The results suggest that EMD has a positive effect on the composition of bacterial species in the post-surgical periodontal wound, by selectively restricting growth of periopathogens that could hamper the wound healing and reduce the outcome of regenerative procedures.

This study investigated the antibacterial effects against Streptococcus mutans of a fine-hybrid resin composite (FH-RC; Tetric ceram), an ion-releasing resin composite (Ariston pHc), a self-curing glass ionomer cement (SC-GIC; Ketac-Molar), a resin-modified GIC (RM-GIC; Photac-Fil), and a zinc oxide eugenol cement (ZOE; IRM). In a novel assay, bacterial suspensions were placed into narrow 20-µl conical cavities within the materials. After 0, 4, 8, 24, 48 h and 1 week of incubation, the suspensions were removed from the restoratives and the numbers of viable bacteria were determined. After incubation periods of 8 h or more, all restorative materials except the FH-RC showed significant growth inhibition when compared with controls. The strongest antibacterial activity was observed with ZOE. The inhibitory effect of Ariston pHc was similar to that of the SC-GIC and the RM-GIC. In the second assay, growth inhibition was evaluated in liquid cultures by incubating eluates of the materials with suspensions of S. mutans. Bacterial growth was determined up to 6 h by measuring absorption at 600 nm. The most marked inhibitory effect was again observed with ZOE. The SC-GIC caused a significant inhibition at all time intervals but the FH-RC, the RM-GIC and Ariston pHc exhibited no significant antibacterial effects. It is recommended to employ more than one method for assessing the antibacterial potential of restorative materials. Long-term clinical trials are necessary to determine whether the antimicrobial effects of dental materials are able to reduce the risk of secondary caries formation.

Background: Chronic inflammation from any source is associated with increased cardiovascular risk. Periodontitis is a possible trigger of chronic inflammation. We investigated the possible association between periodontitis and coronary heart disease (CHD), focusing on microbiological aspects.Methods: A total of 789 subjects (263 patients with angiographically confirmed, stable CHD and 526 populationbased, age-and sex-matched controls without a history of CHD) were included in the Coronary Event and Periodontal Disease (CORODONT) study. Subgingival biofilm samples were analyzed for periodontal pathogens Actinobacillus actinomycetemcomitans, Tannerella forsythensis, Porphyromonas gingivalis, Prevotella intermedia, and Treponema denticola using DNA-DNA hybridization. The need for periodontal treatment in each subject was assessed using the Community Periodontal Index of Treatment Needs (CPITN). The main outcome measures included total periodontal pathogen burden, number of the vari-ous periodontal pathogens in the subgingival biofilm, and periodontal treatment needs (according to the CPITN).Results: In multivariable analyses, we found a statistically significant association between the periodontal pathogen burden (log 10 of the sum of all pathogens) (odds ratio [OR], 1.92; 95% confidence interval [CI], 1.34-2.74; PϽ.001) or the number of A actinomycetemcomitans in periodontal pockets (log 10 ) (OR, 2.70; 95% CI, 1.79-4.07; PϽ.001) and the presence of CHD. In addition, a statistically significant association between an increase in mean CPITN score by 1 and the presence of CHD (OR, 1.67; 95% CI, 1.08-2.58; P =.02) was observed.Conclusions: Our findings suggest an association between periodontitis and presence of CHD. Periodontal pathogen burden, and particularly infection with A actinomycetemcomitans, may be of special importance.

Gutta-percha points containing calcium hydroxide, zinc oxide (ZnO), a mixture of ZnO and chlorhexidine (ZnO/CHX), iodine-polyvinylpyrrolidone (ZnO/J-PVP), or a mixture of CHX and J-PVP and ZnO (ZnO/CHX/J-PVP) were tested for their ability to inhibit growth of pure cultures of bacterial species commonly involved in endodontic infections (Peptostreptococcus micros, Streptococcus intermedius, Enterococcus faecalis, and Porphyromonas gingivalis). To quantitate growth inhibition, an in vitro assay was established that controlled for important parameters of root canal infection. Approximately 10(7) bacteria per assay were suspended in diluted human serum and co-incubated with the gutta-percha points in an anaerobic atmosphere for up to 2 wk. Aliquots used for determination of colony counts were taken on days 0, 1, 2, 4, 7, and 14 of incubation. As judged by colony-forming unit reduction kinetics and final counts, calcium hydroxide had better growth inhibitory activity than ZnO/CHX, ZnO/J-PVP, and ZnO alone for all bacteria tested except Peptostreptococcus micros. The combination of CHX and J-PVP with ZnO did not render results different from those of ZnO/CHX or ZnO/J-PVP. The results of this study support the introduction of standardized assays for testing antibacterial properties of root canal medications under conditions that more closely resemble those encountered in endodontal infections.

According to recent studies, amelin (ameloblastin, sheathlin) is expressed in young odontoblasts at the initiation of dentin formation during odontogenesis. The purpose of the present investigation was to study whether amelin is also expressed at the onset of traumainduced reparative dentin formation. The mandibular developing first molars of 5-day-old rats were surgically taken out, and their pulp tissue briefly separated from the inner dentin surface and immediately repositioned. Then the teeth were re-implanted in their alveoli. At 0, 2, 4, 6, 8, 12 or 14 days after surgery, the animals were sacrificed and the experimental teeth evaluated by histology and immunohistochemistry for amelin. At 2, 4, 6 and 8 days after surgery, the detached and traumatized odontoblasts in the experimental teeth exhibited increasing signs of degeneration and loss of intracellular structures. At days 6 and 8 after surgery, immunohistochemistry revealed a strong staining for amelin in the traumatized odontoblastic layer. Twelve and 14 days after replantation, only necrotic cell remnants of the traumatized odontoblasts were discernible. At this stage, no amelin could be detected by immunostaining. A wide zone of an unorganized mineralized tissue surrounded the odontoblastic cell remnants. On the pulpal side of the unorganized tissue, a new, highly organized tubular reparative dentin layer was observed, bordered by columnar odontoblast-like cells abutting on newly formed predentin.The results indicate that the initiation of trauma-induced reparative dentin formation mimics that of primary dentin formation and that amelin seems to be involved in both processes, possibly as a signaling molecule.