Periodontal diseases and dental caries are the most common diseases of humans and the main cause of tooth loss. Both diseases can lead to nutritional compromise and negative impacts upon self‐esteem and quality of life. As complex chronic diseases, they share common risk factors, such as a requirement for a pathogenic plaque biofilm, yet they exhibit distinct pathophysiologies. Multiple exposures contribute to their causal pathways, and susceptibility involves risk factors that are inherited (e.g. genetic variants), and those that are acquired (e.g. socio‐economic factors, biofilm load or composition, smoking, carbohydrate intake). Identification of these factors is crucial in the prevention of both diseases as well as in their management. Aim To systematically appraise the scientific literature to identify potential risk factors for caries and periodontal diseases. Methods One systematic review (genetic risk factors), one narrative review (role of diet and nutrition) and reference documentation for modifiable acquired risk factors common to both disease groups, formed the basis of the report. Results & Conclusions There is moderately strong evidence for a genetic contribution to periodontal diseases and caries susceptibility, with an attributable risk estimated to be up to 50%. The genetics literature for periodontal disease is more substantial than for caries and genes associated with chronic periodontitis are the vitamin D receptor (VDR), Fc gamma receptor IIA (Fc‐γRIIA) and Interleukin 10 (IL10) genes. For caries, genes involved in enamel formation (AMELX, AMBN, ENAM, TUFT, MMP20, and KLK4), salivary characteristics (AQP5), immune regulation and dietary preferences had the largest impact. No common genetic variants were found. Fermentable carbohydrates (sugars and starches) were the most relevant common dietary risk factor for both diseases, but associated mechanisms differed. In caries, the fermentation process leads to acid production and the generation of biofilm components such as Glucans. In periodontitis, glycaemia drives oxidative stress and advanced glycation end‐products may also trigger a hyper inflammatory state. Micronutrient deficiencies, such as for vitamin C, vitamin D or vitamin B12, may be related to the onset and progression of both diseases. Functional foods or probiotics could be helpful in caries prevention and periodontal disease management, although evidence is limited and biological mechanisms not fully elucidated. Hyposalivation, rheumatoid arthritis, smoking/tobacco use, undiagnosed or sub‐optimally controlled diabetes and obesity are common acquired risk factors for both caries and periodontal diseases.

Mutations in the cathepsin C gene (CTSC) have been identified as causal for the Papillon-Lefèvre syndrome (PLS), which includes prepubertal periodontitis (PP). Some CTSC mutations are causal for PP without PLS. No relationship has been demonstrated between CTSC mutations and other forms of periodontitis. Genetic polymorphisms in a candidate gene approach have been explored as risk factors for periodontitis. There is limited evidence that some polymorphisms in the genes encoding interleukins (IL)-1, Fc gamma receptors (Fc gammaR), IL-10 and the vitamin D receptor, may be associated with periodontitis in certain ethnic groups. However relatively large variations in carriage rates of the Rare (R)-alleles among studies on any polymorphism were observed. The available studies appear under-powered and do not adequately take into account other pertinent risk factors for periodontitis. Future studies should include larger cohorts, should clearly define phenotypes and should adequately control for other risk factors. In addition to the candidate gene approach, alternative strategies need to be considered to elucidate the gene variations, which confer risk for periodontitis.

An association with periodontitis was found for the combined genotype comprising carriage of the R allele for IL1A )889, IL1B +3954 and IL1RN in a sub-group of patients who were non-smokers, and were also culture-negative for P. gingivalis and A. actinomycetemcomitans.-Cases diagnosed as mixed periodontitis status. **63% Caucasian; 22% Asian; 15% Afro-Caribbean.), association not found; +, association found. *R / R is associated with aggressive periodontitis (P = 0.012). Additional genotype information was obtained from the authors. à Cases diagnosed as adult periodontitis. § An association with periodontitis was found for the combined genotype comprising carriage of the R allele for IL1A )889, IL1B +3954 and IL1RN in a sub-group of patients who were non-smokers, and were also culture-negative for P. gingivalis and A. actinomycetemcomitans.-Cases diagnosed as mixed periodontitis status. **The association between the R allele and chronic periodontitis did not quite reach significance (P = 0.07).), association not found; +, association found. *In smokers and N / R genotype only in males. Additional genotype information was obtained from the authors.à Cases diagnosed as adult periodontitis. § An association with periodontitis was found for the combined genotype comprising carriage of the R allele for IL1A)889, IL1B +3954 and IL1RN in a sub-group of patients who were non-smokers, and were also culture-negative for P. gingivalis and A. actinomycetemcomitans.

Our results provide evidence that IL-1RN gene polymorphism is associated with peri-implantitis and may represent a risk factor for this disease.