Dental pulp tissue exposed to mechanical trauma or cariogenic process results in root canal and/or periapical infections, and conventionally treated with root canal procedures. The more recent regenerative endodontic procedure intends to achieve effective root canal disinfection and adequate pulp–dentin tissue regeneration; however, numerous limitations are reported. Because tooth is composed of vital soft pulp enclosed by the mineralized hard tissue in a highly organized structure, complete pulp–dentin tissue regeneration has been challenging to achieve. In consideration of the limitations and unique dental anatomy, it is important to understand the healing and repair processes through inflammatory-proliferative-remodeling phase transformations of pulp–dentin tissue. Upon cause by infectious and mechanical stimuli, the innate defense mechanism is initiated by resident pulp cells including immune cells through chemical signaling. After the expansion of infection and damage to resident pulp–dentin cells, consequent chemical signaling induces pluripotent mesenchymal stem cells (MSCs) to migrate to the injury site to perform the tissue regeneration process. Additionally, innovative biomaterials are necessary to facilitate the immune response and pulp–dentin tissue regeneration roles of MSCs. This review highlights current approaches of pulp–dentin tissue healing process and suggests potential biomedical perspective of the pulp–dentin tissue regeneration.
1 January 2011 in Oral Surgery Oral Medicine Oral Pathology Oral Radiology and Endodontology
The purpose of this study was to investigate the combined effect of mechanical and chemical treatments on the shear bond strength (SBS) of metal orthodontic brackets on zirconia restoration. The zirconia specimens were randomly divided into 12 groups () according to three factors: AL (Al2O3) and CO (CoJet™) by sandblasting material; SIL (silane), ZPP (Zirconia Prime Plus), and SBU (Single Bond Universal) by primer; and N (not thermocycled) and T (thermocycled). The specimens were evaluated for shear bond strength, and the fractured surfaces were observed using a stereomicroscope. Scanning electron microscopy images were also obtained. CO-SBU combination had the highest bond strength after thermocycling (26.2 MPa). CO-SIL showed significantly higher SBS than AL-SIL (). CO-ZPP resulted in lower bond strength than AL-ZPP before thermocycling, but the SBS increased after thermocycling (). Modified Adhesive Remnant Index (ARI) scoring and SEM figures were consistent with the results of the surface treatments. In conclusion, CO-SBU, which combines the effect of increased surface area and chemical bonding with both 10-MDP and silane, showed the highest SBS. Sandblasting with either material improved the mechanical bonding by increasing the surface area, and all primers showed clinically acceptable increase of shear bond strength for orthodontic treatment.
Objective: Supernumerary teeth, a term describing a condition where patients have an abnormally large number of teeth, can be associated with non-syndromic or syndromic phenotypes. PDGFRs are cell surface tyrosine kinase receptors, and are involved in several aspects of tooth development. The purpose of this study was to identify causative genes of familial supernumerary teeth and the molecular pathogenesis of tooth number abnormalities through genetic analysis of a family that showed supernumerary premolars in two successive generations. Material and methods: We recruited a Korean family with supernumerary premolars and performed mutational analyses to identify the underlying molecular genetic aetiology. Results: Targeted exome sequencing identified a missense mutation in PDGFRB (c.C2053T, p.R685C). Sanger sequencing confirmed that three affected individuals in the patient’s family were heterozygous for the mutation. Conclusions: This is the first report of a Korean family that carries a PDGFRB mutation potentially responsible for supernumerary premolars. Our results demonstrate the power of next-generation sequencing in rapidly determining the genetic aetiology of numerical tooth abnormalities.