Can social adversity alter the epigenome, trigger oral disease, and affect future generations?

Abstract

The nature versus nurture debate has intrigued scientific circles for decades. Although extensive research has established a clear relationship between genetics and disease development, recent evidence has highlighted the insufficiency of attributing adverse health outcomes to genetic factors alone. In fact, it has been suggested that environmental influences, such as socioeconomic position (SEP), may play a much larger role in the development of disease than previously thought, with extensive research suggesting that low SEP is associated with adverse health conditions. In relation to oral health, a higher prevalence of caries (tooth decay) exists among those of low SEP. Although little is known about the biological mechanisms underlying this relationship, epigenetic modifications resulting from environmental influences have been suggested to play an important role. This review explores the intersection of health inequalities and epigenetics, the role of early-life social adversity and its long-term epigenetic impacts, and how those living within the lower hierarchies of the socioeconomic pyramid are indeed at higher risk of developing diseases, particularly in relation to oral health. A deeper understanding of these mechanisms could lead to the development of targeted interventions for individuals of low SEP to improve oral health or identify those who are at higher risk of developing oral disease.

Keywords: Allostatic load; Chromatin; DNA methylation; DNA methyltransferase inhibitors; Dental pulp; Epigenetic heredity; Epigenetics; Genetics; Health inequalities; Histone deacetylase inhibitors; Histone modification; Oral cancer; Oral disease; Periodontitis; Pulpitis; Social adversity; Stress.

Fig. 1

a Overview of chromatin organisation. Chromosomal DNA is tightly wrapped around histone proteins to form nucleosomes, which are further condensed into chromatin. Various modifications to the DNA and histones in this structure can stimulate or repress gene expression as required by the cell. b Histone acetylation. Acetyl groups can be added to or removed from histones to alter gene expression. This process is mediated by HATs and HDACs. c DNA methylation. Methyl groups are added to gene promoters in order to repress gene expression