Introduction
There are many endocrinal disorders associated with significant problems in the human body. Many patients with these disorders seek periodontal treatment. Hence, it becomes essential for a periodontist to understand these disorders and provide appropriate treatment to patients with endocrinal disorders. In the following discussion, we shall read about these disorders and periodontal management of these cases. Let us start our discussion with the most common endocrinal disorder, Diabetes Mellitus.
Diabetes mellitus
Diabetes mellitus is a metabolic disorder characterized by chronic hyperglycemia with disturbances of carbohydrate, fat and protein metabolism, resulting from the defects in insulin secretion, insulin action, or both 53. Insulin is a hormone which is produced by the β-cells of the pancreas which controls the blood glucose levels. Diabetes is associated with a range of serious complications which result in reduced quality of life and premature mortality. It is associated with microvascular and macrovascular complications that can cause damage to multiple organ systems in the body. The classical symptoms of marked hyperglycemia include polyuria, polydipsia, weight loss, sometimes with polyphagia, and blurred vision. Long-term complications of diabetes include retinopathy with potential loss of vision; nephropathy leading to renal failure; peripheral neuropathy with risk of foot ulcers, amputations, and Charcot’s joints; and autonomic neuropathy causing gastrointestinal, genitourinary, and cardiovascular symptoms. The uncontrolled diabetic patients usually require periodontal treatment, so a thorough understanding of the disease is essential for a dental health care provider.
Types of diabetes
Based upon the etiology, diabetes can be classified into the following types,
I. Type 1 diabetes: Caused due to β-cell destruction, usually leading to absolute insulin deficiency
A. Immune-mediated.
B. Idiopathic.
II. Type 2 diabetes: May range from predominantly insulin resistance with relative insulin deficiency to a predominantly secretory defect with insulin resistance.
III. Other specific types:
A. Genetic defects of β -cell function.
B. Genetic defects in insulin action.
C. Diseases of the exocrine pancreas.
D. Endocrinopathies.
E. Drug or chemical induced.
F. Infections.
G. Uncommon forms of immune-mediated diabetes.
H. Other genetic syndromes sometimes associated with diabetes.
IV. Gestational diabetes mellitus
In the present discussion, we shall discuss in detail the most common type of diabetes mellitus i.e. Type 2 diabetes mellitus.
Type 2 diabetes mellitus
This form of diabetes accounts for 90-95% of diabetic patients. Previously, it was known as non-insulin-dependent diabetes or adult-onset diabetes. This disease is caused due to insulin resistance in the liver and skeletal muscle, increased glucose production in the liver, overproduction of free fatty acids by fat cells and relative insulin deficiency. The insulin secretion decreases with gradual β-cell failure. Other contributing factors for this disease include obesity, age (onset of puberty is associated with increased insulin resistance), lack of physical activity, genetic predisposition, racial/ethnic background (African-American, Native American, Hispanic and Asian/Pacific Islander) and conditions associated with insulin resistance, (e.g., polycystic ovary syndrome).
This form of diabetes frequently goes undiagnosed for many years because the hyperglycemia develops gradually and at earlier stages, often it is not severe enough for patient to ……. Contents available in the book……. Contents available in the book……. Contents available in the book……. Contents available in the book…….
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Screening of diabetes
Traditionally, the diagnosis of diabetes has been done by identifying plasma glucose levels. The current diagnostic criteria uses glycated hemoglobin (HbA1c) levels, fasting plasma glucose levels, plasma glucose levels during an oral glucose tolerance test (OGTT) or the random plasma glucose levels to diagnose diabetes. The fasting or random plasma glucose levels confirm the glucose level at a particular point of time when the blood is drawn, but do not give any information about the past glucose levels. The HbA1c reflects the average plasma glucose over the previous eight to 12 weeks 54 because the glucose gets bound to the Hb molecules. HbA1c is formed as a result of the addition of a stable glucose molecule to the N-terminal group of an HbA0 molecule via a nonenzymatic glycation process 55. It is considered a reliable indicator of the glycemic status of the previous 3 months 56. Table 32.7 describes the recent criteria suggested for diagnosing diabetes mellitus 57.
| Criteria for the diagnosis of diabetes. |
|---|
| HbA1c ≥ 6.5%. The test should be performed in a laboratory using a method that is NGSP certified and standardized to the DCCT assay.* OR Fasting plasma glucose (FPG) ≥ 126 mg/dl (7.0 mmol/l). Fasting is defined as no caloric intake for at least 8 h.* OR 2-h plasma glucose ≥ 200 mg/dl (11.1 mmol/l) during an oral glucose tolerance test (OGTT). The test should be performed as described by the World Health Organization, using a glucose load containing the equivalent of 75 g anhydrous glucose dissolved in water.* OR In a patient with classic symptoms of hyperglycemia or hyperglycemic crisis, a random plasma glucose ≥ 200 mg/dl (11.1 mmol/l). *In the absence of unequivocal hyperglycemia, criteria 1-3 should be confirmed by repeat testing. |
Treatment of diabetes
Essential components of the treatment for diabetes include diabetes self-management education and support, lifestyle interventions and pharmacological management. There are a number of anti-diabetic agents available these days (Table 32.8, 32.9). There are:
1. α-glucosidase inhibitors (AGIs),
Acarbose.
2. Biguanides,
Metformin hydrochloride.
3. Dipeptidyl peptidase-4 (DPP-4) Inhibitors,
Sitagliptin.
Vildagliptin.
4. Insulin Secretagogues,
Sulphonylureas.
Meglitinides.
5. Thiazolidinediones (TZDs),
Glitazones.
6. Incretin mimetics,
Exenatide.
liraglutide.
7. Insulin.
| Insulins used as anti-diabetic agents. | |
|---|---|
| Rapid-acting insulins | · Regular insulin (Humulin R, Novolin R) · Insulin lispro (Humalog) · Insulin aspart (Novolog) · Insulin glulisine (Apidra) · Prompt insulin zinc (Semilente, Slightly slower acting) |
| Intermediate-acting insulins | · Isophane insulin, neutral protamine Hagedorn (NPH) (Humulin N, Novolin N) · Insulin zinc (Lente) |
| Long-acting insulins | · Extended insulin zinc insulin (Ultralente) · Insulin glargine (Lantus) · Insulin detemir (Levemir) |
Periodontal treatment of diabetic patients
The first step in the treatment of a diabetic patient is asking about the medical history of the patient and the assessment of glycemic control of the patient at the initial appointment. Patients with well-controlled diabetes can be treated similarly as non-diabetic individuals. If the patient is an uncontrolled diabetic the dental treatment is delayed if possible until good metabolic control is achieved.
The patient should be asked about the recent blood glucose levels and frequency of hypoglycemic episodes. The dosage, frequency of intake and time of administration of the anti-diabetic drugs should be noted. The drug interactions with various anti-diabetic drugs may alter the blood glucose levels. For example, the hypoglycemic control of sulfonyl-ureas may be altered by drugs that are highly protein-bound, such as salicylates, dicumarol, β-adrenergic blockers, monoamine oxidase inhibitors, sulfonamides and angiotensin-converting enzyme inhibitors. On the other hand ……. Contents available in the book……. Contents available in the book……. Contents available in the book……. Contents available in the book…….
Scheduling the visits of the patient
It is important to note that most of the complications during the treatment of a diabetic patient are due to hypoglycemia and not hyperglycemia. If the patient has a complication due to hyperglycemia, which is not confirmed, the initial treatment is same as that of hypoglycemia. Reason being, hyperglycemia does not cause any life threatening complication, but hypoglycemia can result in a life-threatening situation. Keeping all these factors in mind the visits of the patient are scheduled.
In general, morning appointments are suitable for a diabetic patient because the endogenous corticosteroid levels are generally high at this time which increases the blood glucose level. If the patient is taking insulin, the visits should be arranged in such a way that the treatment time does not coincide with the peak activity of insulin.
Diet
The patient should take normal diet and medications before the appointment. If the patient skips the breakfast owing to the dental appointment, but still takes anti-diabetic medications, the risk of hypoglycemia increases. If procedures like conscious sedation are planned, the patient is asked to alter the diet. The dosage of medications may also be altered in consultation with the physician.
Estimation of blood glucose level before the procedure
Depending on the diabetic history of the patient, dentist may require the blood glucose level estimation prior to the initiation of treatment. Various commercial blood glucose monitors are available in the market, which provide accurate levels of blood glucose. If the blood glucose level of the patient is <70 mg/dl, an oral carbohydrate should be given to minimize the risk of hypoglycemia. If blood glucose is >200 mg/ dl, an intravenous infusion of 10% ……. Contents available in the book……. Contents available in the book……. Contents available in the book……. Contents available in the book…….
Precautions during the treatment of diabetic patient
As already stated, most of the complications during the treatment of a diabetic patient are due to hypoglycemia, the peak activity of the insulin or other anti-diabetic drugs should be determined to avoid the risk of hypoglycemia. The initial signs of hypoglycemia include decreased spontaneity, mood change, hunger, and weakness. As the condition becomes more severe, the patient may have sweating, incoherence, and tachycardia. If the condition is not treated, the state of the patient even worsens and may result in unconsciousness, hypotension, hypothermia, seizures, coma, and death. It must be noted that stress also precipitate hypoglycemia. The stress response is characterized by the acute metabolization of carbohydrates, proteins, and fats to provide increased levels of glucose. In addition, during stress, resistance to the effects of insulin increases 58. Therefore, stress-reducing protocol should be followed prior to and during the treatment.
| Symptoms and signs of hypoglycemia. | |
|---|---|
| Symptoms | Signs |
| · Anxiety · Shakiness · Increased sweating · Hunger | · Tachycardia · Tremors · Altered consciousness (lethargy and obtundation or personality change) · Blood glucose level: < 60 mg/dl |
If during the treatment, it is suspected that the patient is experiencing hypoglycemia, the dental treatment should be stopped and the patient should be given 15 gm of fast acting carbohydrates in the form of a tablet, candy, juice or soft drink. Then, blood glucose level of the patient should be determined. If appropriate blood glucose levels are achieved, treatment can be continued. If appropriate blood glucose levels are not achieved the carbohydrate dose is repeated. If the patient is unable to swallow or is unconscious, an intravenous line is established and 25-30 ml of 50% dextrose solution is administered. Glucagon injection can also be given intramuscularly or subcutaneously.
| Treatment of hypoglycemia. | |
|---|---|
| Conscious patient | Unconscious patient |
| Administer 15 gm of simple carbohydrates. Repeat finger-stick glucose test after 15 minutes: · Blood glucose level > 60 mg/dl: patient should be asked to eat or drink (for example, a sugar-sweetened beverage). · Blood glucose level < 60 mg/dl: repeat treatment of 15 gm of simple carbohydrates and check blood glucose after 15 minutes. Continue until achieving a blood glucose level > 60 mg/ dl. · Ask the patient to notify his/ her physician. | With intravenous access: · Administer 25-30 ml of 50% dextrose immediately. · Notify the patient's physician. Without intravenous access: · Apply glucose gel inside the mouth in a semi obtunded patient or treat with 1 mg of glucagon intramuscularly or subcutaneously. · Repeat the blood glucose test after 15 minutes. · Establish intravenous access and notify the patient's physician. |
Complications due to hyperglycemia are uncommon during dental treatment. The ketoacidosis or hyperosmolar nonketotic states in Type I and Type II diabetes, respectively usually have prolonged onset. Therefore, risks associated with the hyperglycemic state are much lower than the hypoglycemic state. As already stated, the clinical presentation of hyperglycemias is very similar to hypoglycemia. If in doubt, it should be treated as a hypoglycemia.
Post-treatment precautions
One of the major problems associated with uncontrolled diabetes mellitus is delayed wound healing. Tissues are more prone to infections during the hyperglycemic state. Therefore, the antibiotic cover is necessary for these patients to prevent infections. If it is anticipated that the patient’s diet may be affected by treatment, the dosage of the antidiabetic drugs or insulin should be readjusted in consultation with the patient’s physician. As already stated, salicylates may alter the hypoglycemic control of sulfonylureas and increase insulin secretion and sensitivity resulting in hypoglycemia. Therefore, aspirin-containing compounds should be avoided for post-operative pain control 59.
Thyroid dysfunctions
Thyroid is a small butterfly-shaped gland that lies just under the skin below Adam’s apple in the neck. It secretes hormones that help to regulate the body’s metabolism. There are two main thyroid hormones: T3 (triiodothyronine) and T4 (thyroxine). T3 is the more active form of the hormone, and T4 is converted into T3 by the body as needed. Most of T3 and T4 are bound to proteins in the bloodstream. The hyper and hypothyroidism are two common dysfunctions of the thyroid gland. An estimated 15% of the general population has abnormalities of thyroid anatomy on physical examination, and an unknown percentage of these do not complete a diagnostic evaluation 60. The oral cavity is adversely affected in these abnormalities of the thyroid.
Thyroid function tests (TFTs) are used to evaluate thyroid status. The thyroid function tests include,
- Thyroid-stimulating hormone (TSH) test.
- T4 tests.
- T3 test.
- Thyroid-stimulating immunoglobulin (TSI) test.
- Antithyroid antibody test also called the thyroid peroxidase antibody (TPOab) test.
Thyroid-stimulating hormone (TSH) test:
Thyroid-stimulating hormone (TSH), or thyrotropin, is produced by the pituitary gland in response to thyrotropin-releasing hormone and stimulates production and secretion of thyroid hormones. Measurement of the TSH serum concentration is the initial test of choice for evaluating thyroid function. The normal range of TSH is between 0.7 milli-International Units per millilitre to 5.3 mIU/mL for adults. The TSH levels are elevated in primary hypothyroidism, decreased in secondary hypothyroidism and elevated in subclinical hypothyroidism. Whereas, low or undetectable TSH levels generally suggest hyperthyroidism. Normal TSH levels in the presence of abnormal T3 or T4 concentrations indicate a non-thyroid pathology. Because TSH is ……. Contents available in the book……. Contents available in the book……. Contents available in the book……. Contents available in the book…….
T4 Tests:
The thyroid primarily secretes T4 and only a small amount of T3. It is found in blood in bound or free forms. The protein-bound form is kept in the body as a reserve and is utilized when needed. The free form is the active form of the hormone. High levels of total T4 (bound and free T4) or high level of free T4 suggests hyperthyroidism, and a low level of total T4 or free T4 suggests hypothyroidism.
T3 Test:
If the T4 levels are normal and still it is suspected that the patient may have hyperthyroidism, T3 levels can be tested. The T3 test is not useful in diagnosing hypothyroidism because levels are not reduced until the hypothyroidism is severe.
Thyroid-stimulating immunoglobulin (TSI) test:
Thyroid-stimulating immunoglobulin is an autoantibody present in Graves’ disease. These antibodies stimulate the thyroid hormone in the same way as that by TSH. It causes the excessive secretion of T3 and T4. TSI test detects TSI circulating in the blood. It is done in patients with Grave’s disease and pregnancy.
Antithyroid antibody test:
In Hashimoto’s disease, anti-thyroid antibodies are present in the blood. Two types of antibodies may be present, one which attack the thyroglobulin or another one which attack an enzyme in thyroid cells, called thyroperoxidase.
In association with these basic tests, several other investigations are available to diagnose the thyroid abnormalities. These include an ultrasound of the thyroid, computerized tomography (CT) scan, or nuclear medicine tests.
Clinical features of hyper and hypothyroidism:
Various clinical features associated with hyperthyroidism include the following,
- Nervousness and irritability.
- Palpitations and tachycardia.
- Heat intolerance or increased sweating.
- Tremor.
- Weight loss or gain.
- Alterations in appetite.
- Frequent bowel movements or diarrhea.
- Dependent lower-extremity edema.
- Sudden paralysis.
- Exertional intolerance and dyspnea.
- Menstrual disturbance (decreased flow).
- Impaired fertility.
- Mental disturbances.
- Sleep disturbances (including insomnia).
- Changes in vision, photophobia, eye irritation, diplopia, or exophthalmos.
Various clinical features associated with hypothyroidism are,
- Fatigue.
- Weight gain from fluid retention.
- Dry skin and cold intolerance.
- Yellow skin.
- Coarseness or loss of hair.
- Hoarseness of voice.
- Goiter.
- Reflex delay, relaxation phase.
- Ataxia.
- Constipation.
- Memory and mental impairment.
- Decreased concentration.
- Depression.
- Irregular or heavy menses and infertility.
- Myalgias.
- Hyperlipidemia.
- Bradycardia and hypothermia.
- Myxedema fluid infiltration of tissues.
Oral manifestation of hyper and hypothyroidism:
Hyperthyroidism:
Various oral manifestations of hyperthyroidism include, increased susceptibility to caries, periodontal disease, enlargement of extra-glandular thyroid tissue (mainly in the lateral posterior tongue), maxillary or mandibular osteoporosis, accelerated dental eruption 61 and burning mouth syndrome. In Grave’s disease, on extra-oral examination, the enlargement of the thyroid gland can be seen when the patient is in a supine position in the dental chair.
Hypothyroidism:
In children, hypothyroidism is characterized by the presence of thick lips (due to increased accumulation of subcutaneous mucopolysaccharides), large protruding tongue (macroglossia), malocclusion and delayed eruption of teeth. Hypothyroidism also results in altered tooth morphology and delayed wound healing 62.
Management of thyroid dysfunctions:
Treatment of hypothyroidism:
Thyroxine (or levothyroxine) is the current standard thyroid hormone replacement therapy for hypothyroidism. The goal of treatment of primary hypothyroidism is to reverse the symptoms of hypothyroidism by normalizing the blood TSH level.
Treatment of hyperthyroidism:
The treatment of hyperthyroidism includes the administration of drugs like β-blockers, antithyroid drugs, radioiodine and surgical treatment of thyroid gland.
Periodontal treatment of patients with thyroid dysfunction
The first step in the periodontal treatment of a patient with thyroid dysfunction is obtaining correct information about the kind of thyroid dysfunction and medications which the patient is taking. The physician can be consulted to know the present status of the thyroid function. The thyroid gland should be protected by a thyroid collar while taking patient X-rays. The thyroid is extremely sensitive to radiation, and excessive radiation exposure is a known risk factor for various thyroid conditions.
Periodontal treatment of patients with hypothyroidism:
Hypothyroidism results in increased subcutaneous mucopolysaccharides accumulation due to decrease in their degradation. It may decrease the ability of small blood vessels to constrict when cut and may result in increased bleeding from infiltrated tissues, including mucosa and skin. Local measures to control bleeding are required for proper hemostasis 63. In hypothyroidism patients, the wound healing is delayed due to decreased metabolic activity in fibroblasts. The delayed wound healing is more susceptible to infection. So, the antibiotic cover is given to prevent any kind of infection. Hypothyroidism is associated with increased risk of susceptibility to cardiovascular diseases from arteriosclerosis and elevated LDL. If the patient has atrial fibrillation then he or she might require antibiotic prophylaxis before invasive procedures, depending on underlying cause of atrial fibrillation 64.
An antiseptic that includes iodine (such as Povidone), can increase the risk of thyroiditis or hypothyroidism in these patients, so should be avoided. Along with this many drug interactions should be considered in patients taking thyroxine. The metabolism of thyroxine is increased with phenytoin, rifampicin, and carbamazepine. With thyroxine, an increased effect of warfarin sodium is observed. Because of its gluconeogenic effects, the dosage of oral hypoglycemic agents should be increased.
Central Nervous System (CNS) depressants, sedatives, or narcotic analgesics may cause an exaggerated response in hypothyroid patients. In all patients with severe hypothyroidism, these drugs must be avoided. To avoid any myxedematous complication, patients with severe hypothyroidism should get the medical treatment before dental treatment. If a myxedematous ……. Contents available in the book……. Contents available in the book……. Contents available in the book……. Contents available in the book…….
Periobasics: A Textbook of Periodontics and Implantology
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Periodontal treatment of patients with hyperthyroidism:
Patients with hyperthyroidism show increased heart rate and blood pressure due to the effects of thyroid hormone on sympathetic nervous system activity. The blood pressure should be monitored before starting any surgical treatment and longer duration of local pressure is required to stop bleeding. Local hemostatic agents may also be used to control bleeding. Propylthiouracil (PTU) is an anti-thyroid drug which has anti-vitamin K activity and can cause hypoprothrombinemia and bleeding. So, patients taking PTU must be carefully evaluated before surgery 65. Acetylsalicylic acid (ASA) interferes with the protein binding of T4 and T3, thereby increasing their free form. It may worsen the symptoms of thyrotoxicosis 66. Therefore, combination analgesics containing acetylsalicylic acid (ASA) are contraindicated in patient with hyperthyroidism. Other nonsteroidal anti-inflammatory drugs (NSAIDs) also have this effect, so should be used with caution.
The use of local anesthesia with epinephrine warrants special consideration while treating the patients with hyperthyroidism. The use of epinephrine or other pressor amines (in local anesthesia or gingival retraction cord, or to control bleeding) must be avoided in the untreated or poorly treated thyrotoxic patient. However, a well-managed or euthyroid thyrotoxic patient can be treated normally and may be given normal concentrations of these vasoconstrictors. Special care must be taken while administering LA with epinephrine to patients who are taking nonselective β-blockers. Epinephrine acts on α-adrenergic receptors, causing vasoconstriction and on β2 receptors causing vasodilation. Nonselective β-blockers eliminate the vasodilatory effect, potentiating an α-adrenergic increase in blood pressure 67. Clinical experience has shown that small amounts of epinephrine can be used safely in these patients.
The symptoms of thyrotoxic crisis (thyroid storm) include restlessness, fever, tachycardia, pulmonary edema, tremor, sweating, and finally coma and death. If this situation is faced during periodontal treatment, the treatment is stopped. The patient is cooled with the help of cold towels or ice packs and given an injection of hydrocortisone (100-300 mg). An intravenous ……. Contents available in the book……. Contents available in the book……. Contents available in the book……. Contents available in the book…….
Parathyroid gland disorders
The parathyroid glands are derived from the ectoderm of the pharyngeal pouches. In Humans, usually four parathyroid glands are present, variably located on the back of the thyroid gland. The superior parathyroid glands develop from the fourth pharyngeal pouch and are therefore referred to as “parathyroid IV”. The inferior parathyroid glands are derived from the third pharyngeal pouch and are also referred to as “parathyroid III”. The major function of the parathyroid glands is to maintain the body’s calcium and phosphate levels. Parathyroid glands secrete parathyroid hormone (PTH) which in association with calcitonin (secreted from the thyroid gland) has key role in regulating the amount of calcium in the blood and within the bones. PTH plays an important role in tooth development and bone mineralization and increases bone resorption. It’s coordinated action on the bones, kidney and intestine increases the flow of calcium into the extracellular fluid and increases its concentration in the blood. The parathyroid disorders are of two types, one where the parathyroid is overactive (hyperparathyroidism), and another where the parathyroid is under- or hypoactive (hypoparathyroidism).
Hyperparathyroidism:
The hyperparathyroidism may be primary, secondary or tertiary. The primary hyperparathyroidism is caused due to hyperfunction of one or more parathyroids, usually caused by a tumor (adenoma in 85% of all cases) or hyperplasia of the gland that produces an increase in PTH secretion resulting in hypercalcemia and hypophosphatemia. Secondary hyperparathyroidism occurs in patients with intestinal mal-absorption syndrome or chronic renal failure, which results in ……. Contents available in the book……. Contents available in the book……. Contents available in the book……. Contents available in the book…….
The oral manifestations of hyperparathyroidism are,
1. Dental abnormalities:
a. Widened pulp chambers.
b. Developmental defects.
c. Alterations in dental eruption.
d. Weak teeth.
e. Malocclusions.
2. Brown tumor.
3. Loss of bone density.
4. Soft tissue calcifications.
Hypoparathyroidism:
The state of decreased parathyroid activity is known as hypoparathyroidism. This condition is characterized by hypocalcemia and hyperphosphatemia. One common reason for hypoparathyroidism is damage to the glands or their blood supply during thyroid surgery. Some rare genetic syndromes such as DiGeorge syndrome or an autosomal dominant syndrome are also associated with this condition. It may also develop as an isolated entity of unknown etiology, referred to as idiopathic hypoparathyroidism 69.
The oral manifestations of hypoparathyroidism are,
1. Dental abnormalities:
a. Enamel hypoplasia in horizontal lines.
b. Poorly calcified dentin.
c. Widened pulp chambers.
d. Dental pulp calcifications.
e. Shortened roots.
f. Hypodontia.
g. Delay or cessation of dental development.
2. Mandibular tori.
3. Chronic candidiasis.
4. Paresthesia of the tongue or lips.
5. Alteration in facial muscles.
Dental management of the patient with parathyroid disorders
The clinical management of the patients with hyper or hypoparathyroidism does not warrant any special consideration. A hyperparathyroidism patient is more prone to bone fracture due to the decreased mineral content of bones, so care should be taken during surgical procedures. The brown tumor if present should be diagnosed correctly in these patients. On the other hand, hypoparathyroidism patients have low serum calcium. Before performing dental treatment, serum calcium level should be determined. It must be above 8 mg/100ml to prevent cardiac arrhythmias, seizures, laryngospasms or bronchospasms. Because of dental abnormalities, these patients are more prone to caries. Proper oral hygiene measures and dietary instructions should be given to these patients to prevent caries. The patient should be put on a regular maintenance program according to the periodontal findings.
Adrenal Insufficiency
Adrenal insufficiency (AI) is a life-threatening disorder that can result from the primary adrenal failure or secondary adrenal disease due to impairment of the hypothalamic-pituitary axis (HPA) 70-72. AI can be primary, secondary or iatrogenic. Addison’s disease, the common term for primary AI, occurs when the adrenal glands cannot produce enough of the adrenal hormones, cortisol and aldosterone. The clinical manifestations of cortisol deficiency include hypoglycemia, hypotension, asthenia, muscle weakness, anorexia, nausea, weight loss and diminished resistance to infections and stress. The characteristic melanin pigmentation occurs due to increased synthesis of adrenocorticotropic hormone (ACTH) and melanocyte-stimulating hormone (MSH). Secondary AI occurs due to pituitary or hypothalamic dysfunction or failure caused by tumors, irradiation, infiltration, trauma or surgery 70, 73. The Iatrogenic AI is caused by suppression of the HPA axis due to glucocorticoid therapy in pharmacological doses 74. The suppression of the HPA axis is rarely seen in ……. Contents available in the book……. Contents available in the book……. Contents available in the book……. Contents available in the book…….
Normal cortisol levels:
The glucocorticoids are produced in the zona fasciculata of the adrenal cortex under the regulation of the HPA axis. Hypothalamus synthesizes Corticotropin-releasing hormone (CRH) and arginine vasopressin (AVP) which stimulate secretion of adrenocorticotropic hormone (ACTH) from the pituitary gland 78. ACTH acts on renal cortex and cortisols are produced. These are under negative feedback at the level of both the hypothalamus and the pituitary gland 79. It has been estimated that normally around 10 mg/day endogenous cortisol is produced in our body 80, 81. There are cyclic variations in the plasma cortisol concentrations in the course of the 24-hour in a day, being maximum early in the morning and minimum at evening.
| Corticosteroid dose equivalents. | |
|---|---|
| Steroid | Equivalent Dose |
| Betamethasone | 1.2 mg |
| Dexamethasone | 1.5 mg |
| Methylprednisolone | 8 mg |
| Triamcinolone | 8 mg |
| Prednisone | 10 mg |
| Prednisolone | 10 mg |
| Hydrocortisone | 40 mg |
| Cortisone | 50 mg |
Dental management of patients with adrenal insufficiency:
The periodontal treatment of patients with primary or secondary AI is started with a detailed case history and current status of the patient. In patients taking exogenous corticosteroids, the reason of intake should be determined. The primary AI or Addison’s disease results from idiopathic, surgical, or infectious destruction or tumor of the parenchyma of the adrenal gland or infiltration of the cortex by sarcoidosis, tuberculosis or amyloidosis 82. Most of these patients with Addison’s disease are treated with corticosteroids. The AI other than Addison’s disease is most commonly due to exogenous corticosteroid intake. The dosage of the exogenous corticosteroids determines the degree of adrenal suppression. Also, the ……. Contents available in the book……. Contents available in the book……. Contents available in the book……. Contents available in the book…….
Corticosteroid doses which do not produce adrenal suppression
If the patient is taking < 30 mg of hydrocortisone/day, it is considered as low-dose corticotherapy. There is no need for corticosteroid supplements both for the long-term and short-term corticoid users because this dose does not cause adrenal suppression. The non-surgical and surgical procedures can be safely carried out without giving the patient any corticosteroid supplements.
Corticosteroid dose which produces adrenal suppression
There is some degree of adrenal suppression in patients who are receiving 30-40 mg of hydrocortisone/day. If the patient is highly anxious, or lengthy dental treatment or surgical procedure is to be performed, we must double the daily dose on the day of treatment. If the postoperative pain is expected, we should also double the daily dose on the first postoperative day.
Patients receiving > 40 mg of hydrocortisone/day are on high-dose corticotherapy. This dosage results in blood levels of corticosteroids, which inhibit the HPA axis. In patients who are taking high-dose corticotherapy for less than one month, there is transient suppression of the HPA axis. Within 14 days of cessation of the therapy, the endogenous cortisol levels become normal. So, in patients who have discontinued corticosteroid treatment less than 14 days ago, maintenance dose on the day of treatment is required. There is no set protocol for patients who are taking high-dose corticotherapy for more than one month.
Precautions during the treatment:
The plasma cortisol concentration is maximum in the morning, so preferably morning appointment should be given to the patient. The anxiety and emotional stress should be minimized. The treatment should be as painless as possible. Appropriate management of the post-operative pain should be done. Some drug interactions should also be kept in mind. Drugs like phenytoin, barbiturates and rifampicin accelerate glucocorticoid metabolism. Glucocorticoids increase the requirements of insulin, oral antidiabetic drugs, and hypotensive medication.
Adrenal or Addisonian crisis
Patients with Addison’s disease regularly take corticosteroid replacement drug therapy to compensate for the deficiency of endogenous cortisols due to their inadequate production. Exogenous glucocorticoids can cause adrenal gland suppression and resultant atrophy. With the atrophy of adrenal glands, there is a decreased glucocorticoid response to stress, and this may precipitate an adrenal crisis 86.
As already stated, the cortisol production from the adrenal cortex is under negative feedback. The falling level of cortisol in the blood stimulates the pituitary gland to produce ACTH. During dental treatment, stress stimulates pituitary gland to produce more ACTH, resulting in an even more increase in the production of cortisol. But if the patient is already taking exogenous steroids, it cause suppression of endogenous cortisol production. Because the body is unable to produce natural cortisol, it fails to respond when higher levels are required. Adrenal crisis may precipitate due to sudden withdrawal of exogenous corticoids, or the existence of situations requiring greater amounts of corticoids than those afforded by replacement therapy. It is due to sudden failure of the adrenal cortex function. The patient may show following signs and symptoms,
- Pallor.
- Rapid, weak pulse.
- Nausea.
- Vomiting.
- Abdominal pain.
- Hypotension (drop in blood pressure).
- Loss of consciousness.
Prevention is the best management approach for Addisonian crisis. The patients who are on long-term corticosteroid treatment should carry his/her Steroid Treatment Card which carries details of prescriber, drug given, dosage and duration of treatment. It helps in minimizing the risk of precipitation of adrenal crisis.
| Classification of corticosteroids on the basis of their onset of action | ||
|---|---|---|
| Glucocorticoid | Approximate equivalent dose (mg) | Half-life (hr) |
| Short Acting | ||
| Cortisone | 25 | 8-12 |
| Hydrocortisone | 20 | 8-12 |
| Intermediate Acting | ||
| Methylprednisolone | 4 | 18-36 |
| Prednisolone | 5 | 18-36 |
| Prednisone | 5 | 18-36 |
| Triamcinolone | 4 | 18-36 |
| Long Acting | ||
| Betamethasone | 0.6 – 0.75 | 36-54 |
| Dexamethasone | 0.75 | 36-54 |
If adrenal crisis precipitates during dental treatment of the patient, the treatment is terminated and the vital signs of the patient are monitored. The patient is placed in dorsal decubitus position and the medical emergency service is contacted. If the patient is unconscious, maintenance of the airway is of prime importance. The basic life support should be given immediately as soon as the adrenal crisis is anticipated. The patient ……. Contents available in the book……. Contents available in the book……. Contents available in the book……. Contents available in the book…….
Conclusion
In the above discussion, we studied various endocrine disorders and the management of patients with these disorders in dental practice. However, it should be remembered that in patients with severe endocrinal problems, physician should be consulted before performing the dental treatment. In the upcoming articles, we shall read about various other medical problems and the protocol for the periodontal treatment of patients with these disorders.
References
References are available in the hard-copy of the website.
Periobasics: A Textbook of Periodontics and Implantology
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