Diabetes mellitus is the most common endocrine disorder, characterized by an inability of the body’s cells to utilize glucose. It is a complex metabolic disorder characterized by chronic hyperglycemia. It has varying degrees of systemic and oral complications, depending on the extent of metabolic control, presence of infection and underlying demographic variables.  The cardinal feature of this condition is increased blood glucose level, resulting from decreased production of insulin, insulin dysfunction or lack of insulin receptor responsiveness at target organs, such as the skeletal muscles and liver. Alteration in lipid and protein metabolism is also seen. Diabetes mellitus is a disease of metabolic dysregulation, primarily of carbohydrate metabolism, characterized by hyperglycemia (elevated blood sugar). 

Classification and Pathophysiology

In 1997, American Diabetes Association provided the current classification

1.   Type I diabetes: formerly insulin dependent diabetes

2.   Type II diabetes: formerly non- insulin dependent diabetes

3.   Gestational diabetes

 Type I Diabetes (IDDM)

1.   Cell mediated autoimmune destruction of the insulin producing beta cells of islets of langerhans in the pancreas, which result in insulin deficiency.

2.   Accounts for 5% to 10% of all cases of diabetes

3.   Occurs most often before 30 years, known as juvenile diabetes

4.   Most people with type I diabetes are normal weight or thin in stature

5.   This type of diabetes results from a lack of insulin production and is very unstable and difficult to control.

6.   It has a marked tendency toward ketosis and coma, and requires injectable insulin to be controlled.

7.   Patients with type I diabetes present with the symptoms traditionally associated with diabetes, including polyphagia, polydipsia, polyuria, and predisposition to infection.

8.   The initiation of pathogenesis however precedes the abrupt clinical onset of diabetes by several years, thus there is a prediabetic period during which the standard biochemical tests for diabetes are of little value.

9.   HLA genotyping and detection of complement fixing islet cell antibodies are of greater value.

Type II Diabetes

  1. Much more common, account for 90% of all diabetic cases.
  2. Type II diabetes commonly leads to not only hyperglycemia but also to hypertension, dyslipedemia, central obesity, and atherosclerosis.
  3. The Pathophysiology of type II diabetes is different from type I diabetes. Type II diabetes is characterized by three major abnormalities-
1.    Peripheral resistance to insulin, particularly in muscles
2.    Impaired pancreatic insulin secretion
3.    Increase glucose production by liver

Type II has a stronger genetic component as compared to type I diabetes, with a rate of upto 90% in identical twins.

Unlike the sudden onset of clinical symptoms of type I diabetes, type II diabetes may remain undiagnosed for years. Thus it is estimated that about half of all patients with type II diabetes are unaware of this condition.

Gestational Diabetes

Gestational diabetes usually develops during third trimester of pregnancy but can occur earlier. An increase prevalence of gestational diabetes is seen in women who are overweight, more than 25 years of age, have a family history of diabetes. This disorder appears to have similar Pathophysiology as type II diabetes i.e. it is strongly associated with insulin resistance.

Oral Manifestations of Diabetes

Numerous oral changes have been described in diabetes. Oral complications of diabetes include:

Alteration in salivary flow and constituents, increase incidence of infection, burning mouth, altered wound healing, and increased prevalence of severity of periodontal disease.

1.   Xerostomia and parotid gland enlargement may occur in the diabetic individual.

2.   Diabetic patient may complain of burning mouth syndrome associated with decreased salivary flow. Burning mouth or tongue and altered taste sensation have been reported in diabetes mellitus patients, probably as a result of Xerostomia and/or secondary candidiasis. It has also been suggested, but not clearly established, that burning tongue may occur in patients with severe diabetes mellitus as a result of diabetic neuropathy

3.   Altered taste sensation may occur as a result of Xerostomia and candidiasis; as a direct result of diabetic neuropathy; or by medications that may induce alterations in glucose receptors within taste buds.

4.   Dry mucosal surfaces are easily irritated and often provide a favourable substate for the growth of fungal organisms. The incidence of candidiasis may be increased in patients with diabetes ( Fisher BM,1987).

5.   Dental caries rate may also be altered in diabetes. An increased caries rate may be associated with decreased salivation or with increase glucose concentration in saliva & GCF.

6.   Medications used to manage blood glucose levels, can have xerostomic effects. Therefore, Xerostomia may result not from the diabetic condition itself but from medications taken by the patients.

7.   An association between oral lichen planus and diabetes mellitus has been suggested but not confirmed. Although some reports indicate an increased frequency of oral lichen planus among diabetes mellitus patients, it appears likely that this may represent a lichenoid drug reaction to medications used in treatment of diabetes mellitus or its associated complications (Bagan-Sebastian JV,1992) . 

The rapidly accumulating data regarding the effect of diabetes mellitus on the oral cavity suggest that oral tissues are adversely affected by uncontrolled diabetes mellitus similarly to other body systems.

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