Diabetes

  In the interval between 1990 and 1998 the Atlanta based Centers for Disease Control reports a thirty-three percent increase in diagnosed cases of Diabetes.  Currently it is estimated that there are seven million cases of undiagnosed Diabetes in the U.S. population, most of them Type II (non-insulin dependent) Diabetes.  Diabetes has become the 4th leading cause of death in the United States.  The average dental practice will see six patients with Diabetes and one undiagnosed case in every 100 patients.  In patients with poor control of sugar levels, moderate to advanced Periodontitis left untreated can make glycemic control more difficult.  Unfortunately, as reported in the ADA Journal recently, Type I diabetics are no more preventive behavior oriented nor do they have more information about the oral health complications of Diabetes than the general population.  Consequently, diabetic intraoral changes and accelerated periodontal disease may result.  This edition of the newsletter summarizes recent advances in Diabetes research, identifies current medication protocols for Type II Diabetes and suggests ways to assist your diabetic patients in achieving better oral health.

 

    Type I Diabetes (formerly called insulin-dependent Diabetes Mellitus, IDDM) is caused by the destruction of the B-cells of the pancreas.  These B-cells are lost when a genetically predisposed person experiences an autoimmune response to a sensitizing event, such as a viral infection.  Patients with Type I Diabetes are generally diagnosed early in life due to overt symptoms and extensive fluctuations in blood sugar levels.  Insulin is mandatory as the B-cells are no longer functional and no insulin is produced.

 

    In distinction, Type II (formerly non-insulin dependent Diabetes Mellitus, NIDDM) Diabetes results when either insulin production is defective or the cell receptors for insulin are dysfunctional.  The term for this state is insulin resistance.  Eighty percent of individuals with Type II Diabetes are overweight, and waistline obesity predominates.  Other risk factors include a familial history of Diabetes; races of African, Hispanic, Polynesian, Asian or Native American origin; over 45 years of age, hypertension; serum triglyceride levels over 250 mg/dl; previous history of pregnancy-associated (gestational) Diabetes; or previous tests with impaired fasting blood glucose levels.

 

    According to the American Diabetes Association in their position statement on screening for Type II Diabetes the cutoff values for a preliminary diagnosis of Type II Diabetes are listed below. 

 

Preliminary Diagnosis of Type II Diabetes

1. Fasting plasma glucose over 126 mg/dl

2. Fasting whole blood glucose over 110 mg/dl

3. Random (non-fasting) capillary blood glucose over       140 mg/dl

    

Blood glucose monitors are available which do random capillary whole blood glucose determinations, can be purchased for office use, but will require periodic calibration with a commercial lab.  A positive history of risk factors, symptoms of polyphagia, polydipsia and polyuria; and/or intraoral changes inconsistent with the local factors present should make the practitioner suspicious.  Random capillary blood glucose testing could be used as a second level screening tool with physician referral in the event of a positive blood glucose.  A preliminary assessment of Diabetes must be confirmed by a second determination, most often using a fasting plasma glucose determination.

 

    As noted earlier in this newsletter, insulin resistance is the prime characteristic of Type II Diabetes.  Type II Diabetics also have one or more genetic irregularities that reduce the capacity of pancreatic islet cells to produce insulin but do not cause insulin failure at an early age.  However, over time and with poor management of their glycemic control, these patients also become insulin dependent.  Current treatments are aimed at extending the time until insulin dependence develops by increasing insulin production or reducing insulin resistance. 

Antihyperglycemic Agents

Generic	Trade Name	Mechanism
Repaglinide	Prandin	Increases insulin secretion
Sulfonylureas	Amaryl Glucotrol XL Glynase	Increases insulin secretion
Alpha-Glucosidase Inhibitors	Precose Glyset	Delays intestinal absorption of complex carbohydrates
Metformin	Glucophage	Insulin sensitizer- primary action in the liver
Thiazolidinedione	Rezulin Troglitazone	Insulin sensitizer- primary action in muscle

   

The protocol for therapy is now diet and exercise first, oral agents for the control of insulin resistance second, and oral agents plus intermediate acting insulins upon pancreatic Beta cell depression.  Knowing protocols can help the practitioner assess the need for special care in the dental office.  The lower the protocol relative to insulin resistance the less cautions are required for treatment with the exception noted later in this newsletter.  Diabetics are also two to four times as likely to experience myocardial infarction and for this reason many Type II Diabetics are on cholesterol lowering medications.

   

 The oral medications that your patients report taking for Diabetes act against insulin resistance by one of three mechanisms: increasing insulin secretion, inhibiting the absorption of complex carbohydrates from the intestine, or increasing the sensitivity of cell receptors to insulin. Sulfonylurea use in older individuals more often results in hypoglycemia and makes patients less tolerant of stress and more prone to syncope.  These patients should take medications far enough in advance of their visits that immediate hypoglycemia from rising blood levels of the drug is not probable.  Ideally, Type II diabetics will monitor their blood glucose levels prior to appointments, be sure to eat regularly and report stressful life episodes.  A high sugar content soda can be kept chilled for those patients who may develop hypoglycemia in the office.

   

As reported by Westfelt and co-workers in a five year study of periodontal therapy in diabetics, well controlled diabetics can achieve and sustain successful periodontal treatment results.  In this study, patients received stringent maintenance care and achieved high standards of oral hygiene.

   

 However, when healing tissues in the diabetic experience an inflammatory stimulus such as heavy plaque accumulation impaired tissue responses may occur.  Tissue repair then results in an exuberant growth at sites where connective tissue is exposed.  The gingiva take on a reddened, highly vascular appearance with fine networks of new vessels at or near the denuded epithelial surface.  Tissue appears to be "bubbling out" of the normal contours, bleeds upon the slightest probing and lack organization.

  

  Patients avoid strenuous home care in these areas due to the bleeding, but diligent plaque removal, as noted in the Westfelt study, is required.  Previously, based on observation of amputation specimens from diabetics, it was concluded that the oxygen supply to wounds was hampered by a thickening of the wall of small blood vessels which was irreversible.  Research over the past ten years has established that the poor perfusion of wounds is due to a lessened exchange of nutrients but the problem lies in the red blood cell rather than the wall of the capillaries supplying the wound site, as was previously believed. (Vessel disease in diabetics appears to happen in larger vessels from the accumulation of atherosclerotic plaques in the vessel walls.)  In the diabetic the cell wall of the red blood cell is stiffened because the red blood cell membrane protein, spectrin, becomes glycosated.  This results in the cell wall being less deformed and the red blood cells stagnated as they move through capillaries.  As a result, the capillaries have greater blood viscosity and increased perfusion pressure.  Patients who are on diabetic medications and take diuretics for high blood pressure may see a worsening of this problem in wound repair.  Secondly, hyperglycemia will increase the rate of collagen breakdown by favoring the concentration of collagen degrading enzymes in the tissues which can result in a disorganized granulation tissue during repair.  It may well be that the local response from plaque accumulation is dictated by the chemistry of the local site rather than an all or none process.  When this response occurs, the clinician needs to employ more stringent mechanical plaque control and, if the tissues are unresponsive, soft tissue curettage.

   

 One other finding may be noteworthy in this review.  Diabetics of longer standing do have neurological changes, particularly those who have become insulin dependent.  These changes may occur as a result of fluid increases within the axon sheaths of nerves.  Fluid pressure can result in referred or idiosyncratic discomfort.  A common place for this pain intraorally is the lower anterior segment and patients express it as a deep within the bone "ache."  When lower anterior discomfort of unknown origin is combined with other risk factors the practitioner may want to screen for Type II Diabetes.

   

 We hope that this review has been informative and that it aids you in understanding your diabetic patients medications and management.  Your patients will surely appreciate your concern and awareness of their medical state.  If we can be of further assistance in the periodontal management of your medically compromised patients, please do not hesitate to contact the office.