According to the Centers for Disease Control and Prevention, the prevalence of diagnosed diabetes has increased from less than 1% of the U.S. population in 1958 to more than 7% in 2015 [6]. As of 2019, 11.3% of the U.S. population, or 37.3 million Americans, have diabetes. Unfortunately, 8.5 million of these individuals are unaware of their diagnosis [7,8]. Diabetes has been considered epidemic since the 1972, and the percentage of Americans expected to have diabetes or impaired glucose tolerance is estimated to reach 15% to 20% by the year 2030 [9,53]. In addition, prediabetes is now estimated to affect 96 million Americans [8].

The scope of the diabetes problem is vast and diverse, particularly among geographical regions. In 2018, the prevalence of diagnosed diabetes in the United States was highest among Southern states, including West Virginia (13.4%), Mississippi (12.9%), Louisiana (12.9%), Alabama (12.7%), Arkansas (12.4%), and Kentucky (12.1%) [10]. Genetics, race, age, and lifestyle significantly influence the onset and progression of the disease process [4]. Although all races and ethnicities can develop diabetes, the prevalence is greatest among American Indian/Alaskan Natives [7,8]. In addition, according to 2013–2016 survey data, the incidence of diagnosed and undiagnosed diabetes is estimated to be 19.8% among Hispanic individuals and 17.9% among non-Hispanic Black Americans 20 years of age and older, compared with the overall population rate of 14% [7,8,11]. However, American Indians/Alaskan Natives present the greatest risk for the development of type 2 diabetes; their risk is more than two times greater than that of White Americans. It is estimated that 15.1% of American Indians/Alaskan Natives older than 18 years of age have diabetes [7]. The highest prevalence of diabetes in the United States is observed in American Indians in the Southwest, where an estimated 22.2% of the population has developed diabetes [7].

The adult mouth typically contains 32 permanent teeth, and the primary role of teeth in humans is mastication, although they also affect speech, facial structure/appearance, and social acceptance. Each tooth consists of enamel, dentin, and dental pulp (i.e., the "nerve"). Enamel is the external layer of the tooth and is composed mainly of hydroxylapatite, a crystallized form of calcium phosphate. It is the hardest and most mineralized substance in the body, even more so than bones. Dentin is the substance that underlies the enamel of the tooth. The significantly lower mineral content makes dentin softer than enamel and permits a more rapid progression of decay. Commonly called the "nerve" of the tooth, the dental pulp is a complex configuration of soft connective tissue consisting of blood vessels, nerve fibers, fibroblasts, macrophages, lymph vessels, lymph cells, and T-lymphocytes. The teeth are anchored in place by the periodontal ligament and its attachment to the supporting alveolar bone. The gingiva, or gums, is a thick, fibrous tissue covered with a mucous membrane with a keratinized surface [22]. The gingiva serves various purposes in the oral cavity depending on its location and tissue type.

Both diabetes and periodontal disease share a common pathogenesis that involves enhanced inflammatory response at the local and systemic levels. This inflammatory response is mainly caused by the chronic effects of hyperglycemia and specifically the formation of biologically active glycated proteins and lipids [25,28]. Patients with diabetes, especially uncontrolled diabetes, are at an increased risk for impaired healing, and the periodontal pocket can experience persistent inflammation and bacterial infection in patients with periodontal disease, which can be made worse by this impaired healing [4,27]. Loss of teeth because of aggressive periodontitis may also occur [4].

In addition to vasoconstriction, endothelial dysfunction is correlated with aggregation of platelets, a proinflammatory state characterized by the accumulation of leukocytes and coagulation products on the endothelium. Fibrinolysis is decreased, and thrombosis is increased. As the secretion of prostacyclin and nitric oxide induce vasoconstriction, plasma cytokine and prothrombin factors levels increase. This makes the plasma markedly procoagulant and antifibrinolytic, promoting atherosclerosis [4]. The Insulin Resistance Atherosclerosis Study also demonstrated that chronic hyperglycemia was positively associated with increased intimal-medial wall thickness [28]. These changes in both the microvascular and macrovascular systems lead to reduced vascular reactivity and increased production of glycation end products [29]. The accumulation of advanced glycation end products in the gingival tissues is generally responsible for the oral complications of diabetes. In fact, individuals with poorly controlled diabetes have a two- to three-fold increase in the prevalence of oral lesions and periodontal disease.

In addition to vasoconstriction, endothelial dysfunction is correlated with aggregation of platelets, a proinflammatory state characterized by the accumulation of leukocytes and coagulation products on the endothelium. Fibrinolysis is decreased, and thrombosis is increased. As the secretion of prostacyclin and nitric oxide induce vasoconstriction, plasma cytokine and prothrombin factors levels increase. This makes the plasma markedly procoagulant and antifibrinolytic, promoting atherosclerosis [4]. The Insulin Resistance Atherosclerosis Study also demonstrated that chronic hyperglycemia was positively associated with increased intimal-medial wall thickness [28]. These changes in both the microvascular and macrovascular systems lead to reduced vascular reactivity and increased production of glycation end products [29]. The accumulation of advanced glycation end products in the gingival tissues is generally responsible for the oral complications of diabetes. In fact, individuals with poorly controlled diabetes have a two- to three-fold increase in the prevalence of oral lesions and periodontal disease.

Oral disease has implications in other chronic complications related to diabetes [34]. Not only is the risk of periodontitis greater in individuals with diabetes, evidence suggests that there may be a relationship between chronic periodontitis and cardiovascular disease and that periodontitis may be a risk factor for cardiovascular disease [35,36,37,38,39,40]. Research has shown that treating severe periodontal diseases is associated with improved blood flow, greater arterial elasticity, enhanced endothelial function, and improvement in levels of systemic inflammatory markers (e.g., C-reactive protein, interleukin-6) [35,41]. The American Heart Association has stated that it is reasonable to hypothesize that periodontal disease contributes to the advancement of type 2 diabetes [42]. Dental infection has also been associated with coronary atherosclerosis, and bacterial DNA from periodontal infections has been identified in atherosclerotic plaques [28]. As a result of this relationship, periodontal disease is a predictor of death among individuals with diabetes and associated ischemic heart disease [43].

As with cardiovascular disease, the proposed mechanism for the effect of periodontitis on the development of kidney disease is systemic inflammation [44]. The death rates from nephropathy are higher in individuals with diabetes and severe periodontal disease than those with no or mild periodontal disease [43,45]. Additionally, the risk of mortality from combined diabetic nephropathy and ischemic heart disease is three times higher in patients with diabetes and severe periodontitis than in those without periodontitis [25].

Depending on the severity of the disease, there are several options for the treatment of periodontitis. If oral disease is suspected in the patient with diabetes, referral to a periodontist is the first step. First-line approaches to the treatment of periodontitis include scaling, root planing, and locally administered antibiotics. Localized therapy with controlled-release antimicrobials has been shown to diminish levels of C-reactive protein and additional inflammatory markers [44]. Dosages will be dependent on the manifestation and extent of the infection and the delivery method chosen (e.g., pastilles, lozenges, troches, implanted cords or chips) [28]. With more advanced disease, dental surgery may also be necessary.

Prevention of periodontal disease is the best option, particularly considering the increased risks in patients with diabetes. Education regarding the causes of periodontal disease and how it is related to diabetes-associated macrovascular and microvascular diseases is necessary. For patients with diabetes who have or are at risk for periodontal disease, healthcare providers should [28]: