The epidemic nature of diabetes mellitus in different regions is reviewed. The Middle East and North Africa region has the highest prevalence of diabetes in adults (10.9%) whereas, the Western Pacific region has the highest number of adults diagnosed with diabetes and has countries with the highest prevalence of diabetes (37.5%). Different classes of diabetes mellitus, type 1, type 2, gestational diabetes and other types of diabetes mellitus are compared in terms of diagnostic criteria, etiology and genetics. The molecular genetics of diabetes received extensive attention in recent years by many prominent investigators and research groups in the biomedical field. A large array of mutations and single nucleotide polymorphisms in genes that play a role in the various steps and pathways involved in glucose metabolism and the development, control and function of pancreatic cells at various levels are reviewed. The major advances in the molecular understanding of diabetes in relation to the different types of diabetes in comparison to the previous understanding in this field are briefly reviewed here. Despite the accumulation of extensive data at the molecular and cellular levels, the mechanism of diabetes development and complications are still not fully understood. Definitely, more extensive research is needed in this field that will eventually reflect on the ultimate objective to improve diagnoses, therapy and minimize the chance of chronic complications development.
Diabetes mellitus is a metabolic disorder characterized by relative or absolute insufficiency of insulin and resultant disturbances of carbohydrate metabolism. The major function of insulin is to counter the concerted action of a number of hyperglycemia-generating hormones and to maintain low blood glucose levels [1-4].
Epidemiology
Almost 20% of adult older than 65-year-old have DM. A dental practice serving an adult population of 2,000 can expect to encounter 40-80 persons with diabetes, about half of whom will be unaware of their condition.
Etiologic Classification of DM
There are two main and some other types of Diabetes Mellitus:
Type 1, insulin-dependent or juvenile-onset diabetes (IDDM)
Type 2, non-insulin-dependent or adult-onset diabetes (NIDDM)
Other specific types
Type 1 (IDDM)
Autoimmune destruction of the insulin-producing beta cells of pancreas. It is present in about 5-10% of DM cases. Commonly occurs in childhood and adolescence. Absolute insulin deficiency and high incidence of severe complications. It is prone to autoimmune diseases (Grave’s, Addison, Hashimoto’s thyroiditis) [5].
Type 2 (NIDDM)
It results from impaired insulin function (insulin resistance). Constitutes 90-95% of DM cases (Figure 1 and 2). Specific causes of this form are unknown. Risk factors include: age, obesity, alcohol, diet, family history and lack of physical activity, etc. (Table 1).
Other Specific Types
Genetic defects of beta-cell functions
Decrease of exocrine pancreas
Endocrinopathies
Drug or chemical usage
Infections

Figure 1: Factors Causing DM

Figure 2: Main symptoms of DM
Table 1: Comparison of DM types
Parameters | Type 1 | Type 2 |
| Clinical | onset <20 years, normal weight, decreased blood insulin, anti-islet cell antibodies, ketoacidosis common | onset >30 years, obesity, normal or increased blood insulin, no anti-islet cell antibodies, ketoacidosis rare |
| Genetics | human leukocyte antigen (HLA)-D linked | No HLA association |
| Pathogenesis | autoimmunity, immunopathologic mechanisms, severe insulin deficiency | insulin resistance, relative insulin deficiency |
| Islet Cells | insulitis early, marked atrophy and fibrosis, severe beta-cell depletion | no insulitis, focal atrophy and amyloid deposits, mild beta-cell depletion |
Table 2: Complications of DM
| Major organ/system | Long term complications |
| Cardiovascular system: heart, brain, blood vessels | Myocardial infarction; atherosclerosis; hypertension; microangiopathy; cerebral vascular infarcts; cerebral hemorrhage |
| Pancreas | Islet cell loss: insulitis (type 1), amyloid (type 2) |
| Kidneys | Nephrosclerosis; glomerulosclerosis; arteriosclerosis; pyelonephritis |
| Eyes | Retinopathy, cataracts; glaucoma |
| Nervous system | Autonomic neuropathy; peripheral neuropathy |
| Peripherals | Peripheral vascular atherosclerosis; infections; gangrene |
Table 3: Drugs and their course of action in DM
| Drug Class | Generic (Trade) Drug Names* | Action |
| Sulfonylureas | Chlorpropamide (Diabinese); Glipizide (Glucotrol); Glyburide (DiaBeta, Micronase); Glimepiride (Amaryl) | Stimulate insulin secretion |
| Meglitinides | Repaglinide (Prandin) | Stimulate insulin secretion |
| Biguanides | Metformin (Glucophage) | Decrease glycogenolysis and hepatic glucose production |
| a-Glucosidase Inhibitors | Acarbose (Precose); Miglitol (Glyset) | Decrease gastro-intestinal absorption of carbohydrates |
| Thiazolidinediones | Rosiglitazone maleate (Avandia); Pioglitazone (Actos) | Enhance tissue sensitivity to insulin |
*This information is for educational purposes only, and does not constitute medical advice. Please consult a healthcare professional for any medical concerns or treatment options.
Gestational Diabetes Mellitus (GDM)
Defined as any degree of glucose intolerance with onset or first recognition during pregnancy. Around 4% risk increases in pregnancy [6].
Complications
People with DM have an increased incidence of both microvascular and macrovascular complications (Table 2).
Diagnosis
A casual plasma glucose level of 200 mg/dL or greater with symptoms presented. Fasting plasma glucose level of 126 or greater (Normal <100 mg/dL). Oral glucose tolerance test (OGTT) value in blood of 200 mg or greater. ADA recommend >45-year-old screened every 3 years [3,7].
Medical Management
Objective: Maintain blood glucose levels as close to normal as possible
Good glycemic control inhibits the onset and delay of type 1 DM, similar in type 2 DM
Exercise and diet control
Insulin: rapid, short, intermediate, long acting
Oral antidiabetic agents (Table 3)
Oral Manifestations and Complications
No specific oral lesions associated with diabetes. However, there are a number of problems by presence of hyperglycemia.
Periodontal Disease
Microangiopathy altering antigenic challenge and altered cell-mediated immune response and impaired of neutrophil chemotaxis. Increased Ca+ and glucose lead to plaque formation. Increased collagen breakdown.
Salivary Glands
Xerostomia is common, but reason is unclear. Tenderness, pain and burning sensation of tongue. May cause secondary enlargement of parotid glands with sialosis [4,6,8,9].
Table 4: Dental management of DM patient
| Potential complication | Preventive measures |
Hypoglycaemia | Thorough medical history and consultation with physician to assess glycaemic control, disease severity and medications with hypoglycaemic potential. Monitoring of blood glucose level and dietary intake before treatment. Avoidance of peak activity periods of insulin or oral antidiabetic medications. Recognition of signs and symptoms of low blood glucose level, and timely administration of carbohydrate source (oral, intramuscular, intravenous) [8]. |
Infection and Delayed Wound Healing | Frequent dental visits to assess plaque control and to identify risk factors for periodontal disease, caries and oral candidiasis. Postoperative antibiotic therapy if warranted. Avoidance of smoking. |
Salivary Gland Dysfunction and Oral Burning | Maintenance of adequate oral hydration (water, ice chips, saliva substitutes, sugar-less gum) Restriction of caffeine and alcohol intake [5,7]. |
Dental Caries
Increase caries prevalence in adult with diabetes (xerostomia, increase saliva glucose). Hyperglycemia state shows a positive association with dental caries.
Increased Risk of Infection
Reasons unknown, but macrophage metabolism altered with inhibition of phagocytosis. Peripheral neuropathy and poor peripheral circulation. More include [9];
Immunological deficiency
High sugar medium
Decrease production of Antibodies
Candidal infection are more common and adding effects with xerostomia
Delayed Healing of Wounds
Due to microangiopathy and ultilisation of protein for energy, may retard the repair of tissues. Increase prevalence of dry socket.
Miscellaneous Conditions
Pulpitis: degeneration of vascular
Neuropathies: may affect cranial nerves (facial)
Drug side-effects: lichenoid reaction may be associated with sulphonylureas (chlopropamide)
Ulcers
Dental Management Considerations
To minimize the risk of an intraoperative emergency, clinicians need to consider some issues before initiating dental treatment, like [10];
Medical history: Take history and assess glycemic control at initial appointment
Glucose levels
Frequency of hypoglycemic episodes
Medication, dosage and times
Consultation
Scheduling of Visits
Usually, one should take morning appointments with taking care that appointments do not coincide with peak activity [11].
Diet
Ensure that the patient has eaten normally and taken medications as usual.
Blood Glucose Monitoring
It must be measured before beginning (<70 mg/dL).
Prophylactic Antibiotics
Established infection
Pre-operation contamination wound
Major surgery
During Treatment
The most complication of DM occur is hypoglycemia episode.
After Treatment
Infection control
Dietary intake
Medications: salicylates increase insulin secretion and sensitivity – avoid aspirin
Diabetes mellitus is growing to epidemic proportions, leading to devastating complications if not treated well. There are many challenges in the successful treatment of diabetes mellitus because of personal and economic costs incurred in diabetes therapy. Its long-term consequences translate into enormous human suffering and economic costs. However, comprehensive diabetes care can delay the progression of complications, maximize the quality of life, and minimize healthcare expenditure.
Insulin is indicated for all types of diabetes mellitus. However, diet, exercise, and diabetes education remain the essential components of diabetes management.
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American Diabetes Association. American Diabetes Association, n.d.
Diabetes – Insulin Initiation. University Hospitals of Leicester NHS Trust, May 2008.
American Diabetes Association. “Clinical Practice Recommendations: 2002.” Diabetes Care, vol. 25, suppl. 1, 2002, pp. S64–S68.
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