A vertical root fracture (VRF) is a complex complication that usually leads to tooth extraction. The aim of this article is to review the prevalence, demography, distribution, diagnostic methods, etiology and predisposing factors, clinical features, radiographic characteristics and treatment strategies of VRFs in non-endodontically treated teeth (VRFNETT) and endodontically treated teeth (VRFETT). Search terms for each subject related to VRFNETT and VRFETT were entered into MEDLINE, PubMed and Google Scholar. Systematic reviews, retrospective cohort studies, demographic research, clinical studies, case reports and case series were reviewed. Most of the VRFs were found in patients older than 40 years old. Older populations were discovered in the non-endodontically treated VRF group when compared to the endodontically treated VRF group. Male patients were found at a greater prevalence than females in the non-endodontically treated VRF group. The initial occurrence of a VRF may accompany radiolucent lines within the root canal, unusual space between the canal wall and intracanal material, a widening of the PDL space along the periradicular surfaces, angular bony destruction, step-like bone defects, V-shaped diffuse bone defects, or root resorptions corresponding to the fracture line before the clear separation of the fractured fragment. The indicative clinical and radiographic signs of VRF included a coronally positioned sinus tract, deep-narrow periodontal defects, the displacement of a fractured fragment, periradicular radiolucent halos and the widening of the root canal space. Interestingly, VRFNETT are more often observed in the Chinese population. Some patients with multiple VRFs were observed, suggesting possible predisposing factors in genetics and tooth development. The management of a VRF usually involves a multidisciplinary approach. The common distribution and features of VRFNETT and VRFETT were elucidated to facilitate recognition and diagnosis. Besides extraction, variable therapeutic schemes, such as the repair of the VRF, root amputation and others reported in earlier literature, are available. A long-term prognosis study of the various therapeutic strategies is needed.

Betel quid (BQ) chewing increased the risk of oral cancer and oral submucous fibrosis (OSMF), an oral premalignant disorder (OPMD) with malignant transformation potential. BQ components such as areca nut (AN), trauma by coarse AN fiber, catechin, copper, alkaloids, stimulated reactive oxygen species (ROS), inflammation and cytotoxicity are suggested to be the contributing factors. They may induce tissue inflammation, proliferation of fibroblasts and collagen deposition, myofibroblast differentiation and contraction, collagen cross-links and inhibit collagen phagocytosis, finally leading to the development of OSMF and oral cancer. These events are mediated by BQ components-induced changes of extracellular matrix (ECM) turnover via regulation of TGF-β1, plasminogen activator inhibitor-1 (PAI-1), cystatin, lysyl oxidase (LOX) and tissue inhibitors of metalloproteinases (TIMPs) and metalloproteinases (MMPs). Genetic susceptibility is also involved in these disease processes. Further understanding the molecular mechanisms of BQ-induced OSMF and oral cancer can be helpful for future disease prevention and treatment.

After tooth extraction, alveolar ridge loss due to resorption is almost inevitable. Most of this bone loss occurs during the first six months after the extraction procedure. Many studies have indicated that applying socket-filling biomaterials after extraction can effectively reduce the resorption rate of the alveolar ridge. The purpose of this study was to investigate the clinical efficacy of the application of a hydroxyapatite/β-tricalcium plus collagen (HA/β-TCP + collagen) dental bone graft in dental sockets immediately after tooth extraction, so as to prevent socket resorption. The study was conducted on 57 extraction sockets located in the mandible and maxilla posterior regions in 51 patients. HA/β-TCP + collagen was inserted into all of the dental sockets immediately after extraction, and was covered with a flap. Follow-up was performed for three months after extraction, using radiographs and stents for the vertical and horizontal alveolar ridge measurements. A minimal alveolar bone width reduction of 1.03 ± 2.43 mm (p < 0.05) was observed. The height reduction showed a slight decrease to 0.62 ± 1.46 mm (p < 0.05). Radiographically, the bone height was maintained after three months, indicating a good HA/β-TCP + collagen graft performance in preserving alveolar bone. In conclusion, the HA/β-TCP + collagen graft demonstrated adequate safety and efficacy in dental socket preservation following tooth extraction.

The biocharacteristics of xenogeneic grafts make them a possible substitute for autogenous bone grafts in dental bone graft procedures. This study aimed to develop a novel porcine graft with collagen capable of generating new bone in bone defects via osteoconduction over 8 weeks of healing and to compare it with a porcine graft. The porcine collagen graft was made to undergo a cell viability test (MTT) and alkaline phosphatase assay (ALP). The surgical procedure was performed in 20 male adult New Zealand white rabbits. Four calvarial critical-size defects of 6 mm in diameter were prepared in each rabbit. The upper left defect was filled with a porcine graft of 500–1000 μm, the upper right with a porcine collagen graft, the lower left with hydroxyapatite/beta-tricalcium phosphate and the lower right served as the control without any filling material. The rabbits were divided and sacrificed at 2, 4, 6 and 8 weeks after surgery. Histological and micro-CT scan results showed that the performance of the porcine collagen graft is superior for regenerating new bone. Porcine collagen graft showed cell viability and osteoblast-like cell differentiation in vitro. The results indicate that porcine collagen graft is a potential bone substitute for clinical application.

Butyric acid as a histone deacetylase (HDAC) inhibitor is produced by a number of periodontal and root canal microorganisms (such as Porphyromonas, Fusobacterium, etc.). Butyric acid may affect the biological activities of periodontal/periapical cells such as osteoblasts, periodontal ligament cells, etc., and thus affect periodontal/periapical tissue destruction and healing. The purposes of this study were to study the toxic effects of butyrate on the matrix and mineralization marker expression in MG-63 osteoblasts. Cell viability was determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay. Cellular apoptosis and necrosis were analyzed by propidium iodide/annexin V flow cytometry. The protein and mRNA expression of osteoprotegerin (OPG) and receptor activator of nuclear factor kappa-B ligand (RANKL) were analyzed by Western blotting and reverse transcriptase-polymerase chain reaction (RT-PCR). OPG, soluble RANKL (sRANKL), 8-isoprostane, pro-collagen I, matrix metalloproteinase-2 (MMP-2), osteonectin (SPARC), osteocalcin and osteopontin (OPN) secretion into culture medium were measured by enzyme-linked immunosorbant assay. Alkaline phosphatase (ALP) activity was checked by ALP staining. Histone H3 acetylation levels were evaluated by immunofluorescent staining (IF) and Western blot. We found that butyrate activated the histone H3 acetylation of MG-63 cells. Exposure of MG-63 cells to butyrate partly decreased cell viability with no marked increase in apoptosis and necrosis. Twenty-four hours of exposure to butyrate stimulated RANKL protein expression, whereas it inhibited OPG protein expression. Butyrate also inhibited the secretion of OPG in MG-63 cells, whereas the sRANKL level was below the detection limit. However, 3 days of exposure to butyrate (1 to 8 mM) or other HDAC inhibitors such as phenylbutyrate, valproic acid and trichostatin stimulated OPG secretion. Butyrate stimulated 8-isoprostane, MMP-2 and OPN secretion, but not procollagen I, or osteocalcin in MG-63 cells. Exposure to butyrate (2–4 mM) for 3 days markedly stimulated osteonectin secretion and ALP activity. In conclusion, higher concentrations of butyric acid generated by periodontal and root canal microorganisms may potentially induce bone destruction and impair bone repair by the alteration of OPG/RANKL expression/secretion, 8-isoprostane, MMP-2 and OPN secretion, and affect cell viability. However, lower concentrations of butyrate (1–4 mM) may stimulate ALP, osteonectin and OPG. These effects are possibly related to increased histone acetylation. These events are important in the pathogenesis and repair of periodontal and periapical destruction.

Antimicrobials are important adjuncts in the treatment of caries and periodontitis. However, increased bacterial resistance and hypersensitivity reactions to commonly used antimicrobials have led to an increasing demand for safe and natural substances. The objective of this study was to investigate the antibacterial effects of ε-polylysine against oral pathogens Streptococcus mutans and Porphyromonas gingivalis. Broth dilution assay, scanning electron microscopy (SEM) and confocal laser scanning microscopy (CLSM) analyses were performed to explore the antibacterial effect of ε-polylysine against S. mutans strain ATCC25175 and P. gingivalis strain ATCC332277. For the test solution, ε-polylysine was added to the bacterial suspension to prepare 0.125%, 0.25%, 0.5% and 1% ε-polylysine solutions diluted in broth medium. All four concentrations demonstrated complete inhibition of S. mutans and significantly reduced viable cell counts of P. gingivalis after 24 h. From starting inoculum of 9.15 log CFU/mL, P. gingivalis cell counts reduced to 4.01 log CFU/mL in the 0.125% ε-polylysine treatment group. SEM, CLSM, and the LIVE/DEAD bacterial assay of ε-polylysine application on P. gingivalis biofilm-dentin specimens revealed bacterial cell membrane disruption and irregular cell morphologies. The results indicated satisfactory antibacterial efficacy of ε-polylysine against P. gingivalis and S. mutans in liquid medium and as an application on biofilm-dentin specimens.