Contribution of biomimetic collagen-ligand interaction to intrafibrillar mineralization.

Contemporary models of intrafibrillar mineralization mechanisms are established using collagen fibrils as templates without considering the contribution from collagen-bound apatite nucleation inhibitors. However, collagen matrices destined for mineralization in vertebrates contain bound matrix proteins for intrafibrillar mineralization. Negatively charged, high-molecular weight polycarboxylic acid is cross-linked to reconstituted collagen to create a model for examining the contribution of collagen-ligand interaction to intrafibrillar mineralization. Cryogenic electron microscopy and molecular dynamics simulation show that, after cross-linking to collagen, the bound polyelectrolyte caches prenucleation cluster singlets into chain-like aggregates along the fibrillar surface to increase the pool of mineralization precursors available for intrafibrillar mineralization. Higher-quality mineralized scaffolds with better biomechanical properties are achieved compared with mineralization of unmodified scaffolds in polyelectrolyte-stabilized mineralization solution. Collagen-ligand interaction provides insights on the genesis of heterogeneously mineralized tissues and the potential causes of ectopic calcification in nonmineralized body tissues.

MMP-8-Responsive Polyethylene Glycol Hydrogel for Intraoral Drug Delivery.

Currently available drug delivery systems for oral diseases suffer from short retention time and poor local concentrations at the target site. A biodegradable stimulus-responsive hydrogel was synthesized in the present study to evaluate its application as an environmentally sensitive carrier for on-demand intraoral drug delivery. The hydrogel was synthesized from diacrylate-containing polyethylene glycol-based scaffolds and a cysteine-terminated peptide crosslinker (CGPQG↓IWGQC) via a Michael-type addition reaction. Because CGPQG↓IWGQC can be cleaved by matrix metalloproteinase 8 (MMP-8), minocycline hydrochloride, bovine serum albumin, or an antibacterial peptide (KSL) was incorporated into the scaffolds to evaluate the MMP-8-responsive release behavior of the on-demand drug delivery system. Hydrogel characterization and gelation kinetics were examined with gel time, Fourier-transform infrared spectroscopy, scanning electron microscopy, and measurements of rheologic parameters. Degradation behavior and MMP-8-responsive drug release were performed by high-performance liquid chromatography and protein-specific assay. Biocompatibility evaluation indicated that the hydrogels were noncytotoxic. Antibacterial testing demonstrated that the released drugs were able to maintain bioactivity. Taken together, these results suggest that the MMP-8-sensitive hydrogel is a promising candidate for on-demand intraoral localized drug delivery. Because MMP-8 is one of the most important biomarkers for periodontitis, the MMP-8-responsive hydrogel has potential to be used for in situ adaptive degradation in response to chronic periodontitis and peri-implantitis. This notion has to be tested in animal models of periodontal disease.

Effect of a novel quaternary ammonium silane cavity disinfectant on durability of resin-dentine bond.

OBJECTIVE: The present study examined the effect of a quaternary ammonium silane (QAS) cavity disinfectant on the viability of human dental pulp cells, dentine bond durability and nanoleakage of simplified etch-and-rinse adhesives. METHODS: Etched dentine surface of third molars were randomly divided into two adhesive groups, Adper™ Single Bond 2 and Prime & Bond® NT™. For each adhesive, the teeth were randomly assigned to five cavity disinfectant groups (N=6): Group 1: deionised water (control); Group 2: 2% chlorhexidine (CHX); Group 3: 2% QAS; Group 4: 5% QAS and Group 5: 10% QAS. The cavity disinfectants were applied on etched dentine surfaces for 20s, followed by adhesive application. The bonded teeth were sectioned for bond strength testing at 24h, 6 months and 12 months. Viability of human dental pulpal cells was examined using MTT assay. Bond strength data were analysed using 3-way ANOVA and Tukey test. Interfacial nanoleakage was evaluated after 24h and 12 months and analysed using Kruskal-Wallis test. RESULTS: Significant differences in bond strength were observed for the factors disinfectants (p<0.001) and time (p<0.001); while the factor, adhesive, was not significantly different (p=0.203). The 2% QAS cavity disinfectant preserved bond strength of both adhesives and reduced interfacial nanoleakage after 12 months. Cell viability was the lowest for 2% CHX, followed by 2% QAS and the control. CONCLUSIONS: The 2% QAS cavity disinfectant demonstrated greater cell viability compared to 2% CHX, with no adverse effect on immediate bond strength and preserved bond stability over time. CLINICAL SIGNIFICANCE: Incorporation of 2% quaternary ammonium silane cavity disinfectant in the resin-dentine bonding protocol enhances the success rate of bonded restorations.

Effect of a novel quaternary ammonium silane on dentin protease activities.

OBJECTIVES: Demineralized dentin collagen release C-terminal cross-linked telopeptide (ICTP) and C-terminal peptide (CTX) during degradation. The present study evaluated the effects of dentin pre-treatment with K21, a quaternary ammonium silane (QAS), on matrix metalloproteinase (MMP) and cathepsin K-mediated collagen degradation. METHODS: Dentin beams were demineralized with 10% H3PO4 for 24h. After baseline dry mass measurements, the beams were divided into 5 groups (N=10) according to protease inhibitors. The beams were pre-treated for 2min with 2% chlorhexidine (CHX), 2%, 5% or 10% QAS; no pre-treatment was performed for the control group. The beams were subsequently incubated in calcium- and zinc-containing medium for 3, 7 or 14days, after which changes in dry mass were measured and incubation media were examined for ICTP and CTX release. The MMP-2 and cathepsin K activities in QAS-treated dentin powder were also quantified using ELISA. RESULTS: The two factors (disinfectants and time) had a significant effect on dry mass loss, ICTP and CTX release (p<0.001). The percentage of dry mass loss increased with time and was significantly lower in all experimental groups when compared to the control at 14days (p<0.001). Conversely, the rate of ICTP and CTX release was significantly lower in the experimental groups, compared to the uninhibited control at 7 and 14days (p<0.001). Dentinal MMP-2 and cathepsin K activities were significantly reduced after demineralized dentin was pre-treated with QAS. CONCLUSION: The experimental QAS is a good inhibitor of MMP and cathepsin K activities in demineralized dentin. CLINICAL SIGNIFICANCE: The newly developed antibacterial quaternary ammonium silane increases the resistance of dentin collagen to degradation by inhibiting endogenous matrix metalloproteinases and cysteine cathepsins. The quaternary ammonium silane cavity disinfectant is promising for use as a protease inhibitor to improve durability of resin-dentin bonds.

Effect of polyacrylic acid on dentin protease activities.

OBJECTIVE: This study tested whether treatment of demineralized dentin with polyacrylic acid (PAA) has any activatory or inhibitory activity on dentin matrix metalloproteinases (MMP)s or cathepsin K (CAT-K). METHODS: Dentin beams (1mm×2mm×6mm; n=10) were completely demineralized with EDTA. After initial dry mass assessment, the beams were dipped into 37% phosphoric acid (PA), PA+2% benzalkonium chloride (BAC), PA+2% chlorhexidine digluconate (CHX), 10% PAA, PAA+BAC or PAA+CHX for 20s. Demineralized beams without treatment served as control. All beams were incubated in simulated body fluid (SBF) for 1 week and the dry mass loss was evaluated. Aliquots of SBF were used to analyze solubilized telopeptide fragments using ICTP as indicator of MMP-mediated collagen degradation and CTX for CAT-K-mediated degradation. Additional demineralized beams (n=10) were used to measure the influence of different chemical treatments on total MMP activity of EDTA-demineralized dentin using generic MMP assay. Data were analyzed by ANOVA (α=0.05). RESULTS: Dry mass loss ranged from 6% (PA) to 2% for (PA-BAC) or (PAA-BAC) (p<0.05). ICTP release of PAA-treated group was significantly higher (p<0.05) than the control, and not significantly different from the PA group (p>0.05). PA+CHX or PAA+CHX and PAA+BAC showed significantly lower ICTP than PA or PAA groups (p<0.05). CAT-K activity increased significantly after 10% PAA treatment compared to control (p<0.05) or to PA postreatment. SIGNIFICANCE: Demineralized dentin treated with 10% polyacrylic acid activated CAT-K more than 37% phosphoric acid; 2% chlorhexidine digluconate seems to be a better inhibitor of MMPs and CAT-K than 2% benzalkonium chloride.

Norepinephrine Regulates Condylar Bone Loss via Comorbid Factors.

Degenerative changes of condylar subchondral bone occur frequently in temporomandibular disorders. Although psychologic stresses and occlusal abnormalities have been implicated in temporomandibular disorder, it is not known if these risks represent synergistic comorbid factors that are involved in condylar subchondral bone degradation that is regulated by the sympathetic nervous system. In the present study, chronic immobilization stress (CIS), chemical sympathectomy, and unilateral anterior crossbite (UAC) were sequentially applied in a murine model. Norepinephrine contents in the subjects' serum and condylar subchondral bone were detected by ELISA; bone and cartilage remodeling parameters and related gene expression in the subchondral bone were examined. Subchondral bone loss and increased subchondral bone norepinephrine level were observed in the CIS and UAC groups. These groups exhibited decreased bone mineral density, volume fraction, and bone formation rate; decreased expressions of osterix, collagen I, and osteocalcin; but increased trabecular separation, osteoclast number and surface, and RANKL expression. Combined CIS + UAC produced more severe subchondral bone loss, higher bone norepinephrine level, and decreased chondrocyte density and cartilage thickness when compared to CIS or UAC alone. Sympathectomy simultaneously prevented subchondral bone loss and decreased bone norepinephrine level in all experimental subgroups when compared to the vehicle-treated counterparts. Norepinephrine also decreased mRNA expression of osterix, collagen I, and osteocalcin by mesenchymal stem cells at 7 and 14 d of stimulation and increased the expression of RANKL and RANKL/OPG ratio by mesenchymal stem cells at 2 h. In conclusion, CIS and UAC synergistically promote condylar subchondral bone loss and cartilage degradation; such processes are partially regulated by norepinephrine within subchondral bone.

Role of dentin MMPs in caries progression and bond stability.

Dentin can be described as a biological composite with collagen matrix embedded with nanosized hydroxyapatite mineral crystallites. Matrix metalloproteinases (MMPs) and cysteine cathepsins are families of endopeptidases. Enzymes of both families are present in dentin and collectively capable of degrading virtually all extracellular matrix components. This review describes these enzymes and their presence in dentin, mainly focusing on their role in dentin caries pathogenesis and loss of collagen in the adhesive hybrid layer under composite restorations. MMPs and cysteine cathepsins present in saliva, mineralized dentin, and/or dentinal fluid may affect the dentin caries process at the early phases of demineralization. Changes in collagen and noncollagenous protein structure may participate in observed decreases in mechanical properties of caries-affected dentin and reduce the ability of caries-affected dentin to remineralize. These endogenous enzymes also remain entrapped within the hybrid layer during the resin infiltration process, and the acidic bonding agents themselves (irrespective of whether they are etch-and-rinse or self-etch) can activate these endogenous protease proforms. Since resin impregnation is frequently incomplete, denuded collagen matrices associated with free water (which serves as a collagen cleavage reagent for these endogenous hydrolase enzymes) can be enzymatically disrupted, finally contributing to the degradation of the hybrid layer. There are multiple in vitro and in vivo reports showing that the longevity of the adhesive interface is increased when nonspecific enzyme-inhibiting strategies are used. Different chemicals (i.e., chlorhexidine, galardin, and benzalkonium chloride) or collagen cross-linker agents have been successfully employed as therapeutic primers in the bonding procedure. In addition, the incorporation of enzyme inhibitors (i.e., quaternary ammonium methacrylates) into the resin blends has been recently promoted. This review will describe MMP functions in caries and hybrid layer degradation and explore the potential therapeutic role of MMP inhibitors for the development of improved intervention strategies for MMP-related oral diseases.

Zoledronate and ion-releasing resins impair dentin collagen degradation.

This study analyzed the amounts of solubilized telopeptides cross-linked carboxyterminal telopeptide of type I collagen (ICTP) and C-terminal crosslinked telopeptide of type I collagen (CTX) derived from matrix-metalloproteinases (MMPs) and cysteine cathepsins (CTPs) subsequent to application of a filler-free (Res.A) or an ion-releasing resin (Res.B) to ethylenediaminetetraacetic acid (EDTA)-demineralized dentin with or without zoledronate-containing primer (Zol-primer) pre-treatment. The chemical modification induced following treatments and artificial saliva (AS) storage was also analyzed through attenuated total reflection Fourier transform infrared spectroscopy (ATR-FTIR). Totally EDTA-demineralized specimens were infiltrated with Res.A or Res.B with or without Zol-primer pre-treatment, light-cured, and immersed in AS for up to 4 wk. ICTP release was reduced following infiltration with Res.B and further reduced when Res.B was used with Zol-primer; remarkable phosphate mineral uptake was attained after AS storage. CTX release was increased in Res.A- and Res.B-treated dentin. However, when Zol-primer was used with Res.A, the CTX release fell significantly compared to the other tested resin-infiltration methods. In conclusion, zoledronate offers an additional inhibitory effect to the ion-releasing resins in MMP-mediated collagen degradation. However, Zol-primer induces a modest reduction in CTX release only when used with resin-based systems containing no ion-releasing fillers.

The effect of glutathione on 2-hydroxyethylmethacrylate cytotoxicity and on resin-dentine bond strength.

AIM: To evaluate the influence of reduced glutathione (GSH) application on 2-hydroxyethylmethacrylate (HEMA) cytotoxicity on rat pulpal cells and evaluate the effect of etched-dentine treatment with GSH on the immediate microtensile bond strength (µTBS) of etch-and-rinse adhesive. METHODOLOGY: The cytotoxicity of 10 mmol L(-1) HEMA, 10 mmol L(-1) HEMA + 1 mmol L(-1) GSH, 10 mmol L(-1) HEMA + 5 mmol L(-1) GSH and 10 mmol L(-1) HEMA + 10 mmol L(-1) GSH was compared (6 h and 24 h). Cells viability was measured by means of 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, followed by morphological observation of cells. Etched-dentine surfaces were rinsed and treated with one of the following solutions: 2% GSH, 5% GSH or 10% GSH, bonded with Adper Single Bond Plus (3M, ESPE, St. Paul, MN, USA) and restored with resin composite. The control group received no GSH treatment. After 1 day of water-storage at 37 °C, the specimens were subjected to µTBS testing. Cytotoxicity and µTBS data were analysed by one-way anova and Tukey post hoc tests (P < 0.05). RESULTS: There were significant differences between the groups. HEMA elicited a remarkable toxic effect. 10 mmol L(-1) GSH prevented HEMA-induced damage at both exposure times. Whilst 5 mmol L(-1) GSH lost its protective effect at 24-h exposure time and 1 mmol L(-1) GSH showed no protective effect at both exposure times, GSH had no significant effect on the immediate µTBS; however, 5% GSH had higher bond strength value when compared to 10% GSH (P = 0.003). CONCLUSION: Controlled concentrations of GSH had a protective effect against HEMA cytotoxicity. GSH had neither positive nor negative influence on µTBS.

Effect of phosphoric acid on the degradation of human dentin matrix.

This study determined if dentin proteases are denatured by phosphoric acid (PA) used in etch-and-rinse dentin adhesives. Dentin beams were completely demineralized with EDTA for 30 days. We "acid-etched" experimental groups by exposing the demineralized dentin beams to 1, 10, or 37 mass% PA for 15 sec or 15 min. Control beams were not exposed to PA but were incubated in simulated body fluid for 3 days to assay their total endogenous telopeptidase activity, by their ability to solubilize C-terminal crosslinked telopeptides ICTP and CTX from insoluble dentin collagen. Control beams released 6.1 ± 0.8 ng ICTP and 0.6 ± 0.1 ng CTX/mg dry-wt/3 days. Positive control beams pre-incubated in p-aminophenylmercuric acetate, a compound known to activate proMMPs, released about the same amount of ICTP peptides, but released significantly less CTX. Beams immersed in 1, 10, or 37 mass% PA for 15 sec or 15 min released amounts of ICTP and CTX similar to that released by the controls (p > 0.05). Beams incubated in galardin, an MMP inhibitor, or E-64, a cathepsin inhibitor, blocked most of the release of ICTP and CTX, respectively. It is concluded that PA does not denature endogenous MMP and cathepsin activities of dentin matrices.

Effect of UVA-activated riboflavin on dentin bonding.

Recent studies have reported collagen cross-linking after exposure to riboflavin followed by ultraviolet-A (UVA) exposure. This study is the first to investigate the effect of a riboflavin-containing primer on adhesive interface stability and dentinal matrix metalloproteinase activity. Human dentin was etched with 35% phosphoric acid, treated with 0.1% riboflavin, exposed to UVA for 2 min, and bonded with a two-step etch-and-rinse adhesive. Adhesive was applied to control specimens without riboflavin/UVA. Specimens were subjected to microtensile bond strength tests and pulled to failure after storage for 24 hrs, 6 mos, or 1 yr. Interfacial nanoleakage was evaluated by light and transmission electron microscopy. To investigate dentinal matrix metalloproteinase activity, we performed correlative zymographic assays on protein extracts obtained from phosphoric-acid-etched dentin powder with or without riboflavin/UVA treatment and XP Bond. Ultraviolet-activated riboflavin treatment increased the immediate bond strength to dentin at all aging intervals (p < 0.05 vs. control) and decreased interfacial nanoleakage in aged specimens (1 yr; p < 0.05). Zymograms revealed that riboflavin/UVA pre-treatment inhibited dentinal matrix metalloproteinase activity (especially MMP-9). In conclusion, dentinal collagen cross-linking induced by riboflavin/UVA increased immediate bond strength, stabilized the adhesive interface, and inhibited dentin matrix metalloproteinases, thereby increasing the durability of resin-dentin bonds.

Apical surgery: endoscopic findings at the resection level of 168 consecutively treated roots.

AIM: Endoscopic evaluation of the cut root face after root-end resection during apical surgery. METHODOLOGY: Consecutive cases undergoing apical surgery from June 2006 to May 2008 were enrolled. After root-end resection, the cut root face was inspected with a rigid endoscope and the following findings were assessed: number of canals, presence of isthmus, presence and location of craze lines/cracks, frosted dentine, and gaps between root filling material and dentine. Craze lines/cracks, frosted dentine and gaps were further correlated with the age group of the patient (<45 vs. ≥ 45 years), the type of treated tooth and the presence or absence of a post/screw. RESULTS: The final material included 168 resected roots. The highest frequency of isthmuses was found in mesial roots of mandibular first molars (88.5%). A craze line/crack was seen in 9.5%, frosted dentine in 79.8% and gaps in 83.3% at the cut root faces. Significant differences were observed for the location of the microfindings at the resected root surfaces (buccal vs. mesial vs. lingual vs. distal, P > 0.0001). Premolars had significantly more craze lines/cracks than anterior teeth (P = 0.006) and molars (P = 0.000). Frosted dentine was significantly more frequently seen in premolars (P = 0.027) and molars (P = 0.001) compared to anterior teeth. The age groups and the presence or absence of a post/screw did not significantly influence the findings. CONCLUSIONS: Frosted dentine and gaps were frequently observed with endoscopy at the resected root surfaces. The type of tooth appeared to affect the occurrence of a craze line/crack and of frosted dentine.

Limitations in bonding to dentin and experimental strategies to prevent bond degradation.

The limited durability of resin-dentin bonds severely compromises the lifetime of tooth-colored restorations. Bond degradation occurs via hydrolysis of suboptimally polymerized hydrophilic resin components and degradation of water-rich, resin-sparse collagen matrices by matrix metalloproteinases (MMPs) and cysteine cathepsins. This review examined data generated over the past three years on five experimental strategies developed by different research groups for extending the longevity of resin-dentin bonds. They include: (1) increasing the degree of conversion and esterase resistance of hydrophilic adhesives; (2) the use of broad-spectrum inhibitors of collagenolytic enzymes, including novel inhibitor functional groups grafted to methacrylate resins monomers to produce anti-MMP adhesives; (3) the use of cross-linking agents for silencing the activities of MMP and cathepsins that irreversibly alter the 3-D structures of their catalytic/allosteric domains; (4) ethanol wet-bonding with hydrophobic resins to completely replace water from the extrafibrillar and intrafibrillar collagen compartments and immobilize the collagenolytic enzymes; and (5) biomimetic remineralization of the water-filled collagen matrix using analogs of matrix proteins to progressively replace water with intrafibrillar and extrafibrillar apatites to exclude exogenous collagenolytic enzymes and fossilize endogenous collagenolytic enzymes. A combination of several of these strategies should result in overcoming the critical barriers to progress currently encountered in dentin bonding.

Cysteine cathepsins in human carious dentin.

Matrix metalloproteinases (MMPs) are important in dentinal caries, and analysis of recent data demonstrates the presence of other collagen-degrading enzymes, cysteine cathepsins, in human dentin. This study aimed to examine the presence, source, and activity of cysteine cathepsins in human caries. Cathepsin B was detected with immunostaining. Saliva and dentin cysteine cathepsin and MMP activities on caries lesions were analyzed spectrofluorometrically. Immunostaining demonstrated stronger cathepsins B in carious than in healthy dentin. In carious dentin, cysteine cathepsin activity increased with increasing depth and age in chronic lesions, but decreased with age in active lesions. MMP activity decreased with age in both active and chronic lesions. Salivary MMP activities were higher in patients with active than chronic lesions and with increasing lesion depth, while cysteine cathepsin activities showed no differences. The results indicate that, along with MMPs, cysteine cathepsins are important, especially in active and deep caries.

Zinc reduces collagen degradation in demineralized human dentin explants.

OBJECTIVES: Dentin matrix metalloproteinases are implicated in the pathogenesis of caries and contribute to collagen degradation in resin-dentin interfaces. The objective was to determine if collagen degradation may be modulated by an excess of zinc or zinc chelators. METHODS: Mineralized and phosphoric acid demineralized human dentin specimens were tested. Chlorhexidine digluconate, doxycycline or ZnCl2 were added to the media. In half of the groups, active exogenous metalloproteinase-2 was incorporated into the solution. C-terminal telopeptide determinations (radioimmunoassay) were performed after 24 h, 1 and 3 weeks. RESULTS: Collagen degradation was prominent in demineralized dentin. Doxycycline fully blocked dentin proteolysis. Chlorhexidine digluconate reduced the degradation at the 24-h period. Zinc in excess strongly inhibits hydrolysis of collagen and its effect was maintained for 3 weeks. CONCLUSIONS: Zinc in excess reduces MMP-mediated collagen degradation. The hypothesis that binding of zinc to collagen results in protection of sensitive cleavage sites of metalloproteinases requires further validation.

Biomimetic analogs for collagen biomineralization.

Inability of chemical phosphorylation of sodium trimetaphosphate to induce intrafibrillar mineralization of type I collagen may be due to the failure to incorporate a biomimetic analog to stabilize amorphous calcium phosphates (ACP) as nanoprecursors. This study investigated adsorption/desorption characteristics of hydrolyzed and pH-adjusted sodium trimetaphosphate (HPA-Na(3)P(3)O(9)) to collagen. Based on those results, a 5-minute treatment time with 2.8 wt% HPA-Na(3)P(3)O(9) was used in a single-layer reconstituted collagen model to confirm that both the ACP-stabilization analog and matrix phosphoprotein analog must be present for intrafibrillar mineralization. The results of that model were further validated by complete remineralization of phosphoric-acid-etched dentin treated with the matrix phosphoprotein analog and lined with a remineralizing lining composite, and with the ACP-stabilization analog supplied in simulated body fluid. An understanding of the basic processes involved in intrafibrillar mineralization of reconstituted collagen fibrils facilitates the design of novel tissue engineering materials for hard tissue repair and regeneration.

The effect of ultrasonic removal of various root-end filling materials.

AIM: To compare residual root-end filling material in apical root-end cavities following their removal with ultrasonic retrotips. METHODOLOGY: Thirty single-rooted teeth were filled with Thermafil and AH Plus sealer. Root-ends were resected at 90 degrees, 3 mm from the apex. Root-end cavities were prepared with diamond burs and ultrasonic retrotips and filled with one of three filling materials: group I: Retro-TC (calcium silicate-based cement), group II: IRM (Dentsply, Germany), group III: Vitrebond (3M ESPE, USA). After 30 days of storage, ultrasonic retrotips were used to remove materials from the root-end cavities. The ultrasonic application time was fixed at 60 s. Polyether impressions and replicas of the root-ends were made. Root apices and replicas were examined by one operator under a scanning electron microscope. Remnants of residual materials were evaluated using a four-level scoring system; fractures, smear layer and exposed dentinal tubules were also examined. RESULTS: Forty per cent of the specimens filled with Retro-TC revealed complete removal of the material with exposure of dentinal tubules, whilst 60% contained residual cement. Twenty per cent of specimens filled with IRM were completely devoid of material, whereas 80% had retained material. Ten per cent of specimens filled with Vitrebond retained a moderate amount of material whilst 90% had substantial retention of the material. Statistically significant differences were found (P < 0.05) amongst the three groups of materials. CONCLUSIONS: Retro-TC was successfully removed in 40% of cases using ultrasonics retrotips for 60 s, whereas IRM and Vitrebond specimens had evidence of retained material in 80% and 90% of all specimens respectively.

Clinical evaluation of polypropylene glycol-based caries detecting dyes for primary and permanent carious dentin.

OBJECTIVE: The aim of this study was to compare the clinical efficacy of new caries detecting dye Caries Check Blue (CCB) with Caries Check (CC) and Caries Detector (CD) using a laser fluorescence device (DIAGNOdent). METHOD: Primary and permanent teeth with dentin caries were stained with polypropylene glycol (MW=300) based new caries detecting dyes CCB, CC, or propylene glycol (MW=76) based CD. In the CCB and CC groups, stained dentin was completely removed. In the CD groups, pink-stained dentin was retained according to the manufacturers' instructions. Cavities before and after caries removal were measured with the DIAGNOdent. Data were analyzed using ANOVA and Fisher's PLSD multiple comparison test at alpha=0.05. Regression analyses were performed between DIAGNOdent readings and scores obtained from the clinical parameters. RESULTS: The DIAGNOdent readings after caries removal were: primary-CCB (13.2+/-10.4), primary-CC (14.3+/-16.7), primary-CD (9.0+/-5.2), permanent-CCB (22.7+/-13.4), permanent-CC (10.6+/-6.8) and permanent-CD (9.7+/-9.0). Significant differences were identified between the permanent-CCB and all other groups. Correlation coefficients between DIAGNOdent readings and clinical parameters were low. CONCLUSIONS: When dentin stained with Caries Check Blue or Caries Check was completely removed, the DIAGNOdent readings were higher than those recorded when palely-stained pink dentin was retained with the Caries Detector, with significant difference observed for the permanent-CCB group. Caries Check Blue may be used clinically to avoid excessive removal of caries-affected or sound dentin in permanent teeth but not in primary teeth.

NMR study on the adhesion efficacy of experimental phosphonic acid monomers.

Three experimental self-etching primers - consisting of N-methacryloyl-omega-aminoalkyl phosphonic acid (NMomegaP) with different methylene chain lengths and N-methacryloyl glycine (NMGly) - were formulated. The influence of methylene chain length in NMomegaP derivatives on the chemical nature of calcium salts was examined following their application to tooth components. Bond strengths of experimental self-etching primers created with these monomers to enamel and dentin were also investigated. Nuclear magnetic resonance spectroscopy showed that NMomegaPs decalcified tooth components with formation of calcium salts, which changed from calcium hydrogen phosphonate to calcium phosphonate with increase in methylene chain length within the NMomegaP structure. Disparity in calcium salt formation was related to increases in bond strength to enamel from 18 to 24 MPa. However, bond strength to dentin remained unchanged (22 MPa). The relative dependency of bond strength on monomer methylene chain length was probably attributable to the sites where these NMomegaP calcium salts had deposited on the bonding substrates.

Evaluation of a new caries detecting dye for primary and permanent carious dentin.

OBJECTIVE: This study evaluated the clinical efficacy of a new caries detecting dye using a laser fluorescence device (DIAGNOdent). METHOD: Primary and permanent teeth with dentin caries were stained with Caries Check (CC), containing 1% acid red in polypropylene glycol (MW=300) or Caries Detector (CD), containing 1% acid red in propylene glycol (MW=76). Primary-CC, primary-CD, permanent-CC and permanent-CD groups were prepared. In the CC groups, stained dentin was completely removed. In the CD groups, pink-stained dentin was retained according to the manufacturers' instructions. Cavities before and after caries removal were measured with the DIAGNOdent. Data were analyzed using ANOVA and Fisher's PLSD multiple comparison test at alpha=0.05. Regression analyses were performed between DIAGNOdent readings and scores obtained from the clinical parameters. RESULTS: For all groups, there were no significant differences in the DIAGNOdent readings before treatment. The DIAGNOdent readings after caries removal were: primary-CC (16.0+/-17.6), primary-CD (9.6+/-5.2), permanent-CC (11.0+/-7.0) and permanent-CD (7.1+/-3.8). Significant differences were identified between the permanent-CC and primary-CD, and permanent-CC and permanent-CD subgroups but not for the primary subgroups. Correlation coefficients between DIAGNOdent readings and clinical parameters were low. CONCLUSIONS: When dentin stained with Caries Check was completely removed, the DIAGNOdent readings were higher than those recorded when palely-stained pink dentin was retained with the Caries Detector, with significant difference observed for the permanent teeth. Caries Check may be used clinically to avoid excessive removal of caries-affected or sound dentin in permanent teeth but not in primary teeth.