Chinese researchers describe the advances in treatment options designed to alleviate the discomfort of orthodontic patients. Orthodontic pain is caused by tooth movement, leading to an immune response and local inflammation. Hu Long and colleagues at the West China Hospital of Stomatology in Chengdu review the current understanding of the etiology of orthodontic pain, and the strategies available to treat the suffering of patients. The cellular products of tissue compression and local inflammation act directly on nerve endings to produce painful sensations. Clinical management of this pain can include medication, laser therapy, cognitive approaches (to alleviate the psychological stress), and, potentially, gene therapy. The authors concede that there is more to understand regarding orthodontic pain; however, the techniques described present promising avenues of exploration for effective therapy.

Dental cements containing ammonium-based groups may offer improved material and antibacterial properties for restorative dentistry. Polymers carrying electrically charged chemical groups are known as ionomers and are widely used as dental cements. Unfortunately, secondary decay and fracture cause half of all repairs made using these cements to fail within 10 years. Lei Cheng of Sichuan University, China, and co-workers investigated the effect of adding the ammonium-based compound dimethylaminododecyl methacrylate (DMADDM) to ionomer cements. They identified levels of DMADDM that reduced bacterial microfilm formation and also improved the material properties of the cements. The benefits included better release of protective fluoride ions from the ionomers, good flexibility combined with strength and improved surface texture. Cements with added DMADDM could therefore help avoid secondary decay and fracture after primary decay has been repaired.

Scientists in China have investigated a possible role for the enzyme SIRT-6 in age-related osteoporosis. Xuedong Zhou and co-workers at Sichuan University sought to clarify the mechanisms of senile osteoporosis, which affects women aged at least 65 years and men aged 70 or more. The mechanisms of the condition remain unclear, but previous research suggests a role for the SIRT-6 enzyme, which may regulate a number of genes involved in maintaining bone structure. Zhou’s team created mice in which the gene that codes for the SIRT-6 enzyme had been shut down. They observed significant effects on mouse bone and cartilage, confirming that SIRT-6 is an important regulator of bone metabolism. The researchers now hope to uncover more evidence for the proposed role for SIRT-6 in senile osteoporosis.

A gene implicated in human evolution seems to have helped make our tooth enamel thinner. Scientists previously showed, using statistical analyses, that a variant of the tooth enamel development gene ENAM was favored by natural selection. Frank Roberts from the University of Washington, Seattle, USA, and colleagues compared tooth characteristics with ENAM gene differences in African-Americans, in whom the favored variant and the original variant occur in roughly equal proportions. Controlling for age, sex, tooth number and crown length, the researchers found that changes in the ENAM gene affected the thickness of the tooth enamel. Specifically, the variant that conferred an advantage in our species’ evolutionary past produced thinner dental enamel. According to the authors, this is the first direct evidence linking a gene with a known effect on tooth structure to adaptive evolution.

Loss of the Fam20A gene causes defects in tooth enamel, excessive growth of the gums, and delayed tooth eruption in mice. Mutations in FAM20A have been linked to many of these same dental problems in humans, but the molecular link between the gene and disease was unknown. A team led by Chun-Lin Qin of Texas A&M University Baylor College of Dentistry in Dallas, USA, and Li Chen of the First Affiliated Hospital of Harbin Medical University China generated mouse models to track the expression of Fam20A in dental development and to test the effects of inactivating the gene. They found that cells that deposit tooth enamel began to express the gene in the mandibular first molars within a day of birth and that loss of Fam20A causes dental abnormalities consistent with those seen in humans.

A protein that promotes cell proliferation and differentiation may play a key role in dentin regeneration and repair. Human dental pulp cells (hDPCs) are multipotent stem cells found in the soft tissue inside teeth; they differentiate into other cell types to generate new dentin following injury or infection. Qiong Xu at Sun Yat-sen University in Guangzhou, China, and co-workers investigated a recently discovered protein called TET1 to determine its role in hDPCs during dentin repair. TET1 is known to be expressed in hDPCs, and has been shown to regulate differentiation in various other cell types. The team disabled the TET1 gene, which resulted in reduced expression of TET1 in hDPCs. The loss of TET1 appeared to decrease the hDPCs’ growth rate and prevented differentiation by reducing the expression of key genes and limiting mineralization.

A potential link has been established between bone response and metal corrosion near dental implants. Platform switching, in which smaller diameter restorative components, or abutments, are positioned on large implant platforms, minimizes loss in the bone that supports the tooth—a requirement for successful implantation. However, mechanisms governing this positive peri-implant bone response remain unclear. Haralampos Petridis and coworkers from University College London, UK, investigated the role of corrosion by-products near implants by evaluating metal ion release from platform-switched and matched (matching abutment and implant platform diameters) systems immersed in lactic acid. Active corrosion mainly occurred on the outer edges of the implant–abutment interface for all systems, causing metal ion discharge at their vicinity. Platform-matched systems produced the highest amounts of metal ions, suggesting that platform switching limits bone loss by reducing this discharge.

Analysis of dental casts indicates patients with painful jaw symptoms exhibit significant displacement of the lower jaw bone at the joint. Misalignment of teeth when the jaws are closed is called dental arch displacement (DAD), and can cause headaches and jaw pain. The 3D nature of DAD, particularly the resulting displacement of bone at the jaw joint, has not been fully explored. Frank Cordray at Ohio State University College of Dentistry, USA, investigated DAD using 1192 articulated dental casts taken from patients with and without symptoms. Cordray took casts from each patient when they were relaxed, then measured the 3D displacement that occurred when he manipulated each cast until there was maximum contact between teeth. In symptomatic patients, Cordray found significant downwards and sideways displacement of the lower jaw bone, alongside increased overall DAD displacement.