[[ REFERENCES ]
Definition
and Classification
Incidence and Prevalence
Etiology
Pathophysiology
Systemic Complications
Oral Complications
Dental Management of the Diabetic Patient
Signs and symptoms of acute hypoglycemia
Signs and symptoms of diabetic ketoacidosis
References
DEFINITION
AND CLASSIFICATION
Diabetes mellitus is characterized by increased levels of glucose in the
blood and abnormalities in the metabolism of lipid protein induced by
diminished levels or total absence of insulin. Additionally there is a
vascular aspect to diabetes mellitus which comprises atherosclerosis and
microangiopathy especially of kidneys and eyes.
Of all the best known systemic diseases, diabetes has been the one most
frequently blamed as a risk agent for periodontal disease and other oral
pathologic disorders. Therefore, every dentist should have a basic understanding
of the incidence, etiology, systemic implications and possible oral associated
findings of diabetes.
The National Diabetes Data Group in 1979 classified diabetes as:
| 1. | Diabetes mellitus |
| a. | Type I - insulin-dependent diabetes mellitus (IDDM) |
| b. | Type II - non-insulin-dependent diabetes mellitus (NIDDM) |
| c. | Type III - other types of diabetes |
| Pancreatic disease | |
| Hormonal disease | |
| Drugs - thiazide diuretics, liithium salts | |
| Others | |
| 2. | Impaired glucose tolerance (IGT) |
| a. | Nonobese IGT |
| b. | Obese IGT |
| c. | IGT associated with other conditions |
| Pancreatic disease | |
| Hormonal disease | |
| Drugs | |
| 3. | Gestational diabetes mellitus (GDM) |
| 4. | Previous abnormality of glucose tolerance (pre-AGT) |
| 5. | Potential abnormalities of glucose tolerance (pot-AGT) |
This classification was adopted by the World Health Organization (WHO) and 1980 and slightly modified by WHO in 1985. The American Diabetes Association Expert Committee in 1997 and 1998 has revised the diagnostic criteria for diabetes and has implemented changes in the 1979 classification as follows:
| a) | use of the terms type 1 and type 2 diabetes instead of insulin-dependent (IDDM) and non-insulin-dependent (NIDDM) to refer to the two major types of diabetes mellitus. |
| b) | use two fasting plasma glucose (FPG) determinations and |
| c) | a lower cutoff level for FPG (126 mg/dL) to diagnose diabetes (this level of FPG is equivalent to the 200-mg/dL value in the oral glucose tolerance test - OGTT). |
Type 1 includes autoimmune
and non-autoimmune, with beta-cell destruction. Type 2 has been expanded
to include various degrees of insulin resistance and insulin hyposecretion,
GDM and Other Types where the cause is known, such as endocrinopathies.
A new category Impaired Fasting Glycemia (IFG) is proposed for those values
which are above normal but below the diagnostic cut-off level for diabetes.
All these changes are being considered for adoption by WHO.
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INCIDENCE
AND PREVALENCE
There are over 16 million people in USA with diabetes mellitus which represents
slightly over 6% of the population. The prevalence of type 1 diabetes
in USA is slightly over 2 persons per 1,000 population while the prevalence
of type 2 varies according to age and ethnicity. The prevalence of type
2 diabetes in USA has steadily increased since the beginning of the 20th
century and it continues to increase. The reason for the increase can
be attributed to a rise in incidence of diabetes, a decrease in mortality
or a combination of both factors.
It is estimated that 18% of individuals between the ages of 65 and 75
and 40% of individuals over 80 years of age are affected with type 2 diabetes.
A paper by the San Antonio Heart Study (Burke JP; et al.) in 1988 reported
an incidence of 15.7% of type 2 diabetes among Mexican Americans as opposed
to an incidence of 5.7% among the same ethnic group in 1979. In non-Hispanic
Whites, the incidence increased from 2.6% in 1980 to 9.4% in 1988 this
represent a three fold increase for both ethnic groups.
The following types of diabetes are seen in USA children and adolescents:
| a) | type 1 in all ethnic groups; |
| b) | type 2 mostly found in minority groups; |
| c) | atypical diabetes inherited as an autosomal dominant in African-Americans and |
| d) | the rare maturity-onset diabetes of the young which is seen exclusively in Whites. |
Of all these forms only type 2 diabetes is increasing in incidence in these age groups. An example of the increased incidence of diabetes in Native Americans is seen in the Pima Indian group, where type 2 diabetes represents 30% of new cases between the ages of 10 and 20 years and it is generally associated with obesity. Type 1 diabetes is generally seen in patients below age 40 while type 2 tends to occur after age 40.
Summarizing, epidemiological studies have shown that diabetes in USA:
| a) | is most prevalent in minority ethnic groups; |
| b) | the prevalence of diagnosed diabetes has increased above three-fold in the last 40 years; |
| c) | a considerable proportion of the population has undiagnosed diabetes and |
| d) | the increase in prevalence has resulted in increased complications such as renal disease, blindness and limb amputations. |
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ETIOLOGY
The etiology of diabetes seems to be a combination of intrinsic (genetic)
and environmental factors to the degree that some authors think of diabetes
as a series of diseases that have glucose intolerance in common. Genetics
plays a role but it is not properly understood for type 1 while it plays
a much greater role for type 2. Autoimmunity as well as viral infections
such as congenital rubella, hepatitis, mumps and cytomegalovirus have
been reported to trigger the development of type 1 diabetes. Accurate
evidence for the causative role of viral infections is inconclusive. Hyperthyroidism,
hyperpituitarism, steroid medication as well as the destruction of pancreatic
beta cells by surgery, cancer or inflammation can induce the development
of diabetes in susceptible persons. Susceptibility for type 1 diabetes
is determined by human leukocyte antigens (HLA) which are located on the
surface of T lymphocytes. HLA are genetically controlled.
Type 2 diabetes is not associated with destruction of beta cells of the
pancreas but with resistance to insulin, altered insulin secretion and
elevated liver glucose production. Studies in identical twins have shown
that there is a 90% concordance for both twins to develop diabetes type
2. The genes for type 2 diabetes have not yet been mapped. Obesity plays
an important role in the development of diabetes type 2 and this is well
demonstrated by the fact that the vast majority of young patients which
develop type 2 diabetes are obese. Contributing causative factors for
type 2, besides obesity, are sedentary life and older age. As stated before,
maturity onset diabetes of the young (type 1 diabetes) is inherited as
an autosomal dominant trait.
Gestational diabetes mellitus (GDM) develops, as the name implies, during
pregnancy. Miscarriage is a high possibility for females who develop GDM.
GDM disappears after the birth of the child but the affected mother has
a greater risk, than the population at large, of developing type 2 diabetes
5 to 10 years after delivery.
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PATHOPHYSIOLOGY
Diabetes results in abnormal glucose metabolism. Glucose is needed by
cells for growth, maintenance and energy. Most glucose is obtained by
digestion of food and is then incorporated in the blood. In order for
glucose to go across the cellular membrane it needs insulin to be bound
to special cellular receptors. Central nervous system and brain cells
do not need insulin to utilize glucose. Insulin secretion by the pancreatic
beta cells is stimulated by food digestion and it takes place in two phases.
The first phase is very short with a total insulin production of 3% to
5%. During the second phase, which lasts one hour, the majority of insulin
is produced. Insulin remains in the blood for a few minutes (4 to 10)
and then immediately binds to the insulin cell surface receptors. Insulin-dependent
tissues are muscles, fat and liver which need glucose from the circulating
blood. The basic functions of insulin are to transfer glucose from the
blood to insulin dependent-cells, to facilitate the transfer of circulating
aminoacids into cells, to facilitate triglycerides synthesis and to prevent
triglyceride destruction.
When insulin production is impaired or absent, or when there is interference
with insulin functions, glucose can not be transferred to insulin-dependent
tissues resulting in an increase in the circulating glucose (hyperglycemia).
The contrary can also be seen, that is, excessive insulin accumulation
will produce low levels of circulating glucose (hypoglycemia). The glucose
which is not utilized by the central nervous system, the brain or the
insulin-dependent tissues is stored in the liver as glycogen. When there
is increased need for glucose utilization or when the levels of digestive
glucose are insufficient, the liver will metabolize the stored glycogen
back into glucose. Some hormones such as catecholamines, glucacon, glucocorticoids,
growth hormone and thyroxine antagonize the action of insulin by increasing
the level of circulating glucose. Therefore, under extreme emotional or
physical stress, a type 1 diabetic may release significant amounts of
catecholamines and glucocorticoids (especially cortisol) which, by increasing
blood glucose levels, will induce severe hyperglycemia.
Increased levels of cortisol induce protein disintegration and interference
with amino acids incorporation into proteins, the end result is transformation
of amino acids into glucose with resultant hyperglycemia. The hyperglycemic
stage is characterized by elimination of large amounts of glucose through
the urine with increased urinary volume. Electrolytes and nitrogen are
thus lost through urine. A further complication is the conversion to glucose
of the glycerol portion of body fats, this leads to excessive acetone
and beta-hydroxybutyric acid which are also eliminated through urine.
If this chain of events continues the type 1 diabetic patient will go
into metabolic ketoacidosis which if it is not treated can lead to coma
and even death.
Another important consideration in the pathophysiology of diabetes is
a normal nonenzymatic event known as glycosylation which increases notably
with hyperglycemia. Glycosylation is the process of adding a univalent
radical derived from a cyclic form of glucose to a protein to form an
unstable Schiff base adduct. Progressively a transformation takes place
into a more stable glycoprotein adduct (Amadori product) if the hyperglycemia
is corrected at this point the Amadori product is reversed but if it continues
the Amadori product becomes stable and non-reversible forming what it
is known as advanced glycosalated end products (AGE). AGE and lipids accumulate
in tissues of diabetic patients, especially vascular walls and collagen,
and are thought as the main responsible agents for the micro and macro
pathologic changes observed in the blood vessels of these patients. Low-density
lipoproteins (LDL) cross-link with collagen due to its AGE glycosylation
and contribute to the thickening of vessels' walls. This results in increased
risk of atherosclerosis in diabetic patients.
SYSTEMIC
COMPLICATIONS
The systemic complications of diabetes are related to the deposition of
AGE in various tissues especially those of the vascular and peripheral
nervous systems. The vascular system changes consist of microangiopathy
and formation of atheromas. The microscopic alterations are lipid deposition,
endothelial proliferation and enlargement of the intima in capillaries
throughout the body. The retina and the glomerular microcirculation of
the kidneys are the most severely affected. Diabetic retinopathy is a
frequent finding in patients with type 1 and less prevalent in patients
with type 2. Diabetic retinopathy is the main cause of blindness in USA.
Blindness in diabetics has a three fold prevalence over non-diabetic patients.
Diabetic nephropathy is the principal cause of death in patients with
type 1 due to renal failure. Patients with type 2 diabetes also develop
renal disease but with a lower prevalence. Due to the fact that type 2
is more frequent, the number of diabetic type 1 and type 2 patients with
renal disease is identical.
As stated above, the macro pathologic changes observed in the circulatory
system are essentially related to the formation of atheromas (atherosclerosis).
The atheromas are produced by deposition of AGE and LDL with consequent
calcification in various arteries of the body. Atheromas lead to poor
circulation in the extremities and is responsible for ulcerations and
gangrene of the feet. The most severe complications of atheromas are myocardial
infarction, hypertension, stroke, coronary insufficiency and renal failure.
Most patients with type 2 diabetes die of myocardial infarction.
Diabetic neuropathy is associated to the hyperglycemia and it is a consequence
to increased absorption of glucose by the Schwann cells. There are several
clinical manifestations associated to the neuropathy such as: burning
pain, tingling and numbness, especially of the extremities, muscle weakness
and cramps, oral paresthesia and burning tongue syndrome are among the
most frequently reported.
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ORAL
COMPLICATIONS
The most marked oral complications for both type 1 and 2 diabetes are
seen in uncontrolled diabetic patients. Many studies have shown that when
hyperglycemia is properly controlled the oral manifestations are minimal
and in some patients non-existent. Intraoral findings include, periodontal
disease which is more severe and with a higher prevalence than that seen
in the non-diabetic, xerostomia, burning mouth syndrome, candidiasis,
delayed and abnormal wound healing, increased propensity to infection,
diminished salivary flow and salivary gland enlargement. Some of these
complications can be directly related to the increased loss of fluid associated
to excessive urination in uncontrolled diabetics while some others, especially
xerostomia, could be influenced or directly dependent on the type of medications
that some of these patients are taking.
Xerostomia, consequent to diminished salivary flow, can lead to burning
mouth syndrome and caries as well as facilitate the development of candidiasis.
Some studies have shown increased prevalence of caries in diabetics while
others have demonstrated the contrary. Caries development can be influenced
by increased levels of glucose in the salivary secretion, especially in
the uncontrolled diabetic; while in the properly controlled diabetic it
could be diminished because of a lower intake of carbohydrates.
It has been statistically proven that diabetes is one of the predisposing
factors for the development of periodontal disease. Likewise marked gingival
inflammation, even with low levels of plaque, is more prevalent in the
uncontrolled diabetic than in the non-diabetic. Properly controlled diabetics
seem to have the same prevalence of gingivitis and periodontal disease
than non-diabetics. Young adults and adolescent diabetics have a greater
prevalence of gingival inflammatory hypertrophy and periodontal disease
than their non-diabetic counterpart. Recurrent periodontal absceses are
also typical of diabetic patients. The clinical manifestations of periodontal
disease in adults and young diabetics are more severe than those observed
in the non-diabetic population. These findings have been properly documented
in Pima Indians which have the highest prevalence of diabetes type 2 observed
in any ethnic group. Those with diabetes have a greater prevalence of
attachment loss and bone loss than aged matched controls. Diabetics also
have increased severity of periodontal destruction with subjects 15 to
34 years old having twice the amount of periodontal destruction as normal
subjects.
The increased prevalence of gingival and periodontal disease in diabetics
is assumed to be multifactorial in origin. Deposition of AGE in gingival
capillary walls as well as in the collagen of the periodontal ligament
and the alveolar bone matrix, increased levels of LDL with atheroma formation,
hyperglycemia interfering with normal periodontal wound healing, altered
immune response, increased oxidation, altered polymorphonuclear leukocyte
functions and genetics are all contributing factors to the development
of periodontal disease in the diabetics. Some of those factors are well
understood while others will need to be further evaluated. One factor
is definitely of utmost importance and that is control of hyperglycemia.
As stated above, the poorer the glucose control the more severe is the
periodontal disease.
The most reliable test professionally used for the evaluation of diabetes
control is the glycosylated hemoglobin assay. Glucose permanently binds
to hemoglobin becoming an AGE (glycosylated hemoglobin); this stable compound
remains in the blood for as much as 90 days. There are two glycosylated
hemoglobin tests but the most frequently used is the hemoglobin A1c (HbA1c),
the result of this test shows the percent of glycosylated hemoglobin present
in the circulation.
The recommended values are as follows:
Normal 4 to 6%
Good control <7%
Moderate control 7 to 8%
Control must improve >8%
Several studies have shown that marked improvement in the periodontal health of diabetic patients seems to improve the systemic status of those patients to the degree that many of them require less daily insulin intake. This relationship is based on the observed reduction of AGE in the blood circulation after proper periodontal therapy is instituted.
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DENTAL
MANAGEMENT OF THE DIABETIC PATIENT
A carefully constructed questionnaire can give some indications that a
patient could be at risk of being diabetic or be an undiagnosed diabetic,
especially type 2. Therefore, if positive answers are given to questions
such as: do you urinate frequently especially at night? or are you frequently
thirsty? the patient should be further questioned about personal and family
history of diabetes. The following findings are also indicative of possible
diabetes: recent weight loss, irritability, dry mouth, frequent infections,
history of poor wound healing, if a woman has given birth to an unusually
heavy baby (>10 pounds) or has had several spontaneous abortions. Obese
patients over 40 years of age also should be properly questioned. If one
or more of the above systemic findings is associated to one or more of
the following intraoral findings then the patient should be tested for
diabetes: marked periodontal disease, history of recurrent periodontal
disease, multiple abscesses, history of poor intraoral healing especially
after tooth extraction, dry mouth syndrome, persistent candidiasis, loss
of sensation. It should be remembered that persistent intraoral candidiasis
and weight loss are also main findings in patients with AIDS. Therefore,
a careful differential diagnosis should be undertaken.
The dentist can use any of the commercially available glucometers to further
confirm the suspicion of a patient being diabetic.
It is recommended that a patient suspected by the dentist to be diabetic,
should be referred to a physician for proper evaluation and diagnosis.
Recently the parameters to determine the diagnostic concentration of fasting
plasma glucose (FPG) have been lowered from 140 to 126 mg/dL but this
modification is still under research and several published papers argue
against its validity.
| 1. | Properly controlled type 1 and type 2 diabetic patients usually can undergo all dental treatments without special precautions. |
| 2. | The dentist must know the type and dose of insulin as well as any other medications that the patient is taking. |
| 3. | The dentist should know if the patient has a history of hypoglycemic attacks and the accompanying signs and symptoms. The chances of having a hypoglycemic attack are increased if there have been previous attacks (See Signs and symptoms of acute hypoglycemia below). |
| 4. | In order to avoid an episode of hypoglycemia while undergoing dental treatment it is advisable to schedule the patient based on the time of highest insulin activity which varies from 30 minutes to 8 hours after injection depending on the type of insulin. Therefore, the appointment does not need to be necessarily in the morning. |
| 5. | The patient must be advised not to change the insulin dose and time of application as well as not to change his/her diet. |
| 6. | It is advisable to have in the dental office orange juice or another form of glucose, to be given to the patient at the first sign of hypoglycemia. Generally a 6 oz. dose of any fruit juice or any other drink containing carbohydrates will rapidly reverse the hypoglycemic symptoms. |
| 7. | If the patient practices self-blood glucose monitoring he/she should be advised to bring to the dental office his/her glucometer. |
| 8. | Emotional and physical stress increase the amount of secreted cortisol and epinephrine which induce hyperglycemia. Therefore, if the patient is very apprehensive pre-treatment sedation should be contemplated (See Signs and symptoms of hyperglycemia below). |
| 9. | If a lengthy, especially surgical procedure is to be undertaken, the patient's physician should be consulted. |
| 10. | Consultation with the patient's physician is a must when: |
| a) | the patient has systemic complications of diabetes such as heart or renal disease, or when |
| b) | the patient has a difficult to control diabetes or is under high insulin dosage or when |
| c) | the patient has an acute oral infection such as periapical or periodontal abscess. |
| 11. | Hospitalization may be needed for patients like in 10a or b above. |
| 12. | Antibiotics should be prescribed for patients like in 10 above in order to prevent secondary infections or complication of the pre-existing infection and to facilitate wound healing. |
| 13. | Treatment of severe cases of periodontal disease in diabetic patients, in addition to the indicated surgical procedure, may require use of systemic tetracycline. Tetracycline has proven to help not only the condition of the periodontium but it also may help control hyperglycemia. |
It should be stressed that the dentist should take all the necessary precautions in order to avoid the occurrence of a hypoglycemic attack while the patient is undergoing dental treatment. Hypoglycemic attacks occur when the concentration of blood glucose drops below 60 mg/dL but in some patients it may occur at either lower or higher concentrations. Preparedness should include availability of different forms of orally administered rapidly absorbed carbohydrates such us: fruit juices, sodas, plain sugar, ice cream, candies, etc. Patients with hypoglycemia will recover from the attack within 10 to 20 minutes after orally administering 15 g of carbohydrate, this is equivalent to 4 to 6 ounces of fruit juice or soda, the same result will be achieved with 4 teaspoons of plain sugar.
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SIGNS AND SYMPTOMS OF ACUTE HYPOGLYCEMIA:
- Hunger
- Weakness
- Confusion (incoherence)
- Pallor
- Anxiety (agitation, belligerance)
- Sweating
- Dizziness
- Tachycardia
In severe cases the following can be present:
- Hypotension
- Hypothermia
- Seizures (tonic or clonic movements)
- Unconsciousness
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SIGNS AND SYMPTOMS OF DIABETIC KETOACIDOSIS:
- Deep, rapid breathing (Kussmaul's respiration)
- Nausea (with or without vomiting)
- Abdominal pain
- Disorientation (coma in severe cases)
- Dehydration (dry oral and nasal mucosas)
In severe cases the following can be present:
- Tachycardia
- Hypotension
- Generalized swelling of the skin.
Comparing the signs and symptoms of hypoglycemia with those of diabetic ketoacidosis it can be seen that disorientation (confusion), tachycardia and hypotension are common to both of them. Therefore, it is emphazised once more that it is of utmost importance for the dentist to know if the patient has a history of hypoglycemic attacks and either, have a glucometer in the office, or ask the patient to bring his/her own glucometer to monitor blood glocose levels.
In summary a successful
dental treatment in a type 1 or type 2 diabetic patient will be achieved
if the following are observed:
A) Detail clinical and family history.
B) Consultation with the patient's physician.
C) Collaboration of the patient in perfect glycemic control.
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