periodontal disease occurs more frequently and with greater virulence and severity in patients with type 1 or type 2 diabetes (Denisse et al., 2017).This combination of factors has led to periodontal disease being considered the sixth complication of diabetes (Vesna, 2018). The increased risk for the development of periodontal disease is correlated to the level of glycemic control. Those who control their diabetes well, maintaining a blood glycated hemoglobin A1c (HbA1c) level of 7% or lower, have demonstrated minimal risk for developing periodontal disease, but this risk increases considerably as glycemic control worsens (Denisse, 2017). Periodontal disease is associated with higher HbA1c levels and diabetes-related complications in patients with type 2 diabetes (Graziani et al., 2018). A second consideration is the influence that periodontal disease has on the severity of diabetes. Various studies have evaluated the effect that periodontal therapy has on glycemic control in patients with type 2 diabetes and periodontal disease. The results of studies about the efficacy of scaling and root planing among diabetics, and the influence which these procedures have upon the reduction of HbA1c levels, vary. Some studies have featured overall reductions of 0.29% to 0.4% of HbA1c levels after root planing and scaling with a 3-4 month post-therapy duration (Duda- Sobczak, 2018; Madianos & Koromantzos, 2018). Results of a 2013 randomized controlled trail among type II diabetic patients found no improvement of glycemic control after scaling and root planing, and a 2018 study among type I and type II diabetic patients found no significant improvement in glycemic control. (ADA, 2019). This is an area which needs continued research in an era in which the oral-systemic continuum is receiving increasing interest and attention. Cytokines are another sign of the connection between diabetes and oral disease. They are secreted from the chronically inflamed gingival tissues involved in periodontal disease, and are associated with insulin resistance (Acharva, 2016). The concept of a relationship between oral disease and systemic disease is not new. Near the end of the 19th century, Willoughby D. Miller presented his theory of focal infection. He believed that microorganisms from the mouth could enter the bloodstream to cause systemic diseases and degenerative conditions (Miller, 1891). As a result of improved scientific investigative techniques, contemporary research increasingly supports the idea that periodontal disease and systemic diseases such as diabetes mellitus have a bidirectional relationship. Several pathophysiological mechanisms govern this bidirectional relationship. Pathogenic periodontal bacteria once were considered the sole factor in the initiation and progression of periodontal disease. However, progressive research and studies have revealed that although bacteria play a pivotal role in the initiation of periodontal disease, factors such as genetics, tobacco use, and the host immune-inflammatory response also influence the progression and clinical outcome of periodontal disease (American Academy of Periodontology, 2021). An intact gingival epithelium is a critical barrier to the dissemination of pathogenic periodontal bacteria into the
systemic circulation. During the progression of periodontal disease, the gingival epithelium becomes ulcerated and exposes the underlying connective tissues and capillaries to the pathogenic periodontal bacteria. The chronic inflammation within the gingival sulcus, and its increased perfusion of blood, facilitates the means by which pathogenic bacteria and their toxins have access to the systemic circulation (ADA, 2019). Several mediators of inflammation, such as interleukin (IL)-6, tumor necrosis factor (TNF)-a, and prostaglandin E2, are released via the host immune-inflammatory response (Duda-Sobczak et al., 2018). Both TNF-a and IL-6 can impair intracellular insulin signaling, and thus can contribute to insulin resistance. Cytokines that are released in response to the chronic inflammation associated with periodontal disease can also increase insulin resistance (Shi et al., 2019). The extended hyperglycemic state of types 1 and 2 diabetes helps form advanced glycation end products (AGEs). The AGEs bind to a specific cellular receptor known as the receptor for AGE (RAGE). The AGE-RAGE coupling has been shown to induce a significant and sustained inflammatory response within the gingival tissues (Franco et al., 2017). The AGE-RAGE combination has also been associated with the progressive loss of the soft and hard tissues of the periodontium that results from advancing periodontal disease (Ilea et al., 2018). The reparative ability within the periodontal tissues is also compromised by the AGE-RAGE coupling (Wang et al., 2020). Osteoblasts are the cells that produce bone. Within the structures of the periodontium, they produce the alveolar bone that supports the teeth. The differentiation, growth, and function of the osteoblasts are compromised in the presence of the AGEs (Wang et al., 2020). Thus, AGEs hamper the ability of new bone to replace old bone within the periodontium. Moreover, diabetes types 1 and 2 can compromise the immune system, reducing its ability to respond to the influx of the periodontal pathogenic bacteria. The polymorphonuclear leukocytes, especially the neutrophils, have a critical role in the immune response to periodontal pathogenic organisms (Xiao et al., 2017). The process whereby neutrophils are drawn via a chemical trail to a pathogenic organism is known as chemotaxis . In patients with diabetes, the collective ability of the neutrophils to locate, phagocytize (engulf), and destroy pathogenic periodontal bacteria is compromised (Vesna, 2018). Thus, decreased host resistance can facilitate the advancement of the periodontal pathology. The polymorphonuclear leukocytes and other cells of the immune system, such as monocytes and macrophages, also have RAGEs. The AGE-RAGE coupling that involves these cells of the immune system thus impairs their ability to function properly against pathogenic periodontal bacteria (Asadipooya & Uy, 2019). Continued research in the bidirectional relationship between diabetes mellitus and periodontal disease is needed to reveal the exact mechanisms by which these diseases exert their influence on each other. Such knowledge will help in the development of methods by which this joint destructive influence can be treated.
PERIODONTAL MANIFESTATIONS OF DIABETES
The potential periodontal manifestations of diabetes are many, and they may include gingivitis and features reflecting the Attachment loss The relationship between diabetes and loss of attachment is statistically significant, with the level of glycemic control being a critical factor (Agarwal & Baid, 2017). Several studies have indicated that the risk of clinical attachment loss is three times greater among diabetics compared to nondiabetic individuals (Susanto et al., 2020). Patients with type 2 diabetes mellitus also have a statistically significant higher number of teeth
destruction of the periodontium, such as attachment loss and proximal bone loss.
with attachment loss compared to non-diabetic subjects. When glycemic control worsens, there is a corresponding and statistically significant increase in the amount of clinical attachment loss. Longer durations of inadequate glycemic control will exacerbate the levels of clinical attachment loss (Singh et al., 2019).
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