Endocrine disorders 2 – diabetes mellitus
- • Introduction to diabetes mellitus
- • Type 1 and Type 2 diabetes mellitus
- • Systemic and oral signs and symptoms of diabetes
- • Diabetes, inflammation and periodontal disease
- • Management of diabetes mellius
- • Management of the diabetic patient in the dental clinic
- • Be aware that diabetes mellitus is a condition associated with an absolute or relative deficiency of insulin activity
- • Be aware that diabetes mellitus is not a single condition, and that type 2 diabetes, the more prevalent form, is primarily a “lifestyle” disease
- • Be familiar with the oral signs of diabetes mellitus, as there is significant potential for dental practitioners to pick up undiagnosed type 2 diabetes
- • Be familiar with the link between diabetes (both type 1 and 2) and periodontitis, both in terms of prevalence and severity
- • Be aware that patients with diabetes mellitus can significantly benefit from good oral health management
- • Be familiar with the strategies that should be used to optimise the treatment of the diabetic patients in the dental clinic
Diabetes mellitus represents the most significant endocrine disorder. In particular, type 2 diabetes is considered the fastest-growing chronic disease, being responsible for approximately 5 million deaths per annum. The term diabetes literally means ‘going through’ or overflow, and is used to describe conditions where large volumes of urine are excreted. The term mellitus means ‘sweet’ or ‘honey-like’, referring to the presence of glucose in the urine. Diabetes mellitus is associated with a lack of secretion or a lack of activity of the hormone insulin, which, in uncontrolled diabetes, results in raised blood glucose levels.
It has been long recognized that there is a link between diabetes mellitus and periodontal disease, and it has been suggested that periodontitis should be considered a formal complication of diabetes. All diabetic patients are at risk of poor oral health and periodontal disease, but the problem is greater in those with poor diabetic control. Importantly, this is a two-way link, with periodontal disease impacting on diabetic control. Because of the impacts of diabetes on oral health, dentists are well placed to pick-up undiagnosed diabetes. Other issues that need to be considered in relation to diabetes mellitus, is that your diabetic patients may be more prone to oral infections. In addition, as a dentist, you have to be able to manage diabetic emergencies, and develop strategies to reduce the risk of such events. The risk of diabetic emergencies is higher in those patients receiving insulin therapy.
Diabetes mellitus is a condition associated with an absolute or relative deficiency of insulin activity. One of the functions of the hormone insulin is, along with the hormone glucagon, to regulate blood glucose levels. Insulin promotes the uptake of glucose by cells, thereby lowering blood glucose levels. As mentioned, the term diabetes relates to one of the key symptoms, namely polyuria. When uncontrolled, sufferers will produce large volumes of urine, which, unlike normal urine, contains glucose. Normally all of the glucose present in the glomerular filtrate produced by the kidneys is reabsorbed back into the bloodstream. However, if blood glucose levels are too high (>180 mg/ml), the active transport mechanism becomes saturated, and glucose will be lost in the urine. The presence of glucose in the urine has an osmotic effect, drawing water out with it, thereby causing polyuria. Diabetes mellitus should not be confused with diabetes insipidus, where the polyuria is caused by a deficiency of the hormone anti-diuretic hormone (ADH), or vasopressin. As a result of the polyuria, sufferers may also complain of excessive thirst due to dehydration, causing them to drink large amounts of fluid (polydipsia).
Diabetes mellitus is a disorder of insulin availability, but it is not a single disease. Its classification is based around the cause of the problem. The most basic classification of the disorder is indicated by the terms ‘type 1’ and ‘type 2’ diabetes. While type 1 diabetes represents what most people envisage as the problem, it accounts for less than 10% of sufferers. The much larger, and steadily growing proportion of sufferers are classified as having type 2 diabetes.
Type 1 diabetes mellitus
Type 1 diabetes is characterized by the destruction of the insulin-producing beta cells in the pancreas, and is divided into two subtypes, type 1A and type 1B. In type 1A diabetes, which was formerly referred to as juvenile-onset diabetes, there is an immune-mediated destruction of the insulin-producing beta cells in the pancreas. This autoimmune reaction results in an absolute lack of insulin, elevated blood glucose levels, and the breakdown of body fats and proteins as an alternative energy source. Type 1B, or idiopathic, diabetes describes cases where there is beta cell destruction, but there is no evidence of an autoimmune reaction. With type 1 diabetes, there is strong evidence for a genetic predisposition involving multiple genes, particularly genes that regulate normal immune responses. The onset of the symptoms of diabetes may occur quite suddenly, normally when the beta-cell mass has been reduced by around 80%. However, type 1 diabetes-associated antibodies may exist for years before the onset of the signs of diabetes. As such, there is a potential for predictive testing, as well as prevention and early control.
The absolute loss of insulin function with type 1 diabetes has marked metabolic effects. In uncontrolled diabetes, a person is unable to transport glucose into fat and muscle cells. As a result, these cells are ‘starved’ of glucose, and fat and protein breakdown is increased in order to provide an alternative source of energy. Naturally, insulin inhibits lipolysis, while a lack of insulin activates hormone-sensitive lipase. This leads to the release of significant quantities of free fatty acids into the blood stream, and they become the main energy substrate in most tissues. However, low circulating insulin levels combined with high free fatty acid levels leads the liver to produce high levels of acetoacetic acid which cannot be taken and metabolized by peripheral tissues. Some of the acetoacetic acid is converted into acetone and β-hydroxybutyric acid. This combination of chemicals is commonly referred to as ketone bodies, and causes the problem of ketoacidosis. Ketoacidosis is primarily associated with type 1 diabetes. In severe, uncontrolled diabetes, high levels of ketone bodies can cause severe acidosis, which may lead to a diabetic coma and potentially death.
Individuals with type 1 diabetes require insulin-replacement therapy in order to reverse catabolism, control blood glucose levels, and prevent ketoacidosis.
Type 2 diabetes mellitus
Type 2 diabetes is primarily considered a ‘lifestyle’ disease. Unlike type 1 diabetes, where there is an absolute deficiency of insulin, in type 2 diabetes there is hyperglycaemia associated with a relative insulin deficiency. It is a disorder of both insulin levels (beta cell dysfunction) and insulin function (insulin resistance). Insulin levels may be high, normal or low, but there is insufficient insulin activity to meet the body’s needs. In the presence of insulin resistance, insulin cannot function effectively, and hyperglycaemia results. Type 2 diabetes is not associated with autoantibodies. However, with time, and without effective intervention, type 2 diabetes may progress to a stage where insulin-replacement therapy is required.
Lifestyle plays a big role in the development of type 2 diabetes, with approximately 80% of sufferers being overweight. Individuals with upper body obesity (central obesity) are at greater risk. Previously type 2 diabetes was found more in the older population, but it is becoming more common in obese adolescents. It is a progressive condition associated with insulin resistance. That mismatch between insulin supply and demand, initially produces increased beta cell secretion of insulin (hyperinsulinaemia). However, with time, the insulin response declines because of increasing beta cell dysfunction. There are a number of possible reasons for beta cell dysfunction, including cell exhaustion due to chronic stimulation, cell desensitization due to hyperglycaemia, apoptosis of beta cells and cell toxicity caused by increased free fatty acid levels. Initially blood glucose levels are only high after a meal (post-prandial), but eventually fasting levels will also rise. However, most people with type 2 diabetes do not have an absolute insulin deficiency, and therefore are less prone to ketoacidosis.
Insulin resistance not only contributes to hyperglycaemia, but also plays a role in other metabolic abnormalities. These problems include high plasma triglyceride levels, low HDL levels, hypertension, systemic inflammation and vascular disease. These abnormalities are referred to as ‘insulin resistance syndrome’ or ‘metabolic syndrome’.