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Diabetes Mellitus Effects on Periodontal Disease Research Paper

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Updated: Mar 6th, 2022

Introduction

Diabetes mellitus (DM) is one of the most important metabolic disorders affecting the cellular and biochemical within the body. Patients with diabetes often exhibit depressed host defense, resulting in increased susceptibility to infection. Failure for the pancreas to secrete insulin leads to diabetes mellitus, a disorder characterized by hyperglycemia. Diabetes mellitus is an integral disease that prevails in a wide range of populations in America. About 100 million persons are feared to have this disorder all over the world. Diabetes mellitus has varied effects on oral tissue and it influences the prevalence and severity of periodontal disease. It has been reported that periodontal disease is more severe in diabetics compared to the non-diabetics. Other investigators have reported that periodontitis is a leading complication of diabetes mellitus (Aldridge et al, p. 271). Periodontal disease is a chronic inflammatory disease of the tissues that support and attach the teeth to the jaws. They are caused by gram-negative bacterial infections and are, for the most part, asymptomatic, although much of the actual destructive tissue changes which are observed clinically are result of the inflamatory host response. Periodontal disease (PD) is the second main cause of oral cavity disorders affecting the population with diabetes due to its oral cavity disorders affecting the population due to its high prevalence. It is more frequent in adults in contrast to cavities which are more common and much more frequent in children.

PD is also seen as a mixture of endogenous infection which is caused by microorganism that colonizes the sub-gingival dental-bacterial plaque, in a structure known as a biofilm. Biofilms are bacterial communities that adhere to oral surfaces. An accumulation of about 700 bacterial species capable of colonizing the mouth have been described. Further, research has shown that a person may store up to 150 different species (Taylor and Becker, p. 194).

Diverse studies carried out by the WHO confirm that the prevalence and severity of PD tends to be on the rise in the adult population compared to younger groups. Persons with diabetes mellitus (DM) are at greater risk of developing PD. PD has been ranked as the 6th complication of DM. Not only is it more prevalent in this population, but also the progression of symptoms, in a more aggressive and more rapidly setting mode. The main reasons for this prevalence is inherently lack of information on the importance of oral hygiene, poor metabolic control and the irregularity in visiting dentists, among others. PD causes the loss of dental organs, thereby making the chewing of food difficult. In addition, more pain results and this will eventually lead to inadequate nutrition. Those people with DM experience a difficult time tolerating false dentures due to total bone loss and the sensitivity of the alveolar mucosa tissue (Aldridge et al, p. 271). Oral hygiene plays a vital role in periodontal health and one self oral care determines the extent and prevalence of the disease. This are is not fully studied despite the fact that self care have proved to be important in periodontal health. There is substantial evidence that the control of periodontal inflammation has the potential to influence glucose metabolism. On the contrary, partial work has been done on the capability of periodontal health care in improving diabetes. A literature review has suggested the importance of maintaining oral hygiene especially in patients with diabetes. This will definitely lower the risks of developing the disease. 1.1.1 Anatomy of the tooth The tooth is embedded in and attached to the alveolar process of the mandible. The embedded portion is the root and the visible part is the crown. The nerves and blood capillaries are situated in the innermost part of the tooth referred to as the pulp. The next layer of the tooth is the dentin which contains connective tissue containing tubules that house the cellular processes of the odontoblasts. The enamel is covered by the crown as shown on figure 1. Enamel is a hard substance with connective tissue whereas the cementum covers the root part of the tooth. The tooth is attached to the alveolar bone by periodontal ligaments. The gingiva functions as the protective tissue for the alveolar process. There is a space between the gingival epithelium and the tooth which is referred to as the gingival sulcus. The depth of the sulcus is approximately 2-3 mm. However, the damage of the periodontal ligaments in PD, may lead to the expansion of the sulcus, and such a case is referred to as a gingival pocket (Diaz and Belmont, p. 44).

Anatomy of the tooth
Figure 1: Anatomy of the tooth

Effects of Diabetes Mellitus on the Periodontal State

The function of immune cells, neutrophils, monocytes and macrophages is often altered in cases of diabetes. Neutrophilic adherence, chemotaxis and phagocytosis are changed, inhibiting an adequate defense against bacteria in the periodontal pouch and significantly increasing the destruction of the periodontal membrane (Diaz and Belmont, p. 43). Although neutrophil function is decreased in diabetics, the monocyte/macrophage cell line may be hyper-responding when faced with the bacterial antigenic contact. This hyper-response results in a greater production of pro-inflammatory cytokines. Peripheral monocytes in diabetic patients produce high levels of the tumor necrosis factor-α (TNF- α) in response to the Porphyromonas gingivalis antigens compared to the monocytes of non-diabetic patients. The level of inflammatory cytokines in the crevicular fluid is also related to glycemic control. Loos reported that diabetic patients with periodonitis, whose HbA1c levels were over 8%, had approximately twice the amount of interleukin-1β (IL-1β) in their crevicular fluid in comparison to patients with indexes below 8% (2109). The net effect of these changes in the immune response of diabetics is an increase in periodontal inflammation, a loss of epithelial insertion and alveolar bone.

The gingival sulcus is a labile site for the body to present a hermetic closure to the external environment. In this space, the crevicular fluid increases in the presence of inflammation. The increase in the loss of periodontal insertion and the alveolar bone in diabetic patients are linked to changes in the metabolism of connective tissue where there is a lack of response in resorption and formation. The effect of the hyperglycemic state includes the inhibition of osteoblastic proliferation and collagen production resulting in a reduction in the formation and decrease in mechanical properties of the newly formed bone.

The changes mentioned above might contribute to the pathogenicity of periodontal disease and changes in healing since collagen is the predominating structural protein in the gums. In addition, collagen is vulnerable to degradation due to the action of MMPs as collagenases which are suggested to be in high amounts in the tissues of persons with diabetes. 1.3 Effects of periodontal disease on the state of diabetes

Periodontal disease has a significant impact on the metabolic state of diabetes. The presence of PD increases the risk of worsening glycemic control in time. The increase of HbA1c values are associated with severe periodontal disease in pregestational type 2 diabetic women. Current research has shown the likelihood of periodontal disease inducing or perpetuating an elevated inflammatory state not only locally, but severe periodontitis with the risk of mortality due to cardio-renal disease. Accumulated studies demonstrates that patients with periodontitis, particularly those colonized with Gram negative bacteria such as P. gingivalis, Tannerella forsynthesis, and Prevotella intermedia, have greater inflammatory serum markers such as C-reactive protein (CRP), IL-6, and fibrinogen than patients without periodontitis. Similarly, there is an increase in resistance to insulin which decreases glycemic control. People with periodontal disease are disadvantaged by depressed immune system which fails to remove the main source or cause of inflammation. The main source is the gram negative bacteria which may lead to continuous activation of the immune making the patient more susceptible to chronic inflammation. At this point, the patient produces species that are reactive in oxygen which in turn triggers production of matrix metalloproteinases. The metalloproteinases enzymes damages the collagen of the periodontal ligaments, which loosens the linkage of the tooth to the alveolar process as well as deepening the gingival sulcus. Gingival pockets forms a place where bacteria can potentially proliferate. This leads to an eventual worsening of infection or inflammation. In addition, the condition of low oxygen fosters the growth of anaerobic bacteria, resulting in worsening of infection and/or inflammation. 2.0 Treatment Since improvement in glycemic control is associated with a major decrease in the risk of diabetic complications, it is important to assure normal or near normal glucose levels. There are different tools to determine the level of glucose control, but a safe glycemic range must be considered for each patient, taking into account coexisting medical conditions, age of the patient, ability to follow a treatment program and possible presence of hypoglycemia unawareness. Basically, treatment of patients with periodontal disease involves mechanical methods. Typically, both professional and mechanical cleaning of the plaque or calculus should be observed. This includes the supragingival and infragingival plaque, (which is a part inside the gingival pockets). If the gingival pockets are deep, surgery may be performed to reduce the growth of bacteria (Skaleric et al. 161). Further research has suggested that apart from mechanical cleaning antimicrobial agents should be applied. The widely used antimicrobial agents are the topical and systematic. The reason for using such treatment is to curb the disease since it involves both the growth of bacteria and shift in the microorganisms species. Topical medication with antiseptics and antibiotics is highly recommended since it has the advantage of delivering the antibacterial agent directly to where there are needed. Tetracycline drugs are examples of topical medication and include the doxycycline, metronidazole and minocycline. A topical antiseptic contains chlorhexidine or sodium hypochlorite. Periodontal treatment decreases local inflammation and as a consequence, decreases chemical mediators involved in inflammation, among them IL-6 and CRP, positively contributing to proper glycemic control. It is evident that PD exceeds the local environment affecting the systemic one. The tissue demand for insulin in type I diabetic patients decreases after periodontal treatment including scraping and radicular smoothing, local gingivectomies and selective extractions, scaling and root planning in addition to the use of antibiotics such as penicillin and streptomycin (Skaleric et al, p. 163). 2.1 Conclusion It is clear that periodontal disease and diabetes have a dependable relationship between them. Not only does diabetes increase the chances of developing periodontal disease, it also supplements the progression of more antagonistic and rapid defining signs. There is therefore a bidirectional relationship between the two principals.

The most important concern for applying evidence in the early diagnosis of periodontal disease is educating the patient. Periodontal disease is a silent condition. Diabetics need to be aware of the signs of periodontal disease. Bleeding of the gums is the first sign of subgingival infection. This is when all the personnel involved in the care of diabetic patients should take active participation and therefore opportunely refer patients to the dentist.

Work Cited

  1. Taylor, G., Burt, B. A., and Becker, M. “Severe periodontitis and risk for poor glycemic control in patients with non-insulin – dependent diabetics”. Journal of Clinical Periodontal 23 (1996): 194−202. Díaz, R., Casanova, R., Belmont, J. “Oral Infections and Glycemic Control”. Archives of Medical Research. 36 (2005): 42−48.
  2. Loos, B. G. “Systemic markers of inflammation in periodontitis”. Journal of Periodontol 76.4 (2005): 2106−2115.
  3. Aldridge, P., Lester, V., Watts, T., Collins, A. et al. “Single-blind studies on the effects of improved periodontal health on metabolic control in type 1 diabetes mellitus”. Journal of Clinical Periodontol. 22.8 (1995): 271–275.
  4. Skaleric, U., Schara, R., Medvescek, M. et al. “Periodontal treatment by Arestin and its effects on glycemic control in type 2 diabetes patients”. Journal of International Academy of Periodontol. 6.4 (2004): 160–165.
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