Diabetes And Periodontal Disease

Introduction

Diabetes and periodontal disease are both highly prevalent in the general population. A disease of metabolism, diabetes has far-reaching effects on the body. It affects the body’s capacity to fight infections and regenerate. Periodontal disease, though limited to the oral cavity, can influence systemic health. The effect of diabetes on periodontal disease has been studied extensively in the past. Now, with the advent of periodontal medicine, the effects of periodontal disease on the development and control of diabetes are under scrutiny. We shall be seeing the cyclic relationship between these two diseases, and how control of one can lead to improved control of the other.

Diabetes

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Diabetes mellitus is a systemic disease with several major complications affecting both the quality and length of life. It is an endocrine disorder characterized by chronic hyperglycemia. Diminished insulin production, impaired action of insulin, or both, lead to decreased transport of glucose to the tissues. This leads to an elevated blood sugar level.

There are two types of diabetes, depending on the cause:

1. Type 1 (insulin-dependent diabetes mellitus) is caused due to autoimmune destruction of the β cells of the pancreatic Islets of Langerhans.
2. Type 2 (noninsulin dependant diabetes mellitus)

It is caused by the resistance of peripheral receptors to the action of insulin.

Both types of diabetes are associated with many long-term complications. These include nephropathy, retinopathy, and neuropathy, cardiovascular and cerebrovascular complications. Periodontitis is now considered to be the sixth complication of diabetes.

It is also associated with poor wound healing and susceptibility to infections.

Periodontal disease

Periodontal disease can be defined as ‘An inflammatory disease of the supporting tissues of the teeth caused by specific microorganisms or groups of specific microorganisms, in a susceptible host, resulting in progressive destruction of the periodontal ligament and alveolar bone with pocket formation, recession or both.’

Periodontitis is an ongoing process characterized by phases of destruction and quiescence. The destruction is influenced by many systemic factors like dietary deficiencies, hormonal balance, and host defense. Conditions like vitamin c deficiency, pregnancy, immune deficiency, and diabetes affect periodontal disease.

Diabetes as an aggravating factor of periodontal disease

The oral manifestations of diabetes include mucositis, burning mouth, candidiasis, abscesses, gingival polyps, and periodontal disease. Diabetes, when a complication of Periodontitis, acts as a modifying an aggravating factor in the severity of periodontal infection. Diabetics with periodontitis demonstrate more attachment loss, bone loss, and deeper probing pocket depths than non-diabetic individuals. The earlier the onset of diabetes, and the poorer the control, the more is the susceptibility to periodontal disease. Also, when a diabetic individual contracts the periodontal disease, it is of greater severity than in non-diabetic individuals.

Change in the Microflora

Diabetic individuals show elevated levels of glucose in the blood. This leads to elevated glucose levels in the gingival crevicular fluid (GCF). This changes the environment of the periodontal microflora. There is a qualitative change in micro-organisms between non-diabetic and diabetic individuals. Studies have shown an increase in the number of Capnocytophaga and Aggregatibacter actinomycetemcometans subgingivally in diabetic individuals.

Microvascular Angiopathy:

Diabetes leads to microvascular angiopathy, causing a compromised delivery of blood and nutrients to the periodontal tissues. There is a decrease in the removal of toxic metabolites from the tissues. There is a constant release of toxins from the plaque. Thus microangiopathy can cause tissue destruction.

Collagen Turnover:

Collagen metabolism is defective in diabetics. Hyperglycemia is associated with an increase in protease and collagenase activity. There is an increase in Accumulated Glycation End-products (AGEs). These AGEs cause cross-linkage of collagen fibers. These fibers, then, are not repaired or replaced. This causes decreased wound healing.

Immune Response:

Diabetes also leads to a diminished immune response. Diabetic abnormalities in immune response include impaired neutrophil chemotaxis, phagocytosis, and adhesion. Certain protein factors in diabetic serum competitively bind neutrophil receptors, thereby preventing complement-mediated phagocytosis. The body’s defense system is thus undermined, predisposing to infections.

Cytokine Regulation:

Diabetics show an increase in inflammatory cytokines from monocytes/ polymorphonuclear leukocytes and a reduction in growth factors from macrophages. This predisposes to chronic inflammation, tissue breakdown, and diminished repair capacity. There is an increase in Interleukin1 (IL1) and Tumor necrosis factor α (TNFα). These, in turn, increase the release of enzymes that destroy gingival connective tissue and promote the formation of osteoclasts.

Bone Formation

Diabetes has also been found to impair the ability of new bone formation. It interferes with the process of coupling. This diminished capacity of new bone formation interferes with the ability of a diabetic individual to repair the loss of tissue that occurs in periodontal disease.

Bacterial plaque is the primary etiologic factor of periodontal disease, but diabetes complicates periodontal disease by altering the host response to plaque and reducing the ability to heal following surgery.

Periodontal disease as a modifying factor for diabetes

The interrelationship between Periodontitis and diabetes provides an example of systemic disease predisposing to oral infection, and once that infection is established, the oral infection exacerbates systemic disease.

Effects of Infection on Glycemic Control

Glycemic control is affected by all kinds of infections. Systemic bacterial and viral infections cause resistance in the peripheral tissue receptors to insulin.

In the case of periodontal disease, there is a persistent bacterial infection that acts in a manner similar to other systemic infections. The presence of severe periodontal disease worsens glycemic control. This effect is more pronounced in Gram-negative infections.

Insulin Resistance

The periodontal infection causes an increase in the levels of proinflammatory cytokines, like interleukin1 (IL1) and tumor necrosis factor α (TNFα). Studies have demonstrated that TNFα suppresses insulin action via its specific receptor; hence, it exacerbates insulin resistance, producing an insulin resistance syndrome similar to that observed in diabetes. It initiates the destruction of pancreatic beta cells leading to the development of diabetes.

Insulin resistance prevents glucose uptake into the tissues and increases the blood glucose level. The pancreas, thus, has to step up the production of insulin. This effect is seen in normal individuals as well as diabetics.

Periodontitis, Diabetes, and Pregnancy

Periodontitis is particularly a problem in pregnant, diabetic women. Periodontitis causes an increase in biological fluids, inducing labor. In this manner, it is associated with pre-term, low-birth-weight babies. Diabetic women are more prone to Periodontitis than nondiabetic women. They also tend to have more bone loss, more attachment loss, and deeper pockets than nondiabetic women. Diabetes, independently, also causes complications during childbearing.

The effect of Periodontitis on the duration of pregnancy is exacerbated in diabetics.

Periodontitis can also cause a loss of glycemic control at this crucial time. Thus, it is important that the periodontal health of pregnant, diabetic women be evaluated. Proper treatment modalities should be undertaken to avoid the unfavorable outcome.

Treatment of Periodontitis in Diabetics

Recent evidence suggests that Periodontitis should be treated differently in diabetic individuals. Periodontal surgery and the resultant transient bacteremia can cause an upregulation of TNFα. This aggravates insulin resistance and upsets glycemic control. Thus Periodontitis in diabetic individuals should be treated non-surgically. The treatment of Periodontitis causes the elimination of the bacterial challenge. This leads to better tissue response to insulin. Normal tissue response is restored over time. Treatment of Periodontitis, thus, improves glycemic control. This is more apparent in patients with severe Periodontitis.

CONCLUSION

Periodontal disease is the result of a complex interplay of bacterial infection and host responses and is often modified by various systemic diseases such as diabetes mellitus. Such diseases are capable of affecting the periodontium and/or the treatment of periodontal disease.

On the other hand, recent research indicated that periodontitis too can influence the course of systemic disease like diabetes.

In order to understand the cellular/molecular mechanisms responsible for such a cyclical association, one must identify common physiological changes associated with diabetes and periodontitis that produce a synergy when the conditions coexist. When one of the diseases is under control, control of the other disease is facilitated.

Not only is periodontal disease thereby affected by systemic diseases, but carefully managed periodontal therapy may also have a positive effect on the general health of patients with systemic diseases.

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