IS PERIODONTAL DISEASE A COMORBIDITY…?Relationship Between Periodontal Disease and Diabetes

Periodontitis and Diabetes

Diabetes mellitus and periodontitis have a very complex bidirectional relationship that involves genetic factors and pro-inflammatory mediators. Presence of periodontitis might impair insulin resistance which appears as hyperglycemia that produces advanced glycation end products (AGEs). In turn, AGEs lead to overproduction of IL-6, IL-1 and Tumor Necrosis Factor alpha (TNF-α). As a consequence, presence of AGEs in tissues causes impaired wound healing (improper collagen turnover in fibroblasts) and excessive neutrophil response to periodontal bacteria.

Several meta-analyses have shown that non-surgical periodontal treatment reduces HbA1c levels significantly in the range of 0.31–0.65%. Even such small reductions in HbA1c can be clinically important. Thus, a large British study demonstrated that every percentage point decrease in HbA1c may result in as much as 35% reduction of microvascular complications, and an average reduction in HbA1c of 0.2% was related to a 10% lower mortality rate. Therefore, the reduction by 0.31–0.65%, which can be achieved by periodontal treatment, can have a great impact in terms of systemic health and societal economy.

Smoking as a Predisposing Factor for Periodontal Disease and Diabetes

The most common risk factors for periodontal disease are pathogenic bacteria, calculus, smoking and diabetes. Regardless of the consumption model, tobacco is associated with an increased risk of developing severe forms of periodontal disease. In diabetic patients, periodontal disease is more severe in smokers than in non-smokers. Both active and passive smokers have an increased risk of developing micro-and macrovascular complications.

The mechanisms by which tobacco increases the risk of periodontitis are reduced gingival perfusion (which decreases the transport of nutrients, oxygen, and elimination of final metabolic products), suppression of the immune response (especially inflammation), suppression of morphological and functional regeneration of periodontium, dysbiosis and thus increased infectivity of the oral microbiota. The mechanism of smoking that leads to vasoconstriction is the reduction of endothelial nitric oxide (NO) synthesis. It is caused by suppression of endothelial NO synthase (eNOS) expression in the vascular wall and decreased NO-mediated oxidative stress. The gaseous component of tobacco smoke contains many reactive oxygen species (ROS) which are generated during combustion. Such compounds act on the endothelium, increasing the production of lipid peroxides that destroy NO and inhibit eNOS, thereby decreasing NO’s bioavailability. The reduced NO level increases the vascular tone, leading to vasoconstriction and increased blood pressure.

In diabetic patients, adjuvant systemic antibiotic administration improves the severity of the pocket but does not provide attachment gain. Without neglecting the importance of metabolic control, prescribing antibiotics is based on the severity of periodontal damage and the inflammatory condition. Metabolic control of diabetes is especially to be considered in the context of oral complications of periodontal disease that appear to be amplified by the pathogenic pathways involved in the micro-vascular complications of diabetes. Reasonable control of diabetes or prediabetes avoids the onset of early periodontal changes, which are less evident to the patient at the beginning of the disease because they do not involve tooth loss.

In turn, the effect of periodontal disease on the control and evolution of diabetes patients appears to be significant. Periodontal treatment improves the management of periodontal infection and improves general health, leading to better control of blood glucose in patients with type 2 diabetes. Consequently, given the significant impact of oral complications on quality of life, the prevention of oral pathology and its early management appears to be essential in the care of diabetes.

Even though there a significant effort has been in this area, the therapy of choice of periodontitis is still the removal of supra and subgingival bacterial plaque through mechanical means. This can be aided by other adjuvant therapies such as antibiotics and antiseptic substances, which may or may not be accompanied by the use of adjuvants (local or systemic) such as antiseptics, antimicrobials and host modulators. The improvements obtained through these strategies are temporary and periodontitis can reappear if oral ecology shifts to a pathologic environment once more.

  

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