Capping a pulpotomy with calcium aluminosilicate cement: comparison to mineral trioxide aggregates.

INTRODUCTION: Calcium aluminate cements have shown little affinity for bacterial growth, low toxicity, and immunogenicity when used as a restoration material, but calcium aluminate cements have not been tested in vivo in pulpotomy procedures. METHODS: To address this question, a calcium aluminosilicate cement (Quick-Set) was tested along with 2 mineral trioxide aggregates, ProRoot MTA and MTA Plus. These cements were used as a capping agent after pulpotomy. Control rats had no pulpotomy, or the pulpotomy was not capped. Proinflammatory cytokines interleukin (IL)-1ß and IL-1α were measured, and histology was performed at 30 and 60 days after capping. The nociceptive response was determined by measuring the lengthening of the rat's meal duration. RESULTS: and CONCLUSIONS: IL-1ß and IL-1α concentrations were reduced in the capped teeth, but no differences were observed among the 3 cements. Dentinal bridging could be detected at both 30 and 60 days with each of the 3 cements, and the pulps were still vital 60 days after capping. Meal duration significantly shortened after placement of the 3 different cements, indicating a nociceptive response, but there were no differences among the materials. Calcium aluminosilicate cement had similar properties to mineral trioxide aggregates and is a viable option for pulpotomy procedures.

Antioxidant combinations protect oral fibroblasts against metal-induced toxicity.

OBJECTIVE: In dentistry, the use of metals in fillings, braces, implants, bridges and other prosthodontic restorations is a common practice. Previous studies revealed that zinc (Zn) and copper (Cu) released from gold alloys, and nickel (Ni) released from nickel-chromium alloys, have a highly cytotoxic effect on fibroblast cell cultures. Our working hypothesis is that oral fibroblasts are susceptible to damage from metals because they elevate reaction oxygen species (ROS). In this study, we investigated specific antioxidant (AO) combinations to determine if they counteract the effects of Cu, Ni and Zn on cultured oral fibroblast proliferation and oxidative damage. METHODS: Oral fibroblasts were pretreated with Cu, Ni and Zn for 60min. Thereafter, cells were treated with 10(-5)M combinations of bioactive AO resveratrol (R), ferulic acid (F), phloretin (P) and tetrahydrocurcuminoids (T) (RFT, PFR, PFT) for 24h. Cell viability and DNA synthesis were monitored by 3-[4,5-dimethylthiazol-2-yl]-5-[3-carboxymethoxyphenyl]-2-[4-sulfophenyl]-2H-tetrazolium (MTS) and 5-bromo-2-deoxyuridine (BrDU) assays. ROS was measured using the fluorescence response of dichlorodihydrofluorescein diacetate (DCF). RESULTS: AO compounds increased recovery of cells exposed to Cu and Zn. Moreover, AO treatment induced DNA synthesis in the presence of the metal stressors. Cu and Ni stimulated production of ROS. PFR treatment decreased ROS in the presence of Cu, Ni and Zn. SIGNIFICANCE: These data indicate that pure AOs counteracted the detrimental effects of Cu, Ni, Zn on oral fibroblasts in vitro by increasing cell viability, and DNA synthesis and decreasing ROS activity.

In vitro evaluation of dentinal tubule penetration and biomineralization ability of a new root-end filling material.

INTRODUCTION: Capasio is being developed as a new generation of endodontic material with potential use as a root-end filling material. The aim of this study was to compare the ability of Capasio and mineral trioxide aggregate (MTA) to penetrate human dentinal tubules and examine the interaction of Capasio and MTA with a synthetic tissue fluid (STF) and root canal walls in extracted human teeth. METHODS: Root-end preparations were filled with Capasio or MTA, allowed to set for 4 weeks in STF, and then sectioned at 1, 2, and 3 mm from resected surface. Depth of penetration was evaluated by using scanning electron microscopy (SEM). Next, Capasio and MTA samples were prepared both in 1-g pellets and in root-end preparations. Samples were placed in STF, allowed to set, and then characterized by using SEM, energy dispersive x-ray analysis (EDXA), and x-ray diffraction (XRD) techniques. RESULTS: Penetration of Capasio into dentinal tubules was observed at all levels. No penetration of MTA into dentinal tubules was observed at any level. Both Capasio and MTA formed apatite crystals in the supernatant, on their exposed surfaces, and in the interfacial layers that were similar in structure and elemental composition when evaluated by using SEM and EDXA. XRD analysis of these crystals corresponds with those reported for hydroxyapatite. CONCLUSIONS: When used as a root-end filling material, Capasio is more likely to penetrate dentinal tubules. Both Capasio and MTA promote apatite deposition when exposed to STF.

Bioactive polyphenol antioxidants protect oral fibroblasts from ROS-inducing agents.

BACKGROUND: Oxidative damage to soft oral tissues may result from exposure to the chemicals or biochemicals found in teeth-whitening products, dental restorations, tobacco, and alcohol. Our working hypothesis is that oral tissues are susceptible to the toxic effects of stressors such as hydrogen peroxide (H(2)O(2)), ethanol (EtOH) and nicotine (Nic), which decrease cell viability/DNA synthesis and elevate reactive oxygen species (ROS). In this study, we investigated specific polyphenols and turmeric derivative antioxidants (AO) in combinations that counteracted the effects of these stressors on cultured oral fibroblast proliferation and ROS production. METHODS: Oral fibroblasts were exposed to stressors for 30 min and then treated with 10(-5) M of bioactive AO mixtures [resveratrol, ferulic acid and tetrahydrocurcuminoid (RFT), phloretin, ferulic acid and resveratrol (PFR), phloretin, ferulic acid and tetrahydrocurcuminoid (PFT)] for 24 h. Cell viability and DNA synthesis were monitored using incorporated 3-[4,5-dimethylthiazol-2-yl]-5-[3-carboxymethoxyphenyl]-2-[4-sulphophenyl]-2H-tetrazolium (MTS) and 5-bromo-2-deoxyuridine (BrdU) assays, respectively. Total ROS was measured with dichlorodihydrofluorescein diacetate (H(2)DCFDA). RESULTS: Incubation of oral fibroblasts in the stressors for 30 min resulted in a dose-dependent decrease of DNA synthesis and number of viable cells, and an increased total ROS activity. AO treatment counteracted the insults by restoring DNA synthesis levels and cell viability, and decreasing the total ROS activity. CONCLUSION: The AO combinations of RFT, PFR and PFT protected the oral fibroblasts from the detrimental effects of H(2)O(2), EtOH and Nic by decreasing total ROS and increasing cell viability and DNA synthesis.

Bioactive antioxidant mixtures promote proliferation and migration on human oral fibroblasts.

OBJECTIVE: Antioxidants (AOs) are the first line of defence against free radical damage and are critical for maintaining optimum health and well being. The need for AOs becomes even more critical with increased exposure to free radicals generated by pollution, cigarette smoke, drugs, illness, stress and exercise. Antioxidant supplementation is an excellent way of improving free radical protection. The aim of this study was to provide cytotoxicity, proliferation and migration data on the in vitro effects of bioactive AO mixtures on human oral fibroblasts. METHODS: Human oral fibroblasts were obtained from human gingival (HGF) and periodontal (HPDL) tissues. Each of these oral fibroblasts was cultured separately in three concentrations of the bioactive pure polyphenol and turmeric derivative mixtures; resveratrol (R), ferulic acid (F), phloretin (P) and tetrahydrocurcuminoids (T); [(RFT), (PFR), and (PFT)]. Cell viability, proliferation, morphology and migratory behaviour were analysed in vitro using high throughput in vitro 96 well plate wound assay. RESULTS: RFT decreased (10(-3)M) and increased (10(-5)M) cell number in HGF cells. Three concentrations (10(-3), 10(-4), and 10(-5)M) of PFR and PFT increased DNA synthesis in HGF cells. PFT promoted cell migration but PFR and RFT had no significant change in HGF wound healing rates in a 96 well plate assay monolayer wound. In the HPDL cells, the 10(-4)M concentration of both RFT and PFT increased cell number at 72 h and 96 h whereas the lower concentration 10(-5)M of RFT significantly stimulated cell number at 96 h. PFR (10(-3)M and 10(-5)M) and PFT (10(-3)M) increased DNA synthesis after 48 h treatment in HPDL cells. CONCLUSIONS: High and low concentrations (10(-3)-10(-5)M) of these AOs (RFT, PFR) may have beneficial effects on functional mechanisms regulating fibroblast migration and proliferation during gingival healing or periodontal repair.

Use of antioxidants in oral healthcare.

There is increasing attention to the potential benefit from the use of antioxidants in the field of dental medicine. In general, antioxidants may be available through oral ingestion, diet or vitamin supplements, and in nutraceuticals. In addition, treatment of oral and dental health problems may include drug-free, natural antioxidant remedies that are available in topical oral applications such as mouth rinse, gel, paste, gum, or lozenge compositions. These topical antioxidant remedies help reduce free-radical or reactive-oxygen species, which are causative inflammatory factors in the progression of gingival and periodontal maladies. This review focuses on relationships between antioxidants and free-radical/reactive-oxygen species in the oral environment.

Use of antioxidants in oral healthcare.

There is increasing attention to the potential benefit from the use of antioxidants in the field of dental medicine. In general, antioxidants may be available through oral ingestion, diet or vitamin supplements, and in nutraceuticals. In addition, treatment of oral and dental health problems may include drug-free, natural antioxidant remedies that are available in topical oral applications such as mouth rinse, gel, paste, gum, or lozenge compositions. These topical antioxidant remedies help reduce free-radical or reactive-oxygen species, which are causative inflammatory factors in the progression of gingival and periodontal maladies. This review focuses on relationships between antioxidants and free-radical/reactive-oxygen species in the oral environment.

Cytokine therapy for craniosynostosis.

The birth prevalence of craniosynostosis (premature suture fusion) is 300-500 per 1,000,000 live births. Surgical management involves the release of the synostosed suture. In many cases, however, the suturectomy site rapidly reossifies, further restricts the growing brain and alters craniofacial growth. This resynostosis requires additional surgery, which increases patient morbidity and mortality. New findings in bone biology and molecular pathways involved with suture fusion, combined with novel tissue engineering techniques, may allow the design of targeted and complementary therapies to decrease complications inherent in high-risk surgical procedures. This paper selectively reviews recent advances in i) identifying genetic mutations and the aetiopathogenesis of a number of craniosynostotic conditions; ii) cranial suture biology and molecular biochemical pathways involved in suture fusion; and iii) the design, development and application of various vehicles and tissue engineered constructs to deliver cytokines and genes to cranial sutures. Such biologically based therapies may be used as surgical adjuncts to rescue fusing sutures or help manage postoperative resynostosis.