Use of electronic nicotine delivery systems (ENDS), such as electronic cigarettes (e-cigs), is increasing across the US population and is particularly troubling due to their adoption by adolescents, teens, and young adults. The industry’s marketing approach for these instruments of addiction...

Periodontitis, which is a chronic infection and disease of the periodontium, is a significant global health burden and is linked to other chronic health conditions such as diabetes and cardiovascular diseases. Dietary polyphenols present in a wide variety of plant-based foods, herbs, and botanicals have been shown to exert antimicrobial, anti-inflammatory, and reduced osteoclast and alveolar bone loss activities in animal models of periodontitis. Polyphenol-containing beverages and foods especially green tea and its active catechin epigallocatechin-3-gallate, cranberries, pomegranates, and fruit and vegetable extracts have reported bacteriostatic/bactericidal activity against microbial species such as P. gingivalis and shown total bacterial burden in clinical studies. These polyphenols also exhibit anti-inflammatory and antioxidant effects, which have the potential to impact various biological mechanisms for reducing the initiation and progression of periodontitis. The main objective of this mini-review is to focus on the mechanisms of action of dietary polyphenols in improving the pathophysiology underlying chronic inflammatory diseases like periodontitis based on pre-clinical and clinical models.

Summary: Hypoxia (i.e. oxygen deprivation) activates the hypoxia‐signalling pathway, primarily via hypoxia‐inducible transcription factors (HIF) for numerous target genes, which mediate angiogenesis, metabolism and coagulation, among other processes to try to replenish tissues with blood and oxygen. Hypoxia signalling dysregulation also commonly occurs during chronic inflammation. We sampled gingival tissues from rhesus monkeys (Macaca mulatta; 3–25 years old) and total RNA was isolated for microarray analysis. HIF1A, HIF1B and HIF2A were significantly different in healthy aged tissues, and both HIF1A and HIF3A were positively correlated with aging. Beyond these transcription factor alterations, analysis of patterns of gene expression involved in hypoxic changes in tissues showed specific increases in metabolic pathway hypoxia‐inducible genes, whereas angiogenesis pathway gene changes were more variable in healthy aging tissues across the animals. With periodontitis, aging tissues showed decreases in metabolic gene expression related to carbohydrate/lipid utilization (GBE1, PGAP1, TPI1), energy metabolism and cell cycle regulation (IER3, CCNG2, PER1), with up‐regulation of transcription genes and cellular proliferation genes (FOS, EGR1, MET, JMJD6) that are hypoxia‐inducible. The potential clinical implications of these results are related to the epidemiological findings of increased susceptibility and expression of periodontitis with aging. More specifically the findings describe that hypoxic stress may exist in aging gingival tissues before documentation of clinical changes of periodontitis and, so, may provide an explanatory molecular risk factor for an elevated capacity of the tissues to express destructive processes in response to changes in the microbial biofilms characteristic of a more pathogenic microbial challenge.

Periodontal disease damages tissues as a result of dysregulated host responses against the chronic bacterial biofilm insult and approximately 50% of US adults >30 years old exhibit periodontitis. The association of five blood nutrients and periodontitis were evaluated due to our previous findings regarding a potential protective effect for these nutrients in periodontal disease derived from the US population sampled as part of the National Health and Nutrition Examination Survey (1999–2004). Data from over 15,000 subjects was analyzed for blood levels of cis-β-carotene, β-cryptoxanthin, folate, vitamin D, and vitamin E, linked with analysis of the presence and severity of periodontitis. Moderate/severe disease patients had lower cis-β-carotene levels across all racial/ethnic groups and these decreased levels in moderate/severe periodontitis were exacerbated with age. β-cryptoxanthin demonstrated lower levels in severe disease patients across the entire age range in all racial/ethnic groups. Folate differences were evident across the various age groups with consistently lower levels in periodontitis patients >30 years and most pronounced in females. Lower levels of vitamin D were consistently noted across the entire age range of patients with a greater difference seen in females with periodontitis. Finally, an analytical approach to identify interactions among these nutrients related to age and periodontitis showed interactions of vitamin D in females, and folate with race in the population. These findings suggest that improving specific nutrient intake leading to elevated blood levels of a combination of these protective factors may provide a novel strategy to affect the significant increase in periodontitis that occurs with aging.