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| REVIEW ARTICLE |
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| Year : 2021 | Volume
: 12
| Issue : 3 | Page : 122-126 |
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Interplay between Periodontal Disease and diabetes mellitus
Garima Asthana, Shivjot Chhina
Department of Periodontology, ITS Dental College, Hospital and Research Centre, Greater Noida, Uttar Pradesh, India
| Date of Submission | 19-Oct-2020 |
| Date of Decision | 15-Feb-2021 |
| Date of Acceptance | 09-May-2021 |
| Date of Web Publication | 15-Jul-2021 |
Correspondence Address:
Dr. Garima Asthana
Department of Periodontology, ITS Dental College, Hospital and Research Centre, Greater Noida, Uttar Pradesh
India
 Source of Support: None, Conflict of Interest: None
DOI: 10.4103/injms.injms_132_20
Progress in the management of diabetes mellitus is turning attention toward comorbidities and conditions such as periodontal diseases. This article aims to present the evidence linking diabetes and periodontal disease. The potential effects of modifying factors of inflammatory origin on diabetic control are also discussed. Increased prevalence, extent, and severity of gingivitis and periodontitis are correlated with diabetes. Moreover, many plausible mechanisms have been exemplified to explain the effect of diabetes on the periodontium. While inflammation plays an important role in periodontal diseases, evidence in the medical literature also supports the role of inflammation as an important component in the pathogenesis of diabetes and its complications. Research suggests that periodontal disease has a large amount of inflammatory components that can negatively affect the metabolic control of diabetes. Conversely, treatment of periodontal disease and decrease in oral inflammation have a positive effect on the diabetic control. Diabetic patients who have periodontal disease have two chronic conditions - diabetes and periodontal disease, each of which can impact the other and require regular professional evaluations, patient education, and consistent educational reinforcement by healthcare providers both medical and dental.
Keywords: Diabetes mellitus, inflammation, periodontal diseases, periodontal therapy
How to cite this article:
Asthana G, Chhina S. Interplay between Periodontal Disease and diabetes mellitus. Indian J Med Spec 2021;12:122-6 |
| Introduction | |  |
Periodontitis is a chronic inflammatory disease, characterized by deposition of the supragingival and subgingival dental plaques. Microbial imbalance in the dental plaque leads to a chronic and destructive inflammatory response, which is characterized by the destruction of the periodontal tissues and the consequent loss of connective tissue attachment and alveolar bone. It also leads to the formation of pathological pockets around the diseased teeth. Mild periodontal infection has been observed in nearly half (45%–50%) of the adults, and this figure rises to over 60% in the elderly aged above 65 years. Severe periodontitis affects approximately 11.2% of the adult population globally and is a major reason for tooth loss, compromised nutrition, and an overall poor quality of life. When present as a concomitant factor in patients with chronic kidney disease (CKD), it leads to 41% increase in 10-year all-cause mortality rates and 22% increase in 10-year cardiovascular mortality rates as compared to patients with CKD-only. According to a report by the World Health Organization, severe periodontitis leading to tooth loss was found in 5%–15% of most populations worldwide.[1]
Diabetes mellitus is a chronic noncommunicable disorder, which has a high prevalence and can remain asymptomatic and undiagnosed for long periods. It is associated with widespread morbidity and mortality, with a far-reaching negative impact on the quality of life. It has been estimated that 415 million individuals had diabetes in 2015 and this number is expected to rise to 642 million by 2040 globally. Type 2 diabetes often goes unnoticed as it is asymptomatic during the initial stage. The global percentage of undiagnosed diabetes was estimated at 192.8 million of adults in 2015. Therefore, early detection and timely intervention remain relevant.[2]
Early detection can be more efficient if the interaction of undiagnosed individuals and healthcare providers is increased. In this situation, dental professionals can play an important role and contribute to the early detection of diabetes. It has been observed that many patients visit their dentist more frequently than their physician. A large number of dental patients may have periodontal disease, which is related to type 2 diabetes at pathophysiological and epidemiological level. Participants with periodontitis and no clinical manifestation of diabetes may have a higher level of HbA1c compared with periodontally healthy individuals. Thus, dental visits could well prove to be an ideal opportunity for diabetes screening among patients with periodontitis.
| Prevalence of Gingivitis and Periodontitis in Relation to Diabetes in Indian Adults | | |
Periodontitis is a common oral infection in India, with a prevalence rate of 66.2% among adolescents and about 89.2% among adults of 35–44 years of age. There is an increasing evidence suggesting the relationship between oral and systemic health, and this necessitates that all healthcare workers should have at the back of their mind the need to identify chronic health conditions, which may be asymptomatic at the time of contact with healthcare setting. Early identification of individuals with undiagnosed diabetes and the simultaneous management of oral and overall health in such patients remain of prime importance. However, it is noteworthy that 40% of Indians may have never been to a dental office, despite the fact that the country has one of the maximum numbers of dentists in the world. High prevalence of gingivitis (68.0%) and periodontitis (25.3%) has been reported among diabetics in the Indian population, and these rates are much higher than observed among persons without diabetes. Clinical and behavioral factors are associated with the prevalence of periodontitis among patients with diabetes.[3]
A study conducted in 2019 participants with good, fair, and poor oral hygiene status showed severe periodontitis prevalence as 0.8%, 17%, and 29.4%, respectively. In the participants who had poor glycemic control (HbA1c ≥8%), the prevalence of severe periodontitis in the three groups was 2.5%, 28.1%, and 30.7%, respectively. In another study, compared to healthy individuals, diabetic participants showed a significantly higher prevalence of periodontitis (42.3%).[4]
| Diabetes and Periodontitis: A Two-way Relationship | | |
The high prevalence of periodontitis as well as diabetes indicates that there will be an overlap of both these diseases in the general population. However, do these diseases have a causal or pathogenetic association is what would be interesting to see.
| Periodontitis | | |
Periodontitis has negative and serious impacts on many aspects of overall quality of life, affecting confidence, social interactions, and food choices. Diabetes is a major risk factor for periodontitis. Patients with poor glycemic control often present with severely inflamed gingiva causing periodontal destruction and pathologic migration of teeth, leading to diastemas. They also display more severe gingival bleeding compared to diabetes patients who have good or moderate control, despite similar plaque scores. Patients with poorly controlled type 2 diabetes are at greater risk for periodontal disease progression than patients with well-controlled type 2 diabetes. In addition to medical conditions, attention to oral disease by both medical and dental care providers is likely to improve their ability to identify individuals with undiagnosed diabetes.[5]
| Pathogenesis of Periodontal Disease in Diabetes | | |
Chronic periodontitis may cause systemic changes in diabetic individuals as a response to the microbiota associated with the diseased periodontium. Epidemiological studies reveal a direct correlation between the glycemic control and the risk of developing periodontitis. Overall, there is 2–3 times increased risk for developing periodontitis in patients with diabetes.[5]
To understand cellular and molecular mechanisms responsible for this cyclical association, one must analyze common physiological changes associated with diabetes and periodontitis that produce a harmonious effect when the conditions coexist. Evidence from clinical studies suggests that in uncontrolled or poorly controlled diabetes, the levels of pro-inflammatory cytokines such as interleukin (IL)-1β, tumor necrosis factor (TNF)-α, IL-6, receptor activator of nuclear factor-kappaβ ligand (RANKL) to osteoprotegerin (OPG) ratio, and oxidative stress are elevated within the gingival tissues which may lead to increased periodontal destruction.
The hyperglycemic state in diabetes has several deleterious effects which may be caused by the following biochemical and microbial changes:
- Increased accumulation of advanced glycation end products (AGEs)
- Increased reactive oxygen species/oxidative stress
- Cytokine imbalance and compromised immune response
- Shift in the microbial flora and circulating adipokines
- Increased RANKL/OPG ratio.
The aforementioned changes alter the equilibrium toward enhanced periodontal tissue destruction. The possible pathways establishing a possible relationship between diabetes mellitus and periodontitis are illustrated in [Figure 1]. Importantly, the defined processes are potentially modified by several other factors, such as genetics, age, smoking, and stress. All of these, singly or together, may contribute significantly to interindividual variations in disease experience.[6] | Figure 1: Possible mechanisms involved in the pathogenesis of periodontitis in diabetes. AGEs: Advanced glycation end products, ECM: Extracellulara matrix, PMNs: Polymorphonuclear neutrophils, IL: Interleukins, TNF α: Tumor necrosis factor-α, LPS: Lipopolysaccharides, PGE2: Prostaglandin E2, ROS: Reactive oxygen species, RANKL: Receptor activator of nuclear factor kappa-B ligand, OPG: Osteoprotegrin
Click here to view |
| Accumulation of Advanced Glycation End Products | | |
Accumulation of AGEs as a result of the chronic hyperglycemia of diabetes, along with the presence of infection and an exaggerated host response, may provide a possible explanation for the clinical outcomes observed in diabetic patients with periodontal disease. Furthermore, AGEs have been associated with:
- Increased oxidative stress
- Subsequent expression of endothelial vascular cell adhesion molecule 1
- Altered structure and function of basement membrane in vitro, upregulation of pro-inflammatory cytokines and growth factors such as platelet-derived growth factor.
The irreversible nature of AGEs and their interaction with respective receptors provide an environment in which tissues and cells are constantly exposed to these products, thereby creating a state of heightened cellular activity. Bacterial products such as endotoxin or lipopolysaccharide also play a role in initiating an inflammatory response in the host through the Toll-like protein receptors and thus can induce an inflammatory cascade These receptors play an important role in the innate immune response, particularly in the initial interaction between the infecting microorganisms, such as Porphyromonas gingivalis, and phagocytic cells of the monocyte lineage.[5],[7]
| Effects of Periodontitis on Diabetes Mellitus | | |
Justifying the bidirectional relationship between diabetes mellitus and periodontal disease, periodontitis could also have an adverse effect on glycemic control. The first clear evidence to support this hypothesis was postulated from investigations of individuals in the Gila River Indian community. Severe periodontitis at baseline was related with an increased risk of poor glycemic control (HbA1c >9.0%). After a follow-up (minimum 2 years), it was concluded that severe periodontitis was a risk factor for compromised diabetes management. Periodontitis may commence or propagate insulin resistance similar to that of obesity, by increasing activation of systemic immune response initiated by cytokines [Figure 2]. | Figure 2: Effect of periodontitis on diabetes mellitus. AGEs: Advanced glycation end products, ECM: Extracellular matrix, IL: Interleukins, TNF α: Tumour necrosis factor-α, LPS: Lipopolysaccharides, PGE2: Prostaglandin E2, ROS: Reactive oxygen species, RANKL: Receptor activator of nuclear factor kappa-B ligand, OPG: Osteoprotegrin, GLUT 4: Glucose transporter-4
Click here to view |
Chronic periodontitis causes an increase in oxidative stress and shift in the subgingival microflora, which leads to cytokine imbalance and immune dysfunction. As a result, the levels of HbA1c are elevated in the blood and GLUT-4 receptor transcription is reduced causing impaired insulin secretion, which may result in chronic hyperglycemia. Mediators of inflammation arising from periodontal sources interact with systemically derived lipids, free fatty acids, and AGE, all of which are characteristic of diabetes. Proposed mechanisms promoting insulin resistance showed that in patients with type 2 diabetes and periodontitis, through a positive feedback mechanism, an increased chronic systemic inflammatory state induced by periodontal disease contributes to insulin resistance, thereby worsening glycemic control. This might explain the role of periodontitis in increasing the risk of poor glycemic control among patients with type 2 diabetes.[7]
| Effects of Diabetic Status on Response to Periodontal Therapy | | |
Limited evidence is available to assess the response in diabetic and nondiabetic patients with periodontitis to periodontal therapy.
Although many patients with controlled diabetes show improvement in clinical parameters of periodontal disease immediately after therapy, those with poorer glycemic control show a rapid rate of recurrence of deep pockets and a less favorable prognosis.[8] In a longitudinal study, twenty diabetic and twenty nondiabetic participants received nonsurgical periodontal therapy, surgical intervention at sites with residual pockets of ≥5 mm, and regular maintenance therapy.[8] Five years after the baseline examination, both the groups showed a similar percentage of sites demonstrating gain, loss, or no change in clinical attachment. The HbA1c values explained that most of the diabetic patients in this study were well-controlled or moderately controlled at baseline.
| Effects of Periodontal Therapy on Diabetic Disease Status | | |
Treatment of periodontal disease decreases inflammation of periodontium which may be helpful in restoring insulin sensitivity, thereby improving glycemic control. A Cochrane review[9] supports the hypothesis that improvements in metabolic control can be expected following effective treatment of periodontitis. The mechanisms of action are not clearly defined, but it can probably be related to reduced systemic inflammation (e.g. decreased serum levels of mediators such as TNF-α and IL-6) after the treatment and resolution of periodontal inflammation. Therefore, since periodontal treatment appears to have the same potential to lower HbA1c as other glucose-lowering therapies, it may be suggested as an adjunctive therapy for improving insulin sensitivity and glycemic control in both type 2 diabetes and periodontitis patients.[9],[10]
| Conclusion | | |
Diabetes mellitus and periodontal diseases are closely associated and are highly prevalent chronic diseases with a multitude of similar pathogenetic pathways. Related conditions including obesity and insulin resistance are hypothesized to be one of the responsible factors in this relationship. Diabetes evidently increases the risk of periodontal diseases, and plausible biologically conceivable mechanisms have been demonstrated in abundance. Periodontal diseases may act as an initiator or propagator of insulin resistance similar to that of obesity, thereby adversely impacting glycemic control. Awareness should be spread among people with diabetes about the increased risk for periodontal disease. The dentists also have a fundamental role to play in diagnosing and managing diabetic patients at an early stage.
Financial support and sponsorship
None.
Conflicts of interest
There are no conflicts of interest.
| References | | |
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[Figure 1], [Figure 2]
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