Influence of Different Enamel Substrates on Microtensile Bond Strength of Sealants After Cariogenic Challenge

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Purpose: To evaluate the microtensile bond strength (mu TBS) of resin sealer on enamel substrates after cariogenic challenge. Materials and Methods: Enamel blocks were obtained from human third molars and randomly divided into 6 groups (n = 10) according to enamel substrates (S: sound, CL: caries-like lesion, or CLTF: caries-like lesion + topical fluoride application) and sealant material (F: FluroShield, or H: Helioseal Clear Chroma). Sealants were placed on enamel surfaces, stored in 100% humidity (24 h, 37 degrees C), and longitudinally sectioned into hourglass shapes. According to the groups, pH cycling was applied and the mu TBS test was performed. The fracture patterns were assessed by SEM. Results: Regarding substrates, the highest mu TBS values in MPa were observed for CLTF enamel (26.0 +/- 7.6), followed by S (22.0 +/- 7.4) and CL (15,5 +/- 4.9). A significant interaction was found between material and pH cycling (p = 0.0395). F (23.9 +/- 7.6) showed higher mu TBS values than H (18.3 +/- 7.5) when submitted to pH cycling. The majority of samples presented mixed failure. Conclusions: Enamel substrate significantly affected mu TBS, with the highest values for remineralized caries-like enamel lesions. Furthermore, mu TBS values were dependent on both materials and pH cycling.132131137Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)FAPESP [05/60595-1

Regulation of Cementoblast Gene Expression by Inorganic Phosphate In Vitro

Examination of mutant and knockout phenotypes with altered phosphate/pyrophosphate distribution has demonstrated that cementum, the mineralized tissue that sheathes the tooth root, is very sensitive to local levels of phosphate and pyrophosphate. The aim of this study was to examine the potential regulation of cementoblast cell behavior by inorganic phosphate (P i ). Immortalized murine cementoblasts were treated with P i in vitro , and effects on gene expression (by quantitative real-time reverse-transcriptase polymerase chain reaction [RT-PCR]) and cell proliferation (by hemacytometer count) were observed. Dose-response (0.1–10 mM) and time-course (1–48 hours) assays were performed, as well as studies including the Na-P i uptake inhibitor phosphonoformic acid. Real-time RT-PCR indicated regulation by phosphate of several genes associated with differentiation/mineralization. A dose of 5 mM P i upregulated genes including the SIBLING family genes osteopontin ( Opn , >300% of control) and dentin matrix protein-1 ( Dmp-1 , >3,000% of control). Another SIBLING family member, bone sialoprotein ( Bsp ), was downregulated, as were osteocalcin ( Ocn ) and type I collagen ( Col1 ). Time-course experiments indicated that these genes responded within 6–24 hours. Time-course experiments also indicated rapid regulation (by 6 hours) of genes concerned with phosphate/pyrophosphate homeostasis, including the mouse progressive ankylosis gene ( Ank ), plasma cell membrane glycoprotein-1 ( Pc-1 ), tissue nonspecific alkaline phosphatase ( Tnap ), and the Pit1 Na-P i cotransporter. Phosphate effects on cementoblasts were further shown to be uptake-dependent and proliferation-independent. These data suggest regulation by phosphate of multiple genes in cementoblasts in vitro . During formation, phosphate and pyrophosphate may be important regulators of cementoblast functions including maturation and regulation of matrix mineralization.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/48015/1/223_2005_Article_184.pd

Central Role of Pyrophosphate in Acellular Cementum Formation

Background: Inorganic pyrophosphate (PPi) is a physiologic inhibitor of hydroxyapatite mineral precipitation involved in regulating mineralized tissue development and pathologic calcification. Local levels of PPi are controlled by antagonistic functions of factors that decrease PPi and promote mineralization (tissue-nonspecific alkaline phosphatase, Alpl/TNAP), and those that increase local PPi and restrict mineralization (progressive ankylosis protein, ANK; ectonucleotide pyrophosphatase phosphodiesterase-1, NPP1). The cementum enveloping the tooth root is essential for tooth function by providing attachment to the surrounding bone via the nonmineralized periodontal ligament. At present, the developmental regulation of cementum remains poorly understood, hampering efforts for regeneration. To elucidate the role of PPi in cementum formation, we analyzed root development in knock-out ((-/-)) mice featuring PPi dysregulation. Results: Excess PPi in the Alpl(-/-) mouse inhibited cementum formation, causing root detachment consistent with premature tooth loss in the human condition hypophosphatasia, though cementoblast phenotype was unperturbed. Deficient PPi in both Ank and Enpp1(-/-) mice significantly increased cementum apposition and overall thickness more than 12-fold vs. controls, while dentin and cellular cementum were unaltered. Though PPi regulators are widely expressed, cementoblasts selectively expressed greater ANK and NPP1 along the root surface, and dramatically increased ANK or NPP1 in models of reduced PPi output, in compensatory fashion. In vitro mechanistic studies confirmed that under low PPi mineralizing conditions, cementoblasts increased Ank (5-fold) and Enpp1 (20-fold), while increasing PPi inhibited mineralization and associated increases in Ank and Enpp1 mRNA. Conclusions: Results from these studies demonstrate a novel developmental regulation of acellular cementum, wherein cementoblasts tune cementogenesis by modulating local levels of PPi, directing and regulating mineral apposition. These findings underscore developmental differences in acellular versus cellular cementum, and suggest new approaches for cementum regeneration

Experimental Animal Models in Periodontology: A Review

In periodontal research, animal studies are complementary to in vitro experiments prior to testing new treatments. Animal models should make possible the validation of hypotheses and prove the safety and efficacy of new regenerating approaches using biomaterials, growth factors or stem cells. A review of the literature was carried out by using electronic databases (PubMed, ISI Web of Science). Numerous animal models in different species such as rats, hamsters, rabbits, ferrets, canines and primates have been used for modeling human periodontal diseases and treatments. However, both the anatomy and physiopathology of animals are different from those of humans, making difficult the evaluation of new therapies. Experimental models have been developed in order to reproduce major periodontal diseases (gingivitis, periodontitis), their pathogenesis and to investigate new surgical techniques. The aim of this review is to define the most pertinent animal models for periodontal research depending on the hypothesis and expected results

The Effect of Low-Intensity Laser Therapy on Bone Healing Around Titanium Implants: A Histometric Study in Rabbits

Purpose: This study aimed to histometrically evaluate the influence of low-intensity laser treatment on bone healing around titanium implants placed in rabbit tibiae. Materials and Methods: Each tibia of 12 adult rabbits received a 3.3 x 6-mm titanium implant. The implants placed in the right tibiae were irradiated with a gallium-aluminum-arsenide diode low-intensity laser every 48 hours for 14 days post-operatively, and the left tibiae were not irradiated. After 3 or 6 weeks, the animals were sacrificed (six animals per period), and nondecalcified sections were obtained and analyzed for bone-to-implant contact (BIC) and bone area within the implant threads. Data were subjected to statistical analysis using analysis of variance (ANOVA) and the Tukey test. Results: BIC was significantly increased it) the laser-treated group at both 3 weeks and 6 weeks. BIC did not increase significantly with time (3 weeks versus 6 weeks). Conversely, bone area within the threads was significantly increased with time (3 weeks versus 6 weeks), regardless of whether the laser was used. Considering bone area within the threads, no significant difference was found for treatment, eg, with or without laser. Conclusion: Low-intensity laser therapy did not affect the area of bone formed within the threads, but it may improve BIC in rabbit tibiae. INT J ORAL MAXILLOFAC IMPLANTS 2009;24:47-51241475

Effect of Aluminum Oxide-Blasted Implant Surface on the Bone Healing Around Implants in Rats Submitted to Continuous Administration of Selective Cyclooxygenase-2 Inhibitors

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Purpose: The continual use of selective cyclooxygenase-2 (COX-2) inhibitors may have a negative impact on bone repair around titanium implants. Because modified implant surfaces could be considered an important strategy to increase success rates in some conditions that interfere in bone healing, the aim of this study was to investigate whether an aluminum oxide (Al(2)O(3))-blasted implant surface could reduce the negative action promoted by the continuous administration of selective COX-2 inhibitors on bone healing around implants. Materials and Methods: Thirty Wistar rats received one titanium implant (machined or Al(2)O(3)-blasted surface) in each tibia and were randomly assigned to one of the following groups: saline (n = 14) or meloxicam (n = 16); each was administered daily for 60 days. Bone-to-implant contact (BIC), bone area (BA) within the limits of threads, and bone density (BD) in a zone lateral to the implant were examined in undecalcified sections. Results: The Al(2)O(3)-blasted surface resulted in significantly increased BIC in both groups, and meloxicam significantly reduced bone healing around implants (P < .05). For the machined surface, significant differences were observed for BIC (39.48 +/- 10.18; 25.23 +/- 9.29), BA (60.62 +/- 4.09; 42.94 +/- 8.12), and BD (56.31 +/- 3.64; 49.30 +/- 3.15) in the saline and meloxicam groups, respectively. For the Al(2)O(3)-blasted surface, data analysis also demonstrated significant differences for BIC (45.92 +/- 11.34; 33.30 +/- 7.56), BA (61.04 +/- 4.39; 44.89 +/- 7.11), and BD (58.77 +/- 2.93; 50.04 +/- 3.94) for the saline and meloxicam groups, respectively. Conclusions: The Al(2)O(3)-blasted surface may increase BIC, however, it does not reverse the negative effects promoted by a selective COX-2 inhibitor on bone healing around implants. Int J Oral Maxillofac Implants 2009; 24:226-233242226233Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)FAPESP [04/15825-6, 04/12430-(0)

Parathyroid hormone protects against periodontitis-associated bone loss

Parathyroid hormone (PTH) functions as a major mediator of bone remodeling and as an essential regulator of calcium homeostasis. In addition to the well-established catabolic effects (activation of bone resorption) of PTH, it is now recognized that intermittent PTH administration has anabolic effects (promotion of bone formation). The aim of this study was to investigate whether intermittent administration of PTH in rodents would block the alveolar bone loss observed in rats when a ligature model of periodontitis is used. Morphometric analysis showed that intermittent PTH administration (40 mug/kg) was able to protect the tooth site from periodontitis-induced bone resorption. In addition, there was a significant reduction in the number of inflammatory cells at the marginal gingival area in sections obtained from animals receiving PTH compared with control animals. These findings demonstrated that intermittent PTH administration was able to protect against periodontitis-associated bone loss in a rodent model.821079179