Periodontitis and diabetes mellitus co-morbidity: A molecular dialogue

Periodontal diseases comprise a wide range of inflammatory conditions that affect the supporting structures of the teeth (the gingiva, bone and periodontal ligament), which could lead to tooth loss and contribute to systemic inflammation. Chronic periodontitis predominantly affects adults, but aggressive periodontitis may occasionally occur in children. Periodontal disease initiation and propagation is through a dysbiosis of the commensal oral microbiota (dental plaque), which then interacts with the immune defences of the host, leading to inflammation and disease. This pathophysiological situation persists through bouts of activity and quiescence, until the affected tooth is extracted or the microbial biofilm is therapeutically removed and the inflammation subsides. The severity of the periodontal disease depends on environmental and host risk factors, both modifiable (for example, smoking) and non-modifiable (for example, genetic susceptibility). Prevention is achieved with daily self-performed oral hygiene and professional removal of the microbial biofilm on a quarterly or bi-annual basis. New treatment modalities that are actively explored include antimicrobial therapy, host modulation therapy, laser therapy and tissue engineering for tissue repair and regeneration.

Periodontitis is a dysbiotic inflammatory disease with an adverse impact on systemic health. Recent studies have provided insights into the emergence and persistence of dysbiotic oral microbial communities that can mediate inflammatory pathology at local as well as distant sites. This Review discusses the mechanisms of microbial immune subversion that tip the balance from homeostasis to disease in oral or extra-oral sites.

We aimed to consolidate all epidemiologic data about severe periodontitis (SP) and, subsequently, to generate internally consistent prevalence and incidence estimates for all countries, 20 age groups, and both sexes for 1990 and 2010. The systematic search of the literature yielded 6,394 unique citations. After screening titles and abstracts, we excluded 5,881 citations as clearly not relevant to this systematic review, leaving 513 for full-text review. A further 441 publications were excluded following the validity assessment. A total of 72 studies, including 291,170 individuals aged 15 yr or older in 37 countries, were included in the metaregression based on modeling resources of the Global Burden of Disease 2010 Study. SP was the sixth-most prevalent condition in the world. Between 1990 and 2010, the global age-standardized prevalence of SP was static at 11.2% (95% uncertainty interval: 10.4%-11.9% in 1990 and 10.5%-12.0% in 2010). The age-standardized incidence of SP in 2010 was 701 cases per 100,000 person-years (95% uncertainty interval: 599-823), a nonsignificant increase from the 1990 incidence of SP. Prevalence increased gradually with age, showing a steep increase between the third and fourth decades of life that was driven by a peak in incidence at around 38 yr of age. There were considerable variations in prevalence and incidence between regions and countries. Policy makers need to be aware of a predictable increasing burden of SP due to the growing world population associated with an increasing life expectancy and a significant decrease in the prevalence of total tooth loss throughout the world from 1990 to 2010.