Based on many years of periodontal research, it is now understood that one of the strongest systemic risk factors for periodontal disease is diabetes mellitus.11,12 In addition, a preponderance of evidence indicates that there is a direct relationship between diabetes mellitus and periodontal disease.12,13 Evidence is also steadily mounting and shows that:
Hyperglycemia and hyperlipidemia in patients with diabetes may result in metabolic alterations that exacerbate periodontopathic-induced periodontitis, but there is another plausible hypothesis that proposes interaction of genes and environmental stressors could develop either periodontitis or diabetes or both.14
Both T1D and T2D increases the risk of periodontal disease three- to four-fold.15 Greater incidence and severity of periodontal disease in patients with diabetes may also be due to: diminished neutrophil recruitment and function, a more severe inflammatory response, and delayed wound healing. Another possible explanation for bone loss in periodontal disease modified by diabetes is the reduction of osteoclasts following a bacterial challenge.15 In one particular animal model study where a bacterial challenge was initiated, mice with T2D not only had a reduction in osteoclasts but new bone formation was suppressed which coincided with increased apoptosis of bone-lining cells. Increased apoptosis of bone-lining cells decreases the amount of new bone formation. Mice with T2D also have increased levels of apoptosis in soft tissue wounds which explain the interference with wound healing.15
Many periodontal researchers have described a bidirectional relationship between diabetes and periodontal disease. There is evidence that poor glycemic control has been shown to be associated with significantly greater alveolar bone loss over time compared to individuals with well-controlled diabetes.16 Similarly, a weaker body of evidence has emerged that suggests that effective periodontal therapy may have a positive effect on glycemic control.16 Keep in mind, however, that numerous conflicting studies exist that do not support the bi-directional association between periodontal disease and diabetes.13 A large, multicenter randomized controlled clinical trial (DPTT) which studied the effect of nonsurgical periodontal therapy for individuals with T2D and periodontitis over a six-month period showed no improvement in glycemic control. The periodontal treatment included two or more sessions of scaling and root planing with local anesthesia (more than 2.5 hours in duration) plus supportive periodontal care (periodontal maintenance).17
The DPTT trial (completed in 2012) received a lot of attention because the results weren’t what the dental community expected, and it did not confirm results of previous, smaller clinical trials and meta-analyses which showed improvements in hemoglobin A1c levels as a result of nonsurgical periodontal therapy.34 The DPTT clinical trial did show that periodontal treatment was safe and effective in reducing signs of periodontal disease in these patients. Pihlstrom and Buse concluded the important benefit of improved oral health but not for the purpose of improving glycemic control in the vast majority of patients.34
In 2013, Corbella et al. conducted a systematic review and meta-analysis of clinical trials that assessed whether periodontal therapy improved glycemic control. The best available evidence does not suggest that short-term diabetes outcomes are improved following non-surgical periodontal therapy.17,18
The American Academy of Periodontology and the European Federation of Periodontology wrote a consensus report in 2013 on diabetes, periodontal disease and systemic disease. They reported the epidemiological evidence from cross-sectional, prospective and intervention studies in order to assess the impact of periodontal disease on diabetes incidence, control and complications.36 They cite consistent and robust evidence demonstrating that severe periodontitis adversely affects glycemic control in diabetes and glycemia in non-diabetes individuals.36 They mention that there is no current evidence to support the adjunctive use of antimicrobials for periodontal management of patients with diabetes.36 The joint working group recommends providing guidelines for periodontal care in patients with diabetes.36
A couple of years later (2015), The Cochrane Oral Health Group searched for randomized controlled trials (RCTs) of individuals with T1D or T2D with a diagnosis of periodontitis.35 Interventions included nonsurgical periodontal therapy, surgical treatment and antimicrobial therapy. At a minimum, two review authors independently examined the titles and abstracts, selected the included trials, extracted data and assessed the included trials for bias.35 Thirty-five studies were included in the assessment. The authors concluded that there was low quality evidence that the treatment of periodontal disease by nonsurgical periodontal treatment does improve glycemic control in people with diabetes; however, there is insufficient evidence to demonstrate that this is maintained after four months.35 In clinical practice, ongoing periodontal maintenance will be required to maintain clinical improvements beyond 6 months. Further research is required to determine whether adjunctive drug therapies should be combined with periodontal therapy.35 In conclusion, based on best evidence, periodontal therapy is beneficial to patients with diabetes, but not as a means of improving glycemic control beyond a four-month period following periodontal treatment.17,18,34,35 Future clinical trials with longer follow-up periods are needed in order to better understand the potential of periodontal treatment to improve glycemic control among people with diabetes.35
Populations of individuals with diabetes (T1D and T2D) are exposed to different environmental factors which affect susceptibility and severity of periodontal disease. For example, smoking, socioeconomic status, individual home care, history of dental care, emotional stress, hematologic disorders, hormonal changes, and medications are significant modifiers of periodontal diseases.16 In one particular study, men with diabetes at a VA Medical Center had more severe periodontal disease compared to men without diabetes.18 Those men who smoked with or without diabetes had significantly higher measurements for all parameters of periodontal status studied. Neither the duration of diabetes nor the degree of glycemic control had a significant effect on periodontal status, but it was concluded that diabetes increased the prevalence and severity of periodontal disease.
Since 1965, residents of the Gila River Indian Community of Arizona, most of who are Pima or closely related Tohono O’odham Indians, have participated in a longitudinal population-based study of diabetes and its complications. The National Institute of Diabetes & Digestive & Kidney Diseases (NIDDK) performs biennial (every two year) examinations of each member of the community aged five and over. These standardized health exams include periodic dental exams including periodontal exams based on set criteria. In a periodontal study that analyzed data on the effect of periodontal disease on overall and cardiovascular disease mortality in these Indians withT2D, several significant findings emerged. This study was the first of its kind to study the risk of cardiovascular disease mortality associated with periodontal disease in patients with diabetes.20 It is also important to note that the impact of common risk factors for both diabetes and cardiovascular disease (like smoking) were taken into consideration. Nearly 60% of this particular Indian population studied had severe periodontal disease, and 70% of those with severe periodontal disease were edentulous.
The prevalence of periodontal disease is quite high in Pima Indians, even those who have not yet been diagnosed with T2D but diabetes further increases the risk. Diabetes, in this population group is also a strong, independent risk factor for cardiovascular disease and diabetic nephropathy. Individuals with diabetes are susceptible to microvascular and macrovascular complications like neuropathy, nephropathy, vision disorders, heart disease, and stroke; therefore, they are at increased risk of morbidity and mortality associated with these diseases/disorders. Also, cardiovascular disease and periodontal disease have many common risk factors like diabetes, age, smoking, health behaviors and habits, socioeconomic factors, diet, and access to care. These shared risk factors may confound results of many of the Pima Indian studies. Therefore, whether or not the prevention or treatment of periodontal disease can reduce the death rate from cardiorenal disease in this population group cannot yet be determined.
One revealing statistic, as a result of this Pima Indian study, showed that 204 of the 628 study subjects died during the follow-up period of the study which averaged 11 years. That’s about almost a quarter of the study participants. Forty-four of 54 deaths were attributed to ischemic heart disease (IHD) and most of the diabetes-related deaths (28 of 35) were due to diabetic nephropathy.20
In another Swedish study, smoking followed by A1C levels was discovered to be the best predictor for severe periodontal disease in subjects with T2D. Those individuals who were less controlled also had more cardiovascular complications.21
It seems that many of the risk factors for periodontal disease in individuals with T2D are preventable. This reinforces the notion that individuals with diabetes should be informed about their increased risk for periodontal disease, and these patients need intensive home care intervention and shorter recare intervals, especially if their glycemic control is poor or erratic and their medical visits are infrequent. In addition, patients in the Swedish research study lack sufficient knowledge about oral health complications in relation to diabetes.21
Much of the periodontal research during the last decade has focused on the host immune response that is triggered by periodontal pathogens. Certain components of bacteria have been found to be potent stimulators of a variety of cytokines and growth factors that eventually lead to an increased inflammatory response resulting in eventual tissue damage and destruction.22 In addition to the bacterial component triggers inflammatory mediators of the immune response may play an important role in local periodontal tissue destruction, but the mechanisms are still being studied intensively. In other words, chronic hyperglycemia may create a host hyper-inflammatory response that results in periodontal tissue and bone destruction.