Epithelial attachment via the basal lamina on the tooth surface provides an important structural defence mechanism against bacterial invasion in combating periodontal disease. However, when considering dental implants, strong epithelial attachment does not exist throughout the titanium-soft tissue interface, making soft tissues more susceptible to peri-implant disease. This study introduced a novel synthetic peptide (A10) to enhance epithelial attachment. A10 was identified from a bacterial peptide display library and synthesized. A10 and protease-activated receptor 4-activating peptide (PAR4-AP, positive control) were immobilized on commercially pure titanium. The peptide-treated titanium showed high epithelial cell migration ability during incubation in platelet-rich plasma. We confirmed the development of dense and expanded BL (stained by Ln5) with pericellular junctions (stained by ZO1) on the peptide-treated titanium surface. In an adhesion assay of epithelial cells on A10-treated titanium, PAR4-AP-treated titanium, bovine root and non-treated titanium, A10-treated titanium and PAR4-AP-treated titanium showed significantly stronger adhesion than non-treated titanium. PAR4-AP-treated titanium showed significantly higher inflammatory cytokine release than non-treated titanium. There was no significant difference in inflammatory cytokine release between A10-treated and non-treated titanium. These results indicated that A10 could induce the adhesion and migration of epithelial cells with low inflammatory cytokine release. This novel peptide has a potentially useful application that could improve clinical outcomes with titanium implants and abutments by reducing or preventing peri-implant disease.

Repeated applications of low-level laser therapy during and after orthodontic procedures could help reduce pain and discomfort. Many orthodontic patients experience pain in the hours and days following treatment, which impacts on treatment participation. Wenjing Chen at Nanjing Medical University and co-workers assessed whether low-level laser therapy (LLLT) can reduce pain and sensitivity in teeth and surrounding tissues. They divided 40 patients into two groups; one was given repeated LLLT in the hours and days following procedures, while the other group received a placebo course. They tested both groups for sensitivity to stimuli including heat and pressure, in the mouth and on the hands. LLLT significantly reduced pain in the mouth relative to the placebo group. No differences were found in tests on the hands, suggesting LLLT works as a targeted analgesia.

Streptococcus mutans triggers an early-stage immune response via a chain of events that leads to the activation of immune component, interleukin-1β. A group of academics from Korea’s Pusan National University, led by Jin Chung, tested the response of human immune cell cultures to infection with S. mutans—a common oral bacteria that can cause systemic disease if it enters the bloodstream. The group found that S. mutans infection leads to the activation of protein signaling complexes known as inflammasomes, which in turn activate an enzyme known as caspase-1. Caspase-1 then activates interleukin-1β, a pro-inflammatory molecule that forms part of a host’s defenses against pathogens. The team also identified that ATP release, ion depletion, and integrity of intracellular enzyme containers, also impacted inflammasome activation. This study offers insights into the immune response against S. mutans and may inform future investigations into systematic oral bacteria infections.

MicroRNAs (miRNAs) are critical regulators of the host immune and inflammatory response against bacterial pathogens. In the present review, we discuss target genes, target gene functions, the potential regulatory role of miRNAs in periodontal tissues, and the potential role of miRNAs as biomarkers and therapeutics. In periodontal disease, miRNAs exert control over all aspects of innate and adaptive immunity, including the functions of neutrophils, macrophages, dendritic cells and T and B cells. Previous human studies have highlighted some key miRNAs that are dysregulated in periodontitis patients. In the present study, we mapped the major miRNAs that were altered in our reproducible periodontitis mouse model relative to control animals. The miRNAs that were upregulated as a result of periodontal disease in both human and mouse studies included miR-15a, miR-29b, miR-125a, miR-146a, miR-148/148a and miR-223, whereas miR-92 was downregulated. The association of individual miRNAs with unique aspects of periodontal disease and their stability in gingival crevicular fluid underscores their potential as markers for periodontal disease progression or healthy restitution. Moreover, miRNA therapeutics hold great promise for the future of periodontal therapy because of their ability to modulate the immune response to infection when applied in conjunction with synthetic antagomirs and/or relatively straightforward delivery strategies.

Bone wound healing is a highly dynamic and precisely controlled process through which damaged bone undergoes repair and complete regeneration. External factors can alter this process, leading to delayed or failed bone wound healing. The findings of recent studies suggest that the use of selective serotonin reuptake inhibitors (SSRIs) can reduce bone mass, precipitate osteoporotic fractures and increase the rate of dental implant failure. With 10% of Americans prescribed antidepressants, the potential of SSRIs to impair bone healing may adversely affect millions of patients’ ability to heal after sustaining trauma. Here, we investigate the effect of the SSRI sertraline on bone healing through pre-treatment with (10 mg·kg^-1 sertraline in drinking water, n = 26) or without (control, n = 30) SSRI followed by the creation of a 5-mm calvarial defect. Animals were randomized into three surgical groups: (a) empty/sham, (b) implanted with a DermaMatrix scaffold soak-loaded with sterile PBS or (c) DermaMatrix soak-loaded with 542.5 ng BMP2. SSRI exposure continued until sacrifice in the exposed groups at 4 weeks after surgery. Sertraline exposure resulted in decreased bone healing with significant decreases in trabecular thickness, trabecular number and osteoclast dysfunction while significantly increasing mature collagen fiber formation. These findings indicate that sertraline exposure can impair bone wound healing through disruption of bone repair and regeneration while promoting or defaulting to scar formation within the defect site.

A mutation on a gene involved in healthy tooth development may cause both enamel and dentin disorders. The ameloblastin enamel protein, and its associated gene, AMBN, play vital roles in enamel formation and tooth remodelling. Mutations on AMBN can cause amelogenesis imperfecta (AI), a genetic and hereditory condition resulting in enamel defects and severe tooth decay. Now, Fu Xiong and Bu-Ling Wu at Southern Medical University in Guangzhou, China, and co-workers have identified an AMBN mutation found in both enamel and dentin defect disorders. The researchers analyzed extracted teeth from a Chinese patient with both AI and a severe dentin disorder, along with teeth from affected and non-affected members of the same family, and compared the results with a control group. They identified a rare mutation on AMBN common to all affected individuals.

A glucose-transporting protein is key to helping teeth respond to orthodontic implants, say researchers in China. Implants apply forces to teeth and the periodontal ligament (PDL) that holds them in place, causing bone to grow on one side and be absorbed into the body on the other. Yanheng Zhou and co-workers at Peking University in Beijing showed that GLUT1, a protein that transports glucose through cell membranes, was greatly upregulated in rat, mouse and human PDL cells subjected to mechanical force. They also injected some of the mice with a GLUT1 inhibitor and found that the treatment greatly decreased the distance moved by the teeth. This could be attributed to a decline in the activity of cells that break down bone tissue and a failure in signalling channels when GLUT1 is inhibited.

The “Biofilms, Microbiomes and Oral Diseases: Challenges and Future Perspectives” symposium jointly organized by Penn Dental Medicine and West China School of Stomatology was held on 30 September 2017 at Penn Wharton China Center (PWCC) in Beijing, China. The topics included the pathogenicity of oral biofilms, novel strategies for the control of biofilm-related diseases, oral microbiome and single-cell approaches, and the link between oral diseases and overall health. Researchers from a number of disciplines, representing institutions from China and Penn Dental Medicine, gathered to discuss advances in our understanding of biofilms, as well as future directions for the control of biofilm-related oral and systemic diseases.

During inflammation, increased transforming growth factor (TGF)-β2 inhibits bone formation in dental follicle stem cells (DFSCs). Hitherto, the relationship between inflammation and bone formation has been poorly understood. But a team headed by Byoung-Moo Seo of Seoul National University, Republic of Korea examined the different functions of two types of TGF-β (a protein that is a key regulator of bone formation): TGF-β1 and TGF-β2. By means of cell cultures and in vivo experiments in mice, the team conducted its investigation on DFSCs: stem cells (non-specialised cells) in the dental follicle, which surrounds a tooth before it erupts. The authors found that inflammation led to an increase in TGF-β2, and that increase inhibited bone formation. The results of the study have implications for the future therapeutic application of DFSCs in bone-loss diseases.