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Kendra Bruggink
When the body is suffering from diabetes, the structure of the blood vessels
is altered. This affects the blood flow, and eventually may weaken the gums and
bone which surround the teeth.
Bacteria associated with periodontal infections thrive on sugars, such as
glucose. Hyperglycemia (high blood sugar) in uncontrolled diabetics results in
increased glucose in the gingival crevicular fluid and blood. The high levels of
glucose in the fluid can help the pathogenic bacteria survive and multiply,
increasing the progression of periodontal disease.
In periodontal disease the presence of gram-negative bacteria in the plaque
biofilm initiate the bodies inflammatory response. Biochemical mediators are
attracted to the site. The mediators which play a role in both diabetes and
periodontal disease include polymorphonuclear leukocytes (PMNs), cytokines IL-8,
IL-6 and the tumor necrosis factor-a (TNF-a), prostaglandin E2 (PGE2), and the
matrix metalloproteinases (MMPs). The PMNs play an important role in the
maintenance of gingival and periodontal health. However it is found that in patients
with diabetes the function of PMNs is reduced and the chemotaxis of the PMNs to
the site of inflammation is defective. When the bacteria is not removed an increase
in the amount of biochemical mediators, such as cytokines, PGE2 and MMPs are
sent to the site of infection. The high concentration of these biochemical mediators
leads to the breakdown of tissue and alveolar bone over time.
Diabetic patients with controlled blood sugar levels (good glycemic control)
can prevent or delay the onset and slow the progression of periodontal disease.
Patients with uncontrolled diabetes have higher risks for infections and poor wound
healing. It is estimated that patients with poor glycemic control are at a 2-3 times
Kendra Bruggink
greater risk for developing a periodontal infection than non-diabetic patients. These
patients also have a poor response to nonsurgical and surgical periodontal
therapies, a more rapid recurrence of dry pockets, and less favorable long term
response to treatment. This is why it is key for diabetic patients to achieve and
maintain same level of glycemic control as patients without diabetes.
References
Gehrig, J., & Willmann, D. (2011). Foundations of periodontics for the dental
hygienist (3rd ed., pp. 173-176, 311-312). Philadelphia: Wolters Kluwer
Health/Lippincott Williams & Wilkins.
Herring, M., & Shah, S. (2006). Periodontal Disease and Control of Diabetes Mellitus. The
Journal of the American Osteopathic Association, 106, 416-421. Retrieved April 18, 2015, from
http://jaoa.org/article.aspx?articleid=2093345
Moritz, A., & Mealey, B. (n.d.). PERIODONTAL DISEASE, INSULIN RESISTANCE, AND
DIABETES MELLITUS: A REVIEW AND CLINICAL IMPLICATIONS. Retrieved April 18, 2015, from
http://www.dentistryiq.com/articles/gr/print/volume-1/issue-2/literature-review/periodontal-diseaseinsulin-resistance-and-diabetes-mellitus-a-review-and-clinical-implications.html
Southerland, J., Taylor, G., & Offenbacher, S. (2005). Diabetes And Periodontal
Infection: Making The Connection. Clinical Diabetes, 23(4), 171-178. Retrieved April
18, 2015, from http://clinical.diabetesjournals.org/content/23/4/171.full