Periodontal innate immune mechanisms relevant to obesity

Obesity affects over 35% of the adult population of the USA, and obesity‐related illnesses have emerged as the leading cause of preventable death worldwide, according to the World Health Organization. Obesity's secondary morbidities include increased risk of cardiovascular disease, type II diabetes, and cancer, in addition to increased occurrence and severity of infections. Sedentary lifestyle and weight gain caused by consumption of a high‐fat diet contribute to the development of obesity, with individuals having a body mass index (BMI) score > 30 being considered obese. Genetic models of obesity (ob/ob mice, db/db mice, and fa/fa rats) have been insufficient to study human obesity because of the overall lack of genetic causes for obesity in human populations. To date, the diet‐induced obese (DIO) mouse model best serves research studies relevant to human health. Periodontal disease presents with a wide range of clinical variability and severity. Research in the past decade has shed substantial light on both the initiating infectious agents and host immunological responses in periodontal disease. Up to 46% of the general population harbors the microorganism(s) associated with periodontal disease, although many are able to limit the progression of periodontal disease or even clear the organism(s) if infected. In the last decade, several epidemiological studies have found an association between obesity and increased incidence of periodontal disease. This review focuses on exploring the immunological consequences of obesity that exacerbate effects of infection by pathogens, with focus on infection by the periodontal bacterium Porphyromonas gingivalis as a running example.