Risk factors for periodontitis
The NHANES 2009–2010 survey indicates that severe periodontitis increases with age and is more prevalent in men than in women. Periodontitis is associated with lower levels of education and higher levels of poverty.2 Other risk factors for periodontitis include smoking, HIV, stress, familial traits, obesity, medications such as cyclosporine and phenytoin, and chronic diseases such as osteoporosis and diabetes. 2,3,5,8 Diabetes is a major risk factor for periodontitis.10 Persons with diabetes are three times more likely than persons without diabetes to have periodontitis.10
Systemic effects of periodontitis
Systemic and vascular inflammatory processes, the sequelae of periodontitis, lead to cardiovascular pathogenesis including atherosclerosis.11 Early-phase response proteins such as C-reactive protein and fibrinogen are believed to be responsible for the atherosclerosis. One study found that people who had diabetes and severe periodontitis for an average of 11 years had a 3.2 times higher risk of death from cardiac or renal disease than did people without periodontitis or those with mild to moderate disease.12 Mealey and Rose also indicated that periodontitis is associated with cardiovascular diseases such as myocardial infarction and stroke, as well as negative pregnancy outcomes, such as low birth weight, pre-eclampsia, and preterm birth.4
The bi-directional relationship between periodontitis and diabetes
The literature is replete with discussions about the link between periodontitis and diabetes.3,4,8,9,13 The fact that the periodontium is a vascularized end organ, similar to the retina and the glomerulus, may explain why microvascular and macrovascular complications occur in both periodontitis and diabetes.4 Genco noted that there is a reciprocal relationship between periodontitis and diabetes: periodontitis leads to the development of diabetes over time, and diabetes leads to increased periodontal damage.9 He surmised that the host inflammatory response to periodontitis promotes insulin resistance and subsequently leads to poor glycemic control.
Preshaw posited that inflammation is the focus for the periodontitis–diabetes link.3 She stated that longstanding plaque on the teeth leads to periodontitis, which later causes dysregulated secretion of inflammatory mediators such as IL-1β, TNF-α, and matrix metalloproteinases, all of which promote tissue destruction and perpetuate inflammation. The inflammation in diabetes leads to microvascular and macrovascular complications, and hyperglycemia drives further inflammation, which leads to oxidative stress and apoptosis. The advanced glycation end products (AGEs), which are formed by the irreversible fusing of glucose to protein and lipids during extended hyperglycemia, impair periodontal health.8 The receptor for advanced glycation end products (RAGE) is an immunoglobulin that interacts with several ligands (ion-metal atom complexes) including AGEs. In addition, the AGEs-RAGE pathway increases thrombus formation and vascular permeability, and it leads to diabetic cardiovascular complications. According to Chandna et al., chronic infection, lipopolysaccharide, and AGEs promote an increased inflammatory state that is responsible for tissue destruction in the periodontium of patients with diabetes.5
Boyd and colleagues conducted a systematic review of studies that analyzed the impact of periodontitis on glycemic control.13 In one small pilot study, researchers found that there was a statistically significant 0.21% increase in glycated hemoglobin (A1c) in the periodontitis group, when compared with healthy controls. In a review of the German-based cohort SHIP (Study of Health in Pomerania), which studied nondiabetic participants (n=2,973) for five years, Boyd’s group also noted that when the nonperiodontal persons were compared to those with poor periodontal health at baseline and at the five-year follow-up, the change in A1c was 0.005% versus 0.143%. For those persons with advanced periodontitis at baseline and further worsening of the disease during the five years, 0.13% greater A1c levels were observed. These results indicate that periodontal disease has a significant effect on the A1c measure over time.
Prevention of periodontitis
Although several options are available to treat periodontal disease, the value of preventive strategies cannot be overstated. Research indicating that moderate periodontitis is prevalent in 37% of current smokers implies that smoking cessation is an important periodontitis preventive strategy.2,5 Avoidance of secondhand smoke also appears to be important in the prevention of periodontitis. In an observational study that assessed NHANES data from 1994 to 2004, researchers found that, after controlling for age, sex, and year of survey, persons with high environmental tobacco smoke exposure (cotinine level ≥1.5 ng/ml) were more than twice as likely to develop periodontitis as were those with negligible exposure.7 Persons who smoke should be advised to quit, and those who are at risk for periodontal disease should be advised to avoid environmental tobacco smoke exposure at all cost. As shown in Table 1, other measures that may help prevent periodontitis include avoidance of sugary foods and beverages and alcohol, use of fluoridated toothpaste and a soft-bristle toothbrush, daily flossing, and brushing one’s teeth at least twice daily.6,14 Kobayashi et al. also noted that regular brushing has been associated with reduced periodontal inflammation that ultimately leads to reduced CVD risk.15 Clinicians should advise patients to have dental care twice per year, minimize the use of medications with oral side effects, and assist patients in accessing care.14