Our understanding of erosive tooth wear and its contributing factors has evolved considerably over the last decades. New terms have been continuously introduced, which frequently describe the same aspects of this condition, whereas other terms are being used inappropriately. This has led to unnecessary confusion and miscommunication between patients, professionals, and researchers. A group of 15 experts, selected by the European Organization for Caries Research (ORCA) and the Cariology Research Group of the International Association for Dental Research (IADR), participated in a 2-day workshop to define the most commonly used terms in erosive tooth wear. A modified Delphi method was utilized to reach consensus. At least 80% agreement was achieved for all terms discussed and their definitions related to clinical conditions and processes, basic concepts, diagnosis, risk, and prevention and management of erosive tooth wear. Use of the terms agreed on will provide a better understanding of erosive tooth wear and intends to enable improved communication on this topic.

The focus of this work is to highlight the most recent advances in the understanding of cleft lip and palate occurrence. Information regarding research on long-term outcomes, genes and their interactions with other genes, and gene-environment interactions is compiled to provide the reader with a critical and up-to-date overview on the current knowledge of the etiology of cleft lip and palate. Recent epidemiological evidence strongly suggests that individuals born with clefts have a shorter lifespan and may have a higher incidence of cancer and psychological disorders. IRF6 has been shown to be an important contributor to cleft lip and palate, but the functional variant leading to the defect has not yet been defined. Inactivation of MSX1 and genes in the FGF family has also been shown to lead to cleft lip and palate. In addition, missense mutations in several candidate genes may cause cleft lip and palate, but definitive evidence regarding the biological consequences of these mutations is yet to be unraveled. Maternal cigarette smoking increases the risk of a baby born with clefts, in particular when the mother carries the GSTT1-null variants. The latest approaches in cleft research include the analysis of several additional phenotypical features of the population, with the goal of increasing the statistical power of genetics studies.

Many studies have demonstrated that caries rates are higher in women than in men. This review attempts to provide an explanation for this trend by examining each factor which contributes to caries and how the factor differs in men and women. Evidence has been provided to demonstrate that caries risk factors for women include a different salivary composition and flow rate, hormonal fluctuations, dietary habits, genetic variations, and particular social roles among their family. Systemic diseases that have been found to be associated with caries have also been found to have an association with the female gender. An extended exposure to the oral cavity or a more cariogenic oral microflora has not been proven to contribute to higher caries in women. Further research in these areas could be done in the future to explain their contribution, or lack thereof, to a higher caries rate in women.

Individuals with clefts present considerably more dental anomalies than do individuals without clefts. We used dental development to subphenotype clefts with the goal of identifying cleft subgroups that could have specific genetic contributions. We examined 1000 individuals, 500 with clefts and 500 without. We used several clinical features, such as cleft completeness or incompleteness, laterality, and the presence of dental anomalies to assess each individual’s cleft status. We performed chi-square and Fisher’s exact tests to compare the frequencies of observed anomalies between individuals with and individuals without clefts, and among individuals with different cleft subphenotypes. Agenesis of the lateral incisor on the non-cleft side was the most remarkable observation, and may suggest that such cases could be considered incomplete forms of bilateral clefts of the lip.

The NIH Consensus Development Program released a statement in 2001 (http://consensus.nih.gov/2001/2001DentalCaries115html.htm) and listed six major clinical caries research directions. One of these directions was the need for genetic studies to identify genes and genetic markers of diagnostic, prognostic and therapeutic value. This last decade has seen a steep increase in studies investigating the presence of genetic factors influencing individual susceptibility to caries. This review revisits recent caries human genetic studies and provides a perspective for future studies in order to fulfil their promise of revolutionizing our understanding of and the standard of care for the most prevalent bacteria-mediated non-contagious disease in the world.