell number or differentiation efficiency was observed for poly(P). In particular, the inhibition of pit formation by long chain poly(P) with 300 phosphate residues was stronger than that of shorter chain poly(P). Thus, poly(P) may play an important regulatory role in osteoclastic bone resorption by inhibiting TRAP activity, which is dependent on its chain length.

Inorganic polyphosphate suppresses lipopolysaccharide-induced inducible nitric oxide synthase (iNOS) expression in macrophages.

In response to infection, macrophages produce a series of inflammatory mediators, including nitric oxide (NO), to eliminate pathogens. The production of these molecules is tightly regulated via various mechanisms, as excessive responses are often detrimental to host tissues. Here, we report that inorganic polyphosphate [poly(P)], a linear polymer of orthophosphate ubiquitously found in mammalian cells, suppresses inducible nitric oxide synthase (iNOS) expression induced by lipopolysaccharide (LPS), a cell wall component of Gram-negative bacteria, in mouse peritoneal macrophages. Poly(P) with longer chains is more potent than those with shorter chains in suppressing LPS-induced iNOS expression. In addition, poly(P) decreased LPS-induced NO release. Moreover, poly(P) suppressed iNOS mRNA expression induced by LPS stimulation, thereby indicating that poly(P) reduces LPS-induced iNOS expression by down-regulation at the mRNA level. In contrast, poly(P) did not affect the LPS-induced release of TNF, another inflammatory mediator. Poly(P) may serve as a regulatory factor of innate immunity by modulating iNOS expression in macrophages.

Inorganic polyphosphates stimulate FGF23 expression through the FGFR pathway.

Polyphosphate (polyP) is composed of linear polymers of orthophosphate residues linked by high-energy phosphoanhydride bonds. It has been reported to improve osteoblastic differentiation, stimulate periodontal tissue regeneration, and accelerate bone repair. The aim of this study was to evaluate the effect of polyP on the expression of FGF23, a hormone secreted mostly be mature osteoblasts and osteocytes. In this study, different types of polyP were synthesized and co-cultured with osteoblast-like UMR-106 cells. Real-time PCR and western blot were used to analyze the gene and protein expression of FGF23. We found that 1 mM polyP was able to increase FGF23 expression after 4 h, reaching a peak after 12-24 h, with expression decreasing by 48 h. We also found that polyP could activate the FGFR pathway, as evidenced by increased phosphorylation of FGFR, FRS2, and Erk1/2. When FGFR signaling was inhibited by the specific inhibitor SU5402, the effect of polyP on FGF23 expression was significantly reduced. Our results indicate that polyP is able to stimulate osteoblastic FGF23 expression and that this effect is associated with activation of the FGFR pathway. These findings provide support for the clinical use of polyP by indicating a mechanism for polyP in bone regeneration.

Bone formation without lamina dura in the middle-aged and elderly: possible dependence on enamel.

Bone formation below the crown of mandibular horizontal incompletely impacted third molar is frequently seen in the middle-aged and elderly. The phenomenon shows lamina dura loss without radiolucency and we hypothesized the participation of mature enamel without any influence on the environmental oral status. In order to investigate the characteristics of the phenomenon based on the presence/absence of the lamina dura and radiolucency below the crown, we studied the relationship between 58 men and 43 women with a lamina dura without radiolucency, 12 men and 8 women without a lamina dura with radiolucency, 34 men and 16 women without a lamina dura without radiolucency, and the status of teeth in the ipsilateral mandible. Subjects without a lamina dura without radiolucency were significantly older than those with a lamina dura without radiolucency in both men (P < 0.0001) and women (P <0.01), indicating different chronological causes. Men without lamina dura with radiolucency showed significantly more tooth loss than those with a lamina dura without radiolucency (P < 0.00001) and those without a lamina dura without radiolucency (P < 0.0001), indicating the influence of poor oral health. Thus, the phenomenon without a lamina dura without radiolucency may show the clinical importance of bone formation in the elderly.

Inorganic polyphosphate differentiates human mesenchymal stem cells into osteoblastic cells.

The existence of inorganic polyphosphates [poly(P)] in human cells has been demonstrated. In osteoblasts, it is suggested that the concentration of cellular poly(P) is relatively high. In this study, we examined whether poly(P) accelerates the differentiation of human mesenchymal stem cells (hMSCs) from patients with osteoarthritis (OA) and rheumatoid arthritis (RA) into osteoblastic cells. Alkaline phosphatase (ALP) activity was induced by poly(P) in hMSCs from both OA and RA. In Alizarin Red S and osteocalcin EIA, there was a significant difference between the control and poly(P) group. In real-time PCR, there was a significant difference in ALP, collagen type 1A, osteocalcin, and bone sialoprotein between the control and poly(P) group. Our findings suggest that poly(P) have the potent role of differentiating hMSCs into osteoblastic cells at the early and later stages of osteoblastic differentiation.

Activation of the FGF signaling pathway and subsequent induction of mesenchymal stem cell differentiation by inorganic polyphosphate.

Inorganic polyphosphate [poly(P)] is a biopolymer existing in almost all cells and tissues, although its biological functions in higher eukaryotes have not been completely elucidated. We previously demonstrated that poly(P) enhances the function of fibroblast growth factors (FGFs) by stabilizing them and strengthening the affinity between FGFs and their cell surface receptors. Since FGFs play crucial roles in bone regeneration, we further investigated the effect of poly(P) on the cell differentiation of human stem cells via FGF signaling systems. Human dental pulp cells (HDPCs) isolated from human dental pulp show the characteristics of multipotent mesenchymal stem cells (MSCs). HDPCs secreted FGFs and the proliferation of HDPCs was shown to be enhanced by treatment with poly(P). Cell surface receptor-bound FGF-2 was stably maintained for more than 40 hours in the presence of poly(P). The phosphorylation of ERK1/2 was also enhanced by poly(P). The effect of poly(P) on the osteogenic differentiation of HDPCs and human MSCs (hMSCs) were also investigated. After 5 days of treatment with poly(P), type-I collagen expression of both cell types was enhanced. The C-terminal peptide of type-I collagen was also released at higher levels in poly(P)-treated HDPCs. Microarray analysis showed that expression of matrix metalloproteinase-1 (MMP1), osteopontin (OPN), osteocalcin (OC) and osteoprotegerin was induced in both cell types by poly(P). Furthermore, induced expression of MMP1, OPN and OC genes in both cells was confirmed by real-time PCR. Calcification of both cell types was clearly observed by alizarin red staining following treatment with poly(P). The results suggest that the activation of the FGF signaling pathway by poly(P) induces both proliferation and mineralization of stem cells.

Effect of inorganic polyphosphate in periodontitis in the elderly.

AIM: Inorganic polyphosphate exists as chains of phosphate molecules and is distributed in osteoblasts, and regulates osteoblastic cell differentiation and bone matrix calcification. The purpose of this study was to clarify the effects of inorganic polyphosphate on periodontitis. MATERIAL AND METHODS: Subgingival local irrigation with inorganic polyphosphate was studied in a randomised double-blind study of 33 patients with periodontitis. Scaling and root planing were performed 1 week after the initial examination. RESULTS: No significant differences between the inorganic polyphosphate group and control were detected in each item except IL-1beta. Patients in whom both the bleeding on probing and gingival index at 1 week had improved were significantly older in the inorganic polyphosphate group than in the control group (p < 0.05). Bone regeneration was seen in one case of the inorganic polyphosphate group. CONCLUSIONS: Inorganic polyphosphate was useful in the treatment of periodontitis in the elderly, indicating a probable effect of anti-ageing, with similar bone regenerations occurring in both groups.