disease, specifically the release of cytokines from white blood cells in response to the infection in the periodontium. Periodontally induced cytokines may alter the function of or destroy beta cells (insulin producing cells) in the pancreas. It has been proposed that one particular cytokine, known as tumor necrosis factor-alpha (TNF α ), which is released in response to periodontal disease, may produce an insulin- resistance syndrome by altering insulin signaling and insulin receptors (Santonocito, et al., 2022; Reddy, et al., 2017; Cicalau, et al., 2021). Randomized controlled trials and clinical studies have yielded conflicting findings when investigating periodontal treatment as a means to improve glycemic control in patients with diabetes. In 2018, a systematic review of meta-analyses of randomized controlled trials indicated the nonsurgical periodontal therapy (scaling and root planing) reduces HbA1C levels at a three-month interval and more so at six-month interval (Madianos & Koromantzos, 2018). Another clinical study in 2018 did not reveal any statistically significant change of the glycemic control in patients with Type 1 or Type 2 diabetes after the nonsurgical periodontal therapy regimen of scaling and root planing (Vergnes, et al., 2018). A literature review for the effect of nonsurgical periodontal therapy upon glycemic control revealed that there was only minimal evidence that nonsurgical periodontal therapy (scaling and root planing) improved glycemic control. A mean reduction of the HbA1c of only 0.29% at the 3-4-month interval with insufficient evidence that even this reduced level was maintained after 4 months was noted in this literature review (Simpson, et al., 2018). The increasing interest in the bidirectional relationship between diabetes and periodontal disease has yielded numerous studies about this relationship. The consistent hyperglycemic state of diabetes mellitus causes the formation of advanced glycation end-products (AGE), the accumulation of which adversely effects the chemotactic and phagocytic ability of neutrophils and phagocytes that provide the initial immune response against pathogenic periodontal bacteria. Effective nonsurgical periodontal therapy has been shown to reduce the formation of AGE, which improves periodontal health and given this bidirectional relationship has a positive impact upon glycemic control (Vesna, 2018). A literature search of four databases (Pub Med, Science direct, Scopus, and Cochrane) highlighted nine studies that investigated the effect of periodontal therapy upon glycated hemoglobin and fasting plasma glucose. Five of these studies reported a statistically significant decrease in blood glucose levels upon the completion of periodontal therapy (Benrachadi, Mohamed, & Bouziane, 2019) . Another meta-analysis came to the same conclusion (Teshome & Yitayeh, 2017). A number of the randomized controlled trials that proved successful in reducing blood glucose levels via nonsurgical periodontal therapy actually implemented the use of an antibiotic along with the scaling and root planning, which was more effective in attaining a statistically significant reduction in HbA1c levels at 3 and 6 month intervals (Sanz, 2018). The use of systemic doxycycline coupled with nonsurgical periodontal therapy has also yielded a statistically significant reduction in the HbA1c levels among patients with diabetes who have been treated with this combined therapy Santonnocito, et al., 2022). Other studies that have combined nonsurgical periodontal therapy such as root planing and scaling with antibiotics such as amoxicillin and metronidazole have not yielded statistically significant decreases in HbA1c levels among patients with diabetes (Glick, 2019). It is imperative that research continues in this area given the conflicting results of these studies.
this association (Vesna, 2018; Glick, 2019). Hyperglycemia that results from diabetes decreases the immune functions of neutrophils, monocytes, and macrophages. Neutrophil adherence, chemotaxis, and phagocytosis against pathogenic periodontal bacteria is impaired in a prolonged hyperglycemic state (Santonnocito, 2022). In addition, diabetes induces the release of pro-inflammatory cytokines from white blood cells (Santonocito, et al., 2022). These cytokines cause chronic inflammation, progressive tissue breakdown, and a decreased capacity for tissue repair. Diabetes may also predispose a patient to a number of oral conditions. Diabetes is a contributing factor in oral candidiasis; there are higher levels of Candida species in the oral cavities of subjects with diabetes compared to patients without diabetes (Nouraei, et al., 2021). The majority of those with diabetes have a higher risk of oral candidiasis than those without diabetes and those with type 1 diabetes have been found to exhibit a higher resistance to the antifungal medications used to treat oral candidiasis than patients without diabetes (Lim, et al., 2020). Investigators have suggested that such conditions as mucosal ulcers, taste impairment, and burning mouth can be manifestations of diabetes (Rohani, 2019). Diabetes affects the dental pulpal tissues by impairing circulation and the immune response and increasing the risk of irreversible pulpitis and developing of pulpal necrosis with a higher percentage of radiolucent periapical lesions among diabetics compared to non-diabetic patients (Rohani, 2019). Diabetes has also been shown to increase the risk of hyposalivation due to changes in the microvasculature and the basement membranes of the salivary glands (Rohani, 2019). Eighty percent of subjects with diabetes were found to have xerostomia compared to 10% of the control subjects. In addition, the level of glucose in the saliva has been positively correlated with the severity of the xerostomia (Verhulst, et al., 2019). It is unclear whether the increased incidence of xerostomia among patients with diabetes results from the medication used to treat diabetes or from the disease itself. Some authors suggest an expanded role for dentistry in diagnosing non-oral diseases such as diabetes. Salivary biomarkers have been successfully used as a diagnostic tool for diabetes (Agarwal & Baid, 2017; Mrag, et al., 2020). In addition, gingival crevicular blood may be used by dentists in the future to screen for diabetes. Elevated glucose levels in the gingival crevicular correlate with elevated blood plasma glucose levels (Sande, et al., 2020). However, more recent studies have shown mixed results (Glick, 2019). Periodontal disease has been associated with an increased risk of diabetes. The inflammatory mediators associated with periodontal disease have access to systemic dissemination given the heightened vascularity of the inflamed gingival tissues. These inflammatory mediators can exacerbate cytokine dysregulation associated with diabetes and increase insulin resistance of the target cells that are responsible for the uptake of glucose via the action of insulin Other authors suggest caution and advise that more prospective studies are necessary to determine if in fact a causal link exists between periodontal disease and patients at risk for diabetes (Simpson, et al., 2018; Verhulst, et al., 2019). Periodontal disease is considered the sixth most common complication of diabetes mellitus, with those patients who have poor glycemic control almost three times as likely to develop periodontal disease and about four times as likely to develop destruction of the alveolar bone (Vesna, 2018). The suggested mechanism for this worsening glycemic control is the inflammation produced by periodontal
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