Oral microbial biofilms: an update.

Human oral cavity (mouth) hosts a complex microbiome consisting of bacteria, archaea, protozoa, fungi and viruses. These bacteria are responsible for two common diseases of the human mouth including periodontal (gum) and dental caries (tooth decay). Dental caries is caused by plaques, which are a community of microorganisms in biofilm format. Genetic and peripheral factors lead to variations in the oral microbiome. It has known that, in commensalism and coexistence between microorganisms and the host, homeostasis in the oral microbiome is preserved. Nonetheless, under some conditions, a parasitic relationship dominates the existing situation and the rise of cariogenic microorganisms results in dental caries. Utilizing advanced molecular biology techniques, new cariogenic microorganisms species have been discovered. The oral microbiome of each person is quite distinct. Consequently, commonly taken measures for disease prevention cannot be exactly the same for other individuals. The chance for developing tooth decay in individuals is dependent on factors such as immune system and oral microbiome which itself is affected by the environmental and genetic determinants. Early detection of dental caries, assessment of risk factors and designing personalized measure let dentists control the disease and obtain desired results. It is necessary for a dentist to consider dental caries as a result of a biological process to be targeted than treating the consequences of decay cavities. In this research, we critically review the literature and discuss the role of microbial biofilms in dental caries.

Axin2-expressing cells differentiate into reparative odontoblasts via autocrine Wnt/ß-catenin signaling in response to tooth damage.

In non-growing teeth, such as mouse and human molars, primary odontoblasts are long-lived post-mitotic cells that secrete dentine throughout the life of the tooth. New odontoblast-like cells are only produced in response to a damage or trauma. Little is known about the molecular events that initiate mesenchymal stem cells to proliferate and differentiate into odontoblast-like cells in response to dentine damage. The reparative and regenerative capacity of multiple mammalian tissues depends on the activation of Wnt/ß-catenin signaling pathway. In this study, we investigated the molecular role of Wnt/ß-catenin signaling pathway in reparative dentinogenesis using an in vivo mouse tooth damage model. We found that Axin2 is rapidly upregulated in response to tooth damage and that these Axin2-expressing cells differentiate into new odontoblast-like cells that secrete reparative dentine. In addition, the Axin2-expressing cells produce a source of Wnt that acts in an autocrine manner to modulate reparative dentinogenesis.

MicroRNAs: new insights into the pathogenesis of endodontic periapical disease.

INTRODUCTION: Apical periodontitis is an inflammatory disease of the periradicular tissues caused by the host's immune response to infection of the root canal system. MicroRNAs (miRNAs) have been shown to play an important role in the regulation of inflammation and the immune response; however, their role in the pathogenesis of endodontic periapical disease has not been explored. The purpose of this study was to examine the differential expression of miRNAs in diseased periapical tissues as compared with healthy controls. METHODS: We first compared miRNA profiles in diseased periapical tissues collected from patients undergoing endodontic surgery with those of healthy pulps by using microarray analyses. The target genes of the differentially expressed miRNAs were identified by using miRWalk and PubMed. Selected miRNAs linked to inflammation and the immune response were then confirmed in a separate cohort of diseased and healthy tissues by using quantitative reverse transcription-polymerase chain reaction. Healthy pulps and periodontal ligaments were used as controls. Data were normalized to the level of SNORD 44, which served as an endogenous control. RESULTS: Of the 381 miRNAs identified by using microarray, 24 miRNAs were down-regulated in diseased periapical tissues compared with controls (n = 13) (P < .003). The down-regulation of 7 miRNAs was confirmed from 9 selected miRNAs by using quantitative real-time polymerase chain reaction (n = 19) (P < .05). Target genes of these miRNAs include key mediators in the immune and inflammatory response such as interleukin-6, matrix metalloproteinase-9, and transforming growth factor-ß. CONCLUSIONS: These findings offer new insight into the pathogenesis of endodontic disease and have the potential to impact the development of new methods for prevention, diagnosis, and treatment of apical periodontitis.

Extreme oral manifestations in a Marfan-type syndrome.

A 12-year-old girl with an otherwise typical Marfan syndrome (Ghent criteria fulfilled) presented with highly unusual oral manifestations consisting of supernumerary teeth and severe dental crowding. Pathological examination of the supernumerary teeth revealed an elevated number of pulpoliths. No mutation in the FBN1, TGFBR1 and TGFBR2 genes was identified despite exhaustive screening, suggesting that another gene defect could explain this association of marfanoid features with dental abnormalities.