Oral and Radiological manifestations of endocrinal disorders

The term ‘endocrine’ was coined by Ernest Starling.

The word endocrine has evolved from two Greek words ‘νδο– endo‘inside, within’, and ‘κρίνειν krinein–‘to separate, distinguish’.

Endocrine Glands are ductless glands that secrete hormones within specific organs and release them directly into the intercellular fluid or into the blood.

Based on chemical nature, hormones are of three types:

  1. Steroid hormones
  2. Protein hormones
  3. Derivatives of the amino acid called tyrosine.

1.   Aldosterone.

2.   11-deoxycorticosterone.

3.   Cortisol.

4.   Corticosterone.

5.   Testosterone.

6.   Dihydrotestosterone.

7.   Dehydroepiandrosterone.

8.   Androstenedione.

9.   Estrogen.

10. Progesterone.

1.   Growth hormone (GH).

2.   Thyroid-stimulating hormone (TSH).

3.   Adrenocorticotropic hormone (ACTH).

4.   Follicle-stimulating hormone (FSH).

5.   Luteinizing hormone (LH).

6.   Prolactin.

7.   Antidiuretic hormone (ADH).

8.   Oxytocin.

9.   Parathormone.

10.  Calcitonin.

11.  Insulin.

12.  Glucagon.

13.  Somatostatin.

14.  Pancreatic polypeptide.

15.  Human chorionic gonadotropin (HCG).

16. Human chorionic somatomammotropin.

  1. Thyroxine (T4)
  2. Triiodothyronine (T3)
  3. Adrenaline (Epinephrine)
  4. Noradrenaline (Norepinephrine)
  5. Dopamine.

A.   Anterior pituitary

1. Growth hormone (GH).

2. Thyroid stimulating hormone (TSH).

3. Adreno corticotropic hormone (ACTH).

4. Follicle stimulating hormone (FSH).

5. Luteinizing hormone (LH).

6. Prolactin.

B.   Posterior pituitary

1. Antidiuretic hormone (ADH)

2. Oxytocin

C.   Thyroid gland

1. Thyroxine (T4)

2. Triiodothyronine (T3)

3. Calcitonin

D.  Parathyroid gland

 1. Parathormone.

E.   Pancreas – Islets of Langerhans

1. Insulin

2. Glucagon

3. Somatostatin

4. Pancreatic polypeptide.

F.   Adrenal cortex

1. Mineralocorticoids

a.    Aldosterone

b.   11deoxycorticosterone

2. Glucocorticoids

a.    Cortisol

b.   Corticosterone

3. Sex hormones

a.    Androgens

b.   Estrogen

c.    Progesterone

4. Adrenal medulla

1. Catecholamines

2. Adrenaline (Epinephrine)

3. Noradrenaline (Norepinephrine)

4. Dopamine

  • Hormone receptors are the large proteins that are present in target cells.
  • Each cell has thousands of receptors.
  • Each receptor is specific for one single hormone. In this way a hormone can act on a target cell, only if the target cell has the receptor for that particular hormone.

Hormone receptors are situated either in cell membrane or cytoplasm or nucleus of the target cells as follows:

  1. Cell membrane: In cell membrane receptors of protein hormones and adrenal medullary hormones (catecholamines) are situated.
  2. Cytoplasm: Receptors of steroid hormones are situated in the cytoplasm of target cells
  3. Nucleus: Receptors of thyroid hormones are in the nucleus of the cell.

Hormone does not act on the target cell directly. It combines with receptor to form hormone-receptor complex. This complex executes the hormonal action.

Hormone complex executes the hormonal action by any one of the following mechanisms:

  1. By altering permeability of cell membrane
  2. By activating intracellular enzyme
  3. By acting on genes.

The hormone which acts on a target cell is called first messenger or chemical mediator. It combines with the receptor and forms hormone-receptor complex.

Hormone-receptor complex activates the enzymes of the cell and causes the formation of another substance called the second messenger or intracellular hormonal mediator.

Second messenger produces the effects of the hormone inside the cells.

Protein hormones and catecholamines act through second messenger.

  1. Cyclic AMP
  2. Calcium ions and calmodulin
  3. Inositol triphosphate
  4. Diacylglycerol
  5. Cyclic guanosine monophosphate
  1. Pituitary gland or hypophysis is a small endocrine gland with a diameter of 1 cm and weight of 0.5 to 1 g.
  2. It is situated in a depression called ‘sella turcica’, present in the sphenoid bone at the base of skull.
  3. It is connected with the hypothalamus by the pituitary stalk or hypophyseal stalk.

Pituitary gland has two divisions:

  1. Anterior pituitary or adenohypophysis
  2. Posterior pituitary or neurohypophysis.
  3. Between the two divisions, there is a small and relatively avascular structure called pars intermedia.
  1. Anterior pituitary is ectodermal in origin and arises from the pharyngeal epithelium as an upward growth known as Rathke’s pouch.
  2. Posterior pituitary is neuroectodermal in origin and arises from hypothalamus as a downward diverticulum.

Six hormones are secreted by the anterior pituitary:

  1. Growth hormone (GH) or somatotropic hormone (STH).
  2. Thyroid-stimulating hormone (TSH) or thyrotropic hormone.
  3. Adrenocorticotropic hormone (ACTH).
  4. Follicle-stimulating hormone (FSH).
  5. Luteinizing hormone (LH) in females or interstitial cell- stimulating hormone (ICSH) in males.
  6. Prolactin

Recently, the hormone β-lipotropin was found to be secreted by anterior pituitary.

GH, TSH, ACTH, FSH and LH hormones stimulate the other endocrine glands. GH stimulates the secretory activity of liver and other tissues. Therefore, these five hormones are called tropic hormones.

Follicle-stimulating hormone and the luteinizing hormone are together called gonadotropic hormones or gonadotropins because of their action on gonads.

  1. Human growth hormone (HGH) controls growth of the body and targets the bone, muscle and adipose tissue.
  2. Thyroid stimulating hormone (TSH) controls the secretion of hormones by the thyroid gland and targets thyroid gland.
  3. Adrenocorticotropic hormone (ADH) controls the secretion of hormones by the adrenal cortex and targets the outer portion of the adrenal gland (cortex).
  4. Follicle stimulating hormone (FSH) a gonadotropin which stimulates the maturation of primary sex organs (ovary and testis) and targets the primary sex organs.
  5. Luteinizing hormone (LH) targets primary sex organs and causes ovulation in females and secretion of testosterone in males.
  6. Prolactin (PRL) stimulates the production of milk by the mammary glands and targets the mammary glands.

Posterior pituitary hormones are:

  1. Antidiuretic hormone (ADH) or vasopressin
  2. Oxytocin

Antidiuretic hormone has two actions:

  1. Retention of water
  2. Vasopressor action.

It increases the facultative reabsorption of water from distal convoluted tubule and collecting duct in the kidneys which are totally impermeable to water in absence of ADH. So, reabsorption of water does not occur in the renal tubules and dilute urine is excreted it results in loss of large amount of water through urine. This condition is called diabetes insipidus and the excretion of large amount of water is called diuresis.

ADH acts on blood vessels through V1A receptors. It has vasoconstrictor action in large amount that causes constriction of the arteries in all parts of the body. So blood pressure gets increased. However, the amount of ADH required to cause the vasopressor effect is greater than the amount required to cause the antidiuretic effect.

  • Oxytocin is secreted in both males and females. In females, oxytocin acts on mammary glands and
  • In males, the release of oxytocin increases during It facilitates release of sperm into urethra.

Oxytocin acts on mammary glands and uterus by activating G-protein coupled oxytocin receptor.

The hyperactivity of adenohypophysis, called hyperpituitarism, results in the following disorders: Gigantism, Acromegaly, Acromegalic Gigantism, Cushing’s Disease.

Gigantism is the pituitary disorder characterized by excess growth of the body, due to hypersecretion of GH in childhood or pre-adult life before the fusion of epiphysis of bone with the shaft.

  1. Increase in the length of the dental arches, resulting in spacing of the teeth.
  2. Maxillary widening.
  3. Jaw malocclusion and overbite.
  4. Protruding and prominent mandible due to mandibular and condylar overgrowth.
  5. Increase in the thickness and height of alveolar processes.
  6. Palatal vault is usually flattened
  7. Tongue increases in size and may cause crenations on its lateral border.
  8. Soft tissue growth may produce uniform macroglossia.
  9. Lips are found thick.
  1. True lateral skull, lateral cephalogram, paranasal view, postero-anterior skull view characteristically reveal enlarged supra orbital ridges and underlying frontal sinuses and increased pneumatisation of temporal bone.
  2. Intraoral periapical radiographs reveal macrodontia because the teeth size is proportional to the size of jaws and the body, roots may be larger than normal.

Acromegaly also called adult hyperpituitarism, is a disorder characterized by progressive cosmetic disfigurement and systemic organ manifestation with the enlargement, thickening and broadening of bones, particularly in the extremities of the body.

  1. Acromegalic or gorilla face: Face with rough features such as protrusion of supraorbital ridges, broadening of nose, thickening of lips, thickening and wrinkles formation on forehead and
  2. Jaw malocclusion and overbite.
  3. Enlarged tongue with teeth indentations on the lateral border.
  4. Soft palate hyperplasia causes sleep apnoea and airway obstruction.
  5. Thickening of the skin is due to deposition of glycosaminoglycan and increased collagen synthesis.

Skull radiographs characteristically reveal:

  1. Enlargement (ballooning) of the sella turcica (if an enlarged pituitary adenoma is present).
  2. Prominent supraorbital ridges, paranasal sinuses (frontal sinus).
  3. Increased pneumatisation of temporal bone.
  4. Thickening of the outer table of the skull.
  5. Thickened malar bones and zygomatic arches with enlarged maxilla.

Jaw radiographs reveal:

  1. Enlargement of the mandible (greatest change in the facial bones, leading to chin protrusion, responsible for typical facial appearance).
  2. Excess condylar growth and height of ascending ramus resulting in class III

skeletal relationship.

  1. Increased angle between the ramus and body of the mandible with loss of antegonial notch, this in combination with uniform macroglossia and maxillary widening, may result in anterior flaring of the teeth and development of an apertognathia (anterior open bite).
  2. The thickness and height of alveolar processes may also increase.

Intraoral periapical radiographs reveal:

  1. Large pulp chambers (taurodontism) and excessive deposition of cementum on the roots.

Supraeruption of the posterior teeth (to compensate for the mandibular overgrowth).

  1. Cardio-vascular complications: concentric biventricular hypertrophy or heart failures
  2. Respiratory complications: sleep apnea.
  3. Metabolic complications: impaired glucose intolerance due to growth hormone-induced insulin resistance.
  4. Lipid abnormalities: hypertriglyceridemia.
  5. Muskuloskeletal complications.
  • Acromegalic gigantism is a rare disorder with symptoms of both gigantism and acromegaly.
  • Hypersecretion of GH in children, before the fusion of epiphysis with shaft of the bones causes gigantism and if hypersecretion of GH is continued even after the fusion of epiphysis, the symptoms of acromegaly also appear.
  • Also k/a Corticotroph adenoma, pituitary dependent Cushing’s syndrome.
  • Cushing’s disease is considered a rare condition characterized by the hypersecretion of the adrenocorticotropic hormone (ACTH) due to a pituitary adenoma that ultimately causes endogenous hypercortisolism by stimulating the adrenal glands.

When the secretion of adrenocorticotropic hormone increases due to the ‘pituitary cause’ it is called Cushing disease and when it is due to the ‘adrenal cause’, it is called Cushing syndrome.

Chronic glucocorticoid excess, or Cushing’s syndrome, may be due to ACTH-dependent (80% cases) or –independent (20% cases):

  ACTH dependent

  Cushing’s syndrome

Cushing’s disease or ACTH secreting pituitary adenoma

Ectopic ACTH secretion

  ACTH independent

  Cushing’s syndrome

Adrenal adenoma

Adrenal carcinoma

Bilateral adrenal hyperplasia

Iatrogenic Cushing’s syndrome

(Exogenous glucocorticoid exposure)

  Pseudo-Cushing’s syndrome

Obesity

Alcoholism

Depression

  1.  Clinical characteristics

    Hypercortisolic state may include: Obesity 

    2.   Protein wasting

    a.    Thin skin.

    b.   Abdominal purple to red and white cutaneous striae.

    c.    Easy bruising.

    d.   Slow healing.

    3.   Muscle wasting (lower limbs muscle atrophy).

    4.   Bone wasting leading to osteoporosis.

    5.   High blood pressure.

    6.   Increased rate of infections.

    7.   Gonadal dysfunction and hyperandrogenism.

    8.   Menstrual irregularity (oligoamenorrhea, amenorrhea).

    9.   Anxiety.

    10.  Depression

    11.  Irritability.

  1. Generalized osteoporosis (granular bone pattern).
  2. Pathologic fractures.
  3. Skull radiograph shows diffuse thinning accompanied by a mottled appearance.
  4. The teeth may erupt prematurely.
  5. Partial loss of the lamina dura.
  1. 24-Hour urine-free cortisol test-

In this test, a person’s urine is collected several times over a 24-hour period and tested for cortisol. Levels higher than 50 to 100 micrograms a day for an adult suggest Cushing’s syndrome.

  1. Late night salivary cortisol and serum cortisol tests-
  • Midnight plasma cortisol test measures cortisol concentrations in the blood. Cortisol production is normally suppressed at night, but in Cushing’s syndrome, this suppression doesn’t occur.
  • Late-night or bedtime saliva sample can be obtained at home, then tested to determine the cortisol level.
  1. Low-dose dexamethasone suppression test (LDDST).

In the LDDST, a person is given a low dose of dexamethasone, a synthetic glucocorticoid, by mouth every 6 hours for 2 days. Urine is collected before dexamethasone is administered and several times on each day of the test.

Cortisol and other glucocorticoids signal the pituitary to release less ACTH, so the normal response after taking dexamethasone is a drop in blood and urine cortisol levels. If cortisol levels do not drop, Cushing’s syndrome is suspected.

  1. Dexamethasone-corticotropin-releasing hormone (Crh) test –

This test combines the LDDST and a CRH stimulation test. In the CRH stimulation test, an injection of CRH causes the pituitary to secrete ACTH. Pretreatment with dexamethasone prevents CRH from causing an increase in cortisol in people with pseudo-Cushing’s. Elevations of cortisol during this test suggest Cushing’s syndrome.

  1. High-dose dexamethasone suppression test (hDDST). The HDDST is the same as the LDDST, except it uses higher doses of dexamethasone.
  2. CRH stimulation test- The CRH test, without pretreatment with dexamethasone, As a result of the CRH injection, people with pituitary adenomas usually experience a rise in blood levels of ACTH and cortisol because CRH acts directly on the pituitary.
  1. Radiologic imaging: direct visualization of the endocrine glands- Imaging tests reveal the size and shape of the pituitary and adrenal glands and help determine if a tumor is present. The most common imaging tests are the computerized tomography (CT) scan and magnetic resonance imaging (MRI).
  2. Petrosal sinus sampling- This test is not always required, but in many cases, it is the best way to distinguish pituitary from ectopic causes of Cushing’s syndrome. Samples of blood are drawn from the petrosal sinuses—veins that drain the pituitary––by inserting tiny tubes through a vein in the upper thigh or groin region. 

Treatment depends on the specific reason for excess cortisol and may include surgery, radiation, chemotherapy, or the use of cortisol-inhibiting drugs.

Hypo activity of the adenohypyphysis, called hypopituitarism, results in the following disorders: Dwarfism, Acromicria, Simmond’s disease and Progeria.

Dwarfism (pituitary dwarfs) is pituitary disorder in children characterized by stunted growth or short stature of the affected person, caused by reduction in the GH secretion in infancy or early childhood.

  1. Failure of the development of the jaws (small maxilla and mandible).
  2. The face appears small.
  3. Agenesis of the upper central incisor and solitary maxillary central Incisor.
  4. Amelogenesis imperfecta.
  5. Permanent teeth showing a delayed pattern of eruption.
  6. Often the shedding pattern of deciduous teeth is delayed by several years development of roots of permanent teeth appears to be delayed.
  7. The dental arches are smaller than the normal and therefore cannot accommodate all the teeth resulting in dental malocclusion.

Radiographic features include:

  1. Delayed exfoliation of deciduous teeth for 1-3 years and delayed eruption of permanent teeth for 3-10 years, because of delayed development of the roots of permanent teeth.
  2. Third molar buds may be completely absent, even in the fourth decade of life.
  3. Small jaws (dental arches) and retarded mandibular and maxillary growth.
  4. The anatomical crowns are normal in size but clinical crowns are smaller because of the incomplete eruption of teeth. It is due to roots of the teeth, which are shorter and apices are wide open with the pulp canal diverging towards the apex leading to incomplete eruption.
  5. Over calcification of the substance of the teeth.
  6. Retrusion of chin and supported structures are retarded in growth.

Simmonds’ disease is a rare pituitary disease. It is also called pituitary cachexia. It occurs in panhypopituitarism, i.e. hyposecretion of all the anterior pituitary hormones due to the atrophy or degeneration of anterior pituitary.

  1. Rapidly developing senile decay.
  2. The senile decay is mainly due to deficiency of hormones from target glands of anterior pituitary, i.e. the thyroid gland, adrenal cortex and the gonads.
  3. Loss of hair over the body and loss of teeth.
  4. Skin on face becomes dry and wrinkled.
  5. Marked alveolar resorption.

Progeria characterized by premature senility in an individual of infantile proportions. The condition commences between 3months and 3 years.

  1. Normal at birth but by the age 1or 2 years there is severe growth retardation.
  2. Dwarf individual with normal skeletal maturation.
  3. Short stature and lower weight for height.
  4. Balding, loss of eyebrows and eye lashes.
  5. Skin is lax and wrinkled (widespread loss of cutaneous fat).
  6. Alopecia.
  7. Prominent scalp veins.
  8. Prominent eyes.
  9. Beaked nose and a “plucked bird” appearance.
  10. Thin and high pitched voice.
  11. Pyriform thorax.

Oral manifestations include:

  1. Delayed dentition
  2. Micrognathia
  3. Thin lips.

Radiographic features include:

  1. Osteoporosis of long bones.
  2. Craniofacial disproportion.
  3. Short dystrophic clavicles.
  4. Increased size of the skull is due to over development of frontal and parietal bones, with small mandible and retracted chin. These features resemble that of a wizened old person who has a stature of a small child.
  5. Ossification may be delayed and deficient, arteriosclerosis.
  6. Structure of bone is unaltered except in those areas where teeth have failed to develop when there is deficiency of trabeculae.
  7. Wide variation in number of teeth.
  8. Overcrowding.

Deficiency of GH in adults causes Acromicria. Atrophy of extremities, hyposecretion of adrenocortical hormones and loss of sexual functions are some prominent symptoms.

  1. Deficiency of GH-releasing hormone from
  2. Atrophy or degeneration of acidophilic cells in the anterior pituitary.
  3. Tumor of chromophobes.
  4. Panhypopituitarism.

Hyperactivty of posterior pituitary results in syndrome of inappropriate hypersecretion of antidiuretic hormone (SIADH).

This disease is due to the excessive secretion of antidiuretic hormone from the posterior pituitary. The major symptom of this disorder is reduction in urine output. The urine, that is formed, is concentrated because antidiuretic hormone causes continuous reabsorption of water.

Cerebral tumors, lung tumors and lung cancers because tumor cells and cancer cells secrete ADH.

Diabetes Insipidus: The deficiency of antidiuretic hormone causes diabetes insipidus. This disease is characterized by excessive excretion of water through urine.

This disease is caused by severe depression or suppression of                      neu­rohypophysial hormone vasopressin (ADH) secretion. It is of two types:

1.  Neurogenic

2.  Nephrogenic.

  1. Neurogenic type: Due to damage of hypathalamo-hypophysial system, or de­velopment of hypothalamic tumour, or damage of nervous system,or infections etc.
  2. Nephrogenic type: Due to unresponsive­ness of renal tissue to vasopressin or re­nal infections, or renal defects.
  1. Polyuria (production of large volume of urine).
  2. Poly dypsia (severe thirst).
  3. Hypokalemia (electrolyte disorder).
  4. Physical and mental retardation.
  5. Dilation of urinary bladder.

It results in Dystrophia Adiposogenitals (Frolich’s syndrome or hypothalamic eunuchism): This disease is characterised by obesity and hypogonadism affecting mostly adolescent boys.

Thyroid is an endocrine gland situated at the root of the neck on either side of the trachea. It has two lobes, which are connected in the middle by an isthmus. It weighs about 20 to 40 g in adults. Thyroid is larger in females than in males.

Thyroid gland secretes three hormones:

  1. Tetraiodothyronine or T4 (thyroxine).
  2. Tri-iodothyronine or T3.
  3. 3. Calcitonin.

Thyroid hormones are transported in the blood by three types of proteins:

  1. Thyroxine-binding globulin (TBG).
  2. Thyroxine-binding prealbumin (TBPA).
  3. Albumin.

Thyroid hormones have two major effects on the body:

  1. To increase basal metabolic rate
  2. To stimulate growth in children.

Secretion of thyroid hormones is controlled by anterior pituitary and hypothalamus through feedback mechanism.

Thyroid-stimulating hormone (TSH) secreted by anterior pituitary helps in regulating the synthesis and release of thyroid hormones. It is also necessary for the growth and the secretory activity of the thyroid gland. Thus, TSH influences every stage of formation and release of thyroid hormones.

Thyroid-stimulating hormone increases:

  1. The number of follicular cells of thyroid.
  2. The conversion of cuboidal cells in thyroid gland into columnar cells and    thereby it causes the development of thyroid follicles.
  3. Size and secretory activity of follicular cells.
  4. Iodide pump and iodide trapping in follicular cells.
  5. Thyroglobulin secretion into follicles.
  6. Iodination of tyrosine and coupling to form the hormones.
  7. Proteolysis of the thyroglobulin, by which release of hormone is enhanced    and colloidal substance is decreased.
  8. Immediate effect of TSH is proteolysis of the thyroglobulin, by which    thyroxine is released within 30 minutes.

Hypothalamus regulates thyroid secretion by controlling TSH secretion through thyrotropic-releasing hormone (TRH). From hypothalamus, TRH is transported through the hypothalamo-hypophyseal portal vessels to the anterior pituitary. After reaching the pituitary gland, the TRH causes the release of TSH.

Iodide is an important factor regulating the synthesis of thyroid hormones. When the dietary level of iodine is moderate, the blood level of thyroid hormones is normal. However, when iodine intake is high, the enzymes necessary for synthesis of thyroid hormones are inhibited by iodide itself, resulting in suppression of hormone synthesis. This effect of iodide is called Wolff- Chaikoff effect.

Factors that increase the secretion of thyroid hormones:

  1. Low basal metabolic rate
  2. Leptin
  3. α-melanocyte-stimulating hormone
  4. low body temperature.

Leptin (from adipose tissue) and α-melanocytestimulating hormone (from pituitary) increase the release of TRH and synthesis of T4. However, this occurs only in infants.

Factors decreasing the secretion of thyroid hormones:

  1. Excess iodide intake.
  2. Stress.
  3. Somatostatin.
  4. Glucocorticoids.
  5. Dopamine.

These factors decrease the secretion of thyroid hormones, by inhibiting the release of TRH.

Hypothyroidism is defined by a decrease in thyroid hormone production and thyroid gland function.

Hypothyroidism leads to myxedema in adults and cretinism in children.

  1. Chronic thyroiditis (Hashimoto’s disease).
  2. Radioactive iodine.
  3. Surgery.
  4. Pharmacological agents e.g lithium and amiodarone.
  1. Slower metabolic rate.
  2. Weight gain.
  3. Lethargy.
  4. Intolerance to cold.
  5. Dry and cool skin.
  6. Frog-like husky voice.
  7. Extreme somnolence with sleeping up to 14 to 16 hours per day.
  8. Menorrhagia and polymenorrhea.
  9. Puffiness of the face and eyelids.
  10. The blood pressure appears to be normal, but the heart rate is slow.
  1. Thick lips.
  2. Macroglossia.
  3. Malocclusion and delayed eruption of teeth.
  4. Impaction of the mandibular second molars.
  5. Dysgeusia.
  6. Delayed eruption.
  7. Poor periodontal health.
  8. Altered tooth morphology.
  9. Delayed wound healing.

It is severe and long term effect due to dissociation of ramus growth and failure of normal resorption of the internal aspect of the ramus, resulting in insufficient space for proper eruption of these teeth.

  1. Fontanelle remain open for an abnormal length of time.
  2. Delayed closing of epiphysis and skull sutures with the production of numerous worming bones (accessory bones in the sutures).
  3. Marked disproportion between the head and body (wide head).
  4. Relatively small maxilla and mandible.
  5. Delayed eruption of permanent teeth.
  6. Short roots.
  7. Thinning of lamina dura.
  8. Maxilla and mandible are relatively small.
  1. Delayed permanent teeth eruption.
  2. Enamel hypoplasia in both dentitions.
  3. Loss of teeth.
  4. Loss of lamina dura.
  5. Micrognathia.
  6. Separation of teeth as a result of enlargement of tongue.
  7. External root resorption.
  8. Open bite due to lack of condylar and mandibular growth.
  9. Generalized osteoporosis leading to decreased height of the alveolar bone.
  1. Consulting the patients’ physician and carrying out a detailed general clinical history before performing dental treatment is indicated.
  2. In uncontrolled patients, oral infection, central nervous depressants such as narcotics and barbiturates should be avoided because they may cause an exaggerated response.
  3. In controlled patients, narcotics and barbiturates drugs should be used sparingly, with a reduced dosage. Presence of oral infection, drugs and surgical procedures can precipitate a myxedematous coma.
  4. Myxedematous coma includes: Hypothermia, bradycardia, severe hypotension and epileptic seizure. If that happens, dental treatment should be discontinued and access to emergency medical services should be available.
  5. Drug interactions of 1-thyroxine includes:
  • Metabolism increases upon use of phenytoin, rifampin and carbamazepine.
  • Absorption is impaired when iron sulfate, sucralfate and aluminum hydroxide are used.
  • Concomitant use of tricyclic antidepressants elevates, 1-thyroxine levels.
  1. Patients are susceptible to cardiovascular disease; therefore they may be on anticoagulation therapy so complete blood count is required to evaluate coagulation factors.
  2. Antibiotic prophylaxis must be assessed in valvular pathology and atrial fibrillation.

Hyperthyroidism is a condition caused by unregulated production of thyroid hormones. It is characterized by:

  1. Tremor.
  2. Emotional instability
  3. Intolerance to heat.
  4. Sinus tachycardia
  5. Marked chronotropic and ionotropic effects.
  6. Increased cardiac output (increased susceptibility to congestive heart failure).
  7. Systolic heart murmur.
  8. Hypertension
  9. Increased appetite and weight loss.
  10. Toxic goiter.
  11. Oligomenorrhea or amenorrhea.
  12. Exophthalmos.

Hyperthyroidism is caused by:

  1. Graves’ disease
  2. Thyroid adenoma.

It is autoimmune disease and common cause of hyperthyroidism. In this B lymphocytes (plasma cells) produce autoimmune antibodies called thyroid-stimulating autoantibodies (TSAbs). These antibodies act like TSH by binding with membrane receptors of TSH and activating cAMP system of the thyroid follicular cells. This results in hypersecretion of thyroid hormones.

Sometimes, a localized tumor develops in the thyroid tissue. It is known as thyroid adenoma and it secretes large quantities of thyroid hormones.

  1. Increased susceptibility to caries.
  2. Periodontal disease.
  3. Enlargement of extraglandular thyroid tissue.
  4. Maxillary or mandibular osteoporosis.
  5. Accelerated dental eruption.
  6. Burning mouth syndrome.
  7. Sjogren’s syndrome.
  1. Consult the patients’ physician and carrying out a detailed general clinical history before performing dental treatment is indicated.
  2. In controlled patients- Avoid severe stress situations and the spread of infectious foci.
  3. In uncontrolled cases- Restrict the use of epinephrine or other pressor amines because the myocardium of these patients is sensitive to adrenaline and may unleash arrhythmias, palpitations and chest pain.
  4. Avoid surgical procedures because presence of acute oral infection and severe stress may precipitate thyroid storm crisis.
  5. If emergency dental treatment is required, consult endocrinologist.
  6. Treatment should be discontinued if signs or symptoms of a thyrotoxic crisis develop and access to medical emergency.
  7. Symptoms of thyrotoxic crisis are tachycardia, irregular pulse, sweating, hypertension, tremor, nausea, vomiting, abdominal pain & coma.
  8. Patients taking propylthiouracil must be monitored for agranulocytosis,  hypoproteinemia or bleeding, and complete blood count, prothrombin  time before invasive procedures.
  9. These patients are susceptible to central nervous system depressant  drugs such as barbiturates.
  10. NSAIDs should also be used with caution and who take β-blockers, as the former can decrease the efficiency of the latter.

Goiter means enlargement of the thyroid gland. It occurs both in hypothyroidism and hyperthyroidism.

Goiter in Hyperthyroidism – Toxic Goiter

Toxic goiter is the enlargement of thyroid gland with increased secretion of thyroid hormones, caused by thyroid tumor.

Goiter in Hypothyroidism – Non-toxic Goiter

Non-toxic goiter is the enlargement of thyroid gland without increase in hormone secretion. It is also called hypothyroid goiter. Based on the cause, the non-toxic hypothyroid goiter is classified into two types.

  1. Endemic colloid goiter
  2. Idiopathic non-toxic goiter.

Endemic colloid goiter is the non-toxic goiter caused by iodine deficiency. It is also called iodine deficiency goiter. Iodine deficiency occurs when intake is less than 50 μg/day.

Idiopathic non-toxic goiter is the goiter due to unknown cause. Enlargement of thyroid gland occurs even without iodine deficiency. It may be due to thyroiditis and deficiency of enzymes such as peroxidase, iodinase and deiodinase, which are required for thyroid hormone synthesis.

Calcitonin is secreted by the parafollicular cells or clear cells (C cells), situated amongst the follicles in thyroid gland.

  • Calcitonin decreases the blood calcium level and thereby counteracts parathormone.
  • Calcitonin reduces the blood calcium level by acting on bones, kidneys and intestine.

Calcitonin stimulates osteoblastic activity and facilitates the deposition of calcium on bones. At the same time, it suppresses the activity of osteoclasts and inhibits the resorption of calcium from bones. It inhibits even the development of new osteoclasts in bones.

Calcitonin increases excretion of calcium through urine, by inhibiting the reabsorption from the renal tubules.

  1. Measurement of plasma level of T3 and T4: For hyperthyroidism or hypothyroidism, the most accurate diagnostic test is the direct measurement of concentration of “free” thyroid hormones in the plasma, i.e. T3 and T4.
  2. Measurement of TRH and TSH: There is almost total absence of these two hormones in hyperthyroidism. It is because of negative feedback mechanism, by the increased level of thyroid hormones.
  3.  Measurement of basal metabolic rate: In hyperthyroidism,basal metabolic rate is increased by about 30% to 60%. Basal metabolic rate is decreased in hypothyroidism by 20% to 40%.
  • There are four parathyroid glands, situated on the posterior surface of upper and lower poles of thyroid gland.
  • These are very small in size, measuring about 6 mm long, 3 mm wide and 2 mm thick, with dark brown color.

Parathormone secreted by parathyroid gland.

Parathormone is essential for the maintenance of blood calcium level within a very narrow critical level. Maintenance of blood calcium level is necessary because calcium is an important inorganic ion for many physiological functions.

PTH maintains blood calcium level by acting on:

  1. Bones
  2. Kidney
  3. Gastrointestinal tract.

It enhances the resorption of calcium from bones (osteoclastic activity) by acting on osteoblasts and osteoclasts of the bone via two phases:

  1. Rapid phase
  2. Slow phase.

Rapid phase

  • Occurs within minutes after the release of PTH.
  • Immediately after reaching the bone, PTH gets attached with the receptors on the cell membrane of osteoblasts and osteocytes that increases the permeability of membranes of these cells for calcium ions so that calcium ions move out of these bone cells and enter the blood at a faster rate.

Slow phase

Slow phase of calcium resorption from bone is due to the activation of osteoclasts by PTH.

PTH increases the reabsorption of calcium from renal tubules along with magnesium ions and hydrogen ions from distal convoluted tubule and proximal part of collecting duct. It increases the formation of 1, 25- dihydroxycholecalciferol (activated form of vitamin D) from 25-hydroxycholecalciferol in kidneys.

PTH increases the absorption of calcium ions from the GI tract indirectly. 1,25- dihydroxycholecalciferol increases the absorption of calcium from GI tract. So activated vitamin D is very essential for the absorption of calcium and PTH plays important role in formation of activated vitamin D.

In liver and kidney vitamin D has to be converted into 1, 25-dihydroxycholecalciferol in the presence of PTH. The 1,25-dihydroxycholecalciferol is active product.

  • Important form of vitamin D is vitamin D3(cholecalciferol).
  • It synthesized in the skin from 7-dehydrocholesterol, by the action of ultraviolet rays from the It is also obtained from dietary sources. Activation of vitamin D3 occurs in two steps:

First step:

Cholecalciferol (vitamin D3) is converted into 25- hydroxycholecalciferol in the liver. This process is inhibited by 25-hydroxycholecalciferol itself by feedback mechanism for two reasons:

  1. Regulation of the amount of active vitamin D
  2. Storage of vitamin D for months together.

Second Step:

25-hydroxycholecalciferol is converted into 1,25- dihydroxycholecalciferol (calcitriol) in kidney in presence of PTH . It is the active form of vitamin D3.

If vitamin D3 is converted into 25-hydroxycholecalciferol, it remains in the body only for 2 to 5 days. But vitamin D3 is stored in liver for several months.

  • When blood calcium level increases, it inhibits the formation of 1, 25-dihydroxycholecalciferol.
  • Increase in calcium ion concentration decreases the PTH secretion, that also suppress the formation of 1, 25-dihydroxycholecalciferol.
  • When the PTH synthesis is inhibited, the conversion of 25-hydroxycholecalciferol into 1, 25-hydroxycholecalciferol is also inhibited. Lack of 1, 25-dihydroxycholecalciferol, decreases the absorption of calcium ions from the intestine, from the bones and from the renal tubules. This makes the calcium level in the plasma to fall back to normal.
  • PTH decreases blood level of phosphate by increasing its urinary excretion.
  • PTH increases phosphate absorption from the bones.
  • Phosphaturic action: It is the effect of PTH by which phosphate is excreted through urine. PTH increases phosphate excretion by inhibiting reabsorption of phosphate from renal tubules.
  • Parathormone increases the absorption of phosphate from GI tract through calcitriol.

Hyperparathyroidism is characterized by hypersecretion of PTH.

Hyperparathyroidism is of three different types:

  • Primary
  • Secondary
  • Tertiary
  1. Primary hyperparathyroidism- Is due to the development of tumour in one or more parathyroid glands, resulting in overproduction of excess PTH.
  2. Secondary hyperparathyroidism- Is due to the physiological compensatory hypertrophy of parathyroid glands in response to hypocalcaemia. Occurs due to:
    • Chronic renal failure.
    • Vitamin D deficiency.
    • Rickets.
  3. Tertiary hyperparathyroidism-Is due to hyperplasia (abnormal increase in the number of cells) of all the parathyroid glands that develops due to chronic secondary hyperparathyroidism.

In primary HPT there will be no symptoms and problem is picked up as an incidental finding (via raised calcium or characteristic X-ray appearances [subperiosteal resorption of the phalanges of the index and middle fingers]).

Nonspecific symptoms:

1.   Musculoskeletal problems:

·         Weakness.

·         Back pain.

·         Muscle soreness.

2.   Gastrointestinal complaints:

·         Vomiting.

·         Nausea.

·         Constipation.

·         Loss of appetite.

Other clinical manifestations of HPT are:

1.   Bone disease:

·         Ribs, clavicles, pelvic girdle and mandible are mostly involved.

·         Pathological fracture.

·         Bone pain and joint stiffness.

2.   Renal calculi.

3.   Patients with HPT have skeletal lesions in the advanced stages.

Generalized Osteoporosis (due to loss of calcium)

  1. Brown tumor.
  2. Loss of bone density.
  3. Mobility in teeth.
  4. Complain of vague jaw bone pain.
  5. Sensitive teeth in mastication and percussion.
  6. Soft tissue calcifications.
  7. Dental abnormalities such as developmental defects, alterations in dental eruption.
  8. Malocclusion due to drifting of teeth with definite spacing of the teeth.
  9. Pseudocystic lesion can also be presents, radiolucent lesion at the apex of tooth.
  • Brown tumor presents itself as a friable red-brown mass.
  • I presents as osteolytic lesion (which may be associated with pain and swelling) that develops due to changes in bone metabolism
  • Caused by high serum concentration of PTH.
  • It is an erosive bony lesions caused by rapid osteolysis and peritrabecular fibrosis resulting in a local destructive phenomenon.
  • Bone lesion may produce significant cortical expansion.
  • Mandible involvement is common (premolars and molars area), rare in the maxilla.
  • Well-defined uni or multilocular radiolucent areas.
  • Widespread loss of the lamina dura
  • Changes in trabeculae pattern bone of the jaws.
  • Significant expansion of cortical bone.
  • Root resorption
  • Displacement of roots.

Aneurismal bone cyst, cherubism, central giant cell granuloma.

Sagliker syndrome includes uglifying appearance to the face (unique facial bone changes), short stature, extremely severe maxillary and mandibular changes, class II malocclusion of upper and lower jaws, teeth/dental abnormalities, fingertip changes, knee and scapula deformities, hearing abnormalities, neurological and severe psychological problems.

  • Rare disease, with involvement of other family members.
  • Patient presents with bilateral or recurrent mandibular radiolucencies diagnosed histopathologically as cemento-ossifying fibromas. It is due to mutation of genes.

Oral radiographs (intraoral and panoramic) reveal:

  • Generalized rarification of the jaws.
  • Loss of medullary trabecular pattern.
  • Jaw appears finely radiopaque described as clear “ground glass” appearance.
  • Serum parathyroid hormone (normal range 15-65 pg/ml).
  • Serum calcium (normal range 9-11 mg/dl).
  • Parathyroid immunoassay.
  • Very high serum calcium level may indicate primary HPT.
  • Low or normal calcium level may indicate secondary HPT.
  • Tertiary HPT has a high PTH and high serum calcium. It is differentiated from primary HPT by a history of chronic kidney failure and secondary HPT.

Serum phosphate (normal range: 2.4-5 mg/dl)

  • In primary HPT, serum phosphate levels are abnormally low.
  • In secondary HPT, serum phosphate levels are generally elevated because of renal disease.

Alkaline phosphatase (normal range 500-750 IU/L)

  • Alkaline phosphatase levels are usually elevated in HPT.

In primary hyperthyroidism, levels may remain within the normal range, however, this is “inappropriately normal” given the increased levels of plasma calcium.

  1. The clinical management of patients does not require any special consideration.
  2. There is a higher risk of bone fracture, so precautions must be taken in surgical treatments.
  3. It is important to recognize brown tumour, as spontaneous regression of the lesion often occurs. However sometimes brown tumor do not disappear. In these cases, brown tumor resection should be done.
  4. Jaw enlargement is treated by recontouring of the maxilla and mandible.
  5. Finding of periapical radiolucency on a radiograph should not automatically lead to access opening and root canal therapy by the dentist.

Hypoparathyroidism is a metabolic disorder characterized by low serum calcium and high serum phosphorus concentrations due to deficiency or absence of PTH secretion.

  • Parathyroidectomy.
  • Removal of parathyroid glands during surgical removal of thyroid gland (thyroidectomy).
  • Autoimmune disease.
  • Deficiency of receptors for PTH in the target cells.

Types of Hypoparathyroidism:

  • Primary hypoparathyroidism-Parathyroid gland is either not present or atrophied or do not function normally or due to damage of parathyroid gland after surgical excision (acquired hypoparathyroidism). Concentration of PTH in the serum is often low.
  • In pseudohypoparathyroidism– Parathyroid gland function is normal, but kidneys fail to respond to PTH due to deficient receptor. So parathyroid glands secrete the hormone in excess, and serum-PTH is increased.
  1. Hypocalcemia with consequent circumoral numbness.
  2. Paresthesias of distal extremities (finger and toes).
  3. Muscle pain.
  4. Abdominal pain or muscle cramping which can progress to spasm or tetany.
  5. Laryngospasm or bronchospasm
  6. Seizures.

Disorders of ectodermal tissues:

  1. Alopecia.
  2. Loss of axillary and pubic hair.
  3. Coarsening of body hair.
  4. Scaling of the skin.
  5. Deformities of the nails.
  6. Increased neuromuscular irritability (due to hypocalcemia).
  7. Chvostek’s or Trousseau’s sign.

In positive Chvostek’s sign on tapping the facial nerve at its point of origin (anterior to ear tragus) will cause spasm of facial musculature particularly of the lip and the alae of the nose.

In Trousseau’s sign, carpal spasm occurs after inflating the blood pressure cuff.

Tetany is an abnormal condition characterized by violent and painful muscular spasm (spasm = involuntary muscular contraction), particularly in feet and hand.

It occurs due to hyperexcitability of nerves and skeletal muscles due to calcium deficiency.

  1. Hyper-reflexia and convulsions.
  2. Carpopedal spasm.
  3. Laryngeal stridor.
  4. Dry skin with brittle nails.
  5. Hair loss.
  6. Grand mal, petit mal or other seizures.
  7. Signs of mental retardation in children or dementia in adults.
  1. Round face.
  2. Short stature.
  3. Obesity.
  4. Ectopic soft tissue ossification.
  5. Cataract.
  6. Short hands and feet due to irregular shortening of the small tubular bones.
  7. Reduction in the length of the 3rd and 4th fingers and toes.
  8. Memory loss and mental deficiency.
  9. These specific patterns of physical findings are called as Albright hereditary osteodystrophy (because kidney responds as if PTH are absent).
  1. Enamel hypoplasia (enamel is thin).
  2. Delayed eruption.
  3. Multiple unerupted teeth.
  4. Teeth appear dull white in color with hypoplastic pitting.
  5. Microdontia and the roots are often short with blunt ends.
  6. Malformed roots, resulting from nontreated hypocalcemia during the developmental phase of the dentition.
  7. Cessation of dental growth and development.
  8. Hypodontia.
  9. Ankylosis.
  10. Jaws are short and wide with high arch palate.
  11. Severe dental caries in the deciduous and permanent teeth.
  12. Loss of teeth.
  13. Chronic candidiasis of oral mucosa and nail.
  14. Paresthesia of the tongue or lips.
  15. Facial twitching.
  1. Thickening of the lamina dura.
  2. Widened root canals.
  3. Poorly calcified dentine with multiple resorptions in the cementum.
  4. Large pulp chambers
  5. Dental pulp calcifications.

In primary hypoparathyroidism

  • Low serum calcium and PTH
  • High serum phosphate level
  • Normal alkaline phosphatase level

In pseudohypoparathyroidism:

  • Low serum calcium
  • PTH is high or normal.
  1. Dental management includes the prevention of caries with periodic check-up, advice is given regarding diet and oral hygiene maintenance.
  2. The serum calcium levels should be above 8 mg/100 ml to prevent cardiac arrhythmias, seizures, laryngospasms or bronchospasms before dental treatment.
  3. Due to enamel hypoplasia there is an increased chance of dental caries.
  4. As pulp chambers are large, caries easily involves the pulp causing pulpitis, hence requiring endodontic treatment.
  5. Pulp calcification and malformed root cause difficulty in endodontic treatment.
  6. Ankylosis causes difficulty in extraction.
  7. Delayed eruption and hypodontia causes malposition and has to be treated by orthodontist.

Adrenal glands are called the ‘life-saving glands’ or ‘essential endocrine glands’, as the absence of adrenocortical hormones causes death within 3 to 15 days and absence of adrenomedullary hormones decreases the resistance to mental and physical stress.

There are two adrenal glands. Each gland is situated on the upper pole of each kidney. Because of the situation, adrenal glands are otherwise called suprarenal glands.

Adrenal gland is made of two distinct parts:

  1. Adrenal cortex: Outer portion, constituting 80% of the gland.
  2. Adrenal medulla: Central portion, constituting 20% of the gland.

Adrenocortical hormones are steroids in nature, hence the name ‘corticosteroids’. Based on their functions, corticosteroids are classified into three groups:

  1. Mineralocorticoids.
  2. Glucocorticoids.
  3. Sex hormones.

All adrenocortical hormones are synthesized mainly from cholesterol that is absorbed directly from the circulating blood.

Mineralocorticoids are the corticosteroids that act on the minerals (electrolytes), particularly sodium and potassium. Mineralocorticoids are:

  1. Aldosterone (90%).
  2. 11-deoxycorticosterone(10%).
  • It maintains the osmolarity and volume of ECF.
  • Aldosterone increases:
  1. Reabsorption of sodium from renal tubules.
  2. Excretion of potassium through renal tubules.
  3. Secretion of hydrogen into renal tubules.

It is regulated by following factors:

  1. Increase in potassium ion (K+) concentration in ECF.
  2. Decrease in sodium ion (Na+) concentration in ECF.
  3. Decrease in ECF volume.
  4. 4. Adrenocorticotropic hormone (ACTH).

Glucocorticoids act mainly on glucose metabolism. Glucocorticoids are:

  1. Cortisol (95% activity)
  2. Corticosterone (4% activity)
  3. Cortisone (1% activity)

Glucocorticoids prevents the inflammatory changes by:

  1. Inhibiting the release of chemical substances from damaged tissues and prevent vasodilatation and erythema in the affected area.
  2. Causes vasoconstriction through the permissive action on catecholamines, prevents rushing of blood to the injured area.
  3. Decreasing the permeability of capillaries and preventing loss of fluid from the plasma into the affected tissue.
  4. Inhibiting the migration of leukocytes into the affected area.
  5. Suppressing T cells and other leukocytes, so that there is reduction in the reaction of tissues which enhance the inflammatory process.
  1. It suppresses the immune system by decreasing the number of circulating T lymphocytes. It is done by suppressing proliferation of T cells and the lymphoid tissues (lymph nodes and thymus).
  2. Glucocorticoids also prevent the release of interleukin-2 by T cells.
  3. Hypersecretion or excess use of glucocorticoids decreases the immune reaction.
  • Adrenocorticotropic hormone (ACTH) regulates glucocorticoid secretion from anterior pituitary.
  • ACTH secretion is regulated by hypothalamus through corticotropin-releasing factor (CRF).
  • Maintenance of structural integrity and vascularization of zona fasciculata and zona reticularis of adrenal cortex.
  • Conversion of cholesterol into pregnenolone, which is the precursor of glucocorticoids.
  • Release of glucocorticoids.
  • Prolongation of glucocorticoid action on various cells.
  • Hypothalamus controls the secretion of ACTH through corticotropin-releasing factor (CRF).
  • It is also called corticotropin-releasing hormone.
  • CRF reaches the anterior pituitary through the hypothalamohypophyseal portal vessels.
  • CRF stimulates the corticotropes of anterior pituitary and causes the synthesis and release of ACTH.

Adrenal cortex secretes mainly the male sex hormones, which are called androgens. But small quantity of estrogen and progesterone are also secreted by adrenal cortex.

Exogenous steroids are extracted from adrenal cortex of animals or prepared artificially.

  • Cortisone and hydrocortisone – used for replacement therapy having both glucocorticoid and mineralocorticoid effects.
  • Prednisolone -has more glucocorticoid activity.
  • Fludrocortisone (9-fluorocortisol) has more mineralocorticoid activity than glucocorticoid activity.
  • It has most potent mineralocorticoid effect.
  • Dexamethasone has only glucocorticoid effect.

Hypersecretion of adrenocortical hormones leads to the following conditions:

  1. Cushing syndrome.
  2. Hyperaldosteronism.
  3. Adrenogenital syndrome.

Hyposecretion of adrenocortical hormones leads to the following conditions:

  1. Addison disease or chronic adrenal insufficiency.
  2. Congenital adrenal hyperplasia.

Addison’s disease occurs due to failure of adrenal cortex to secrete Corticosteroids.

This disease is named after Thomas Addison, who first described patients affected by this disorder in 1855, in the book titled “On the constitutional and local effects of the disease of supra renal capsule”.

  • Primary Addison’s disease due to adrenal cause.
  • Secondary Addison’s disease due to failure of anterior pituitary to secrete ACTH.
  • Tertiary Addison’s disease due to failure of hypothalamus to secrete corticotropin-releasing factor (CRF).
  • Autoimmune
  • Tuberculosis

Other causes:

  • Fungal infection.
  • Hemochromatosis.
  • Metastatic neoplasm.
  • X‑linked adrenoleukodystrophy.
  • Muscle weakness and fatigue.
  • Weight loss and decreased appetite.
  • Hyperpigmentation.
  • Salt craving.
  • Nausea, diarrhea or vomiting.
  • Muscle or joint pains.
  • Irritability Metabolic acidosis.
  • Depression.
  • Weakness.
  • Dehydration.
  • Sweating.
  • Changes in mood and personality.

• Early morning serum cortisol, ACTH level and plasma renin activity.
• Hypoglycemia.
• Hyponatraemia.
• Hyperkalemia.
• Eosinophilia.
• Lymphocytosis.
• Low blood pressure.

Pale brown to deep chocolate pigmentation over the buccal mucosa, angles of the mouth, gingiva, tongue, lips.

Melanoma, Pigmented maculae, Peutz-Jeghers syndrome.

Routine procedures (excluding extractions and surgery)

  1. Patients presently using corticoids: No supplementing required.
  2. Patients with a history of regular corticoid use:
  • HDC (high dose corticoids) for a maximum of 30 days or equivalent:

If less than 2 weeks before, administer a maintenance dose on the day of treatment; if more than 2 weeks before, provide supplementing.

  • HDC for more than one month or equivalent: no established regimen.
  • LDC (low dose corticoids) or the equivalent: no supplementing required.
  1. Patients receiving corticotherapy on alternate days for at least 30 days: on the non-corticoid days, no supplementing is required. Conservative management is indicated on the rest of days.

Extractions or surgery, very extensive treatments, or involving highly anxious patients

Patients presently using corticoids:

  • Up to 30 mg / day of hydrocortisone or the equivalent, no supplementing required.
  • 30 – 40 mg / day of hydrocortisone or the equivalent, double the daily dose on the day of treatment; if postoperative pain is expected, also double the daily dose on the first postoperative day.
  • More than 40 mg / day of hydrocortisone for at least 30 days or the equivalent, no supplementing required.

Patients with a history of regular corticoid use: 

  • HDC (high dose corticoids) for a maximum of 30 days or the equivalent:

If less than 2 weeks before, administer double the normal dose on the day of treatment; if more than 2 weeks before, no supplementing required.

LDC (low dose corticoids) or the equivalent: no supplementing required.

Adrenal crisis is a common symptom of Addison disease, characterized by sudden collapse associated with an increase in need for large quantities of glucocorticoids.

  • Exposure to even mild stress.
  • Hypoglycemia due to fasting.
  • Trauma.
  • Surgical operation.
  • Sudden withdrawal of glucocorticoid treatment.

Depending on the consciousness level of the patient, proper management of an emergency situation of acute adrenal insufficiency includes the following steps:

Conscious patient:

  1. Terminate dental treatment as soon as the initial signs of adrenal insufficiency, such as mental confusion, abdominal pain, nausea and/or vomiting, become evident in a person on glucocorticoisteroid therapy.
  2. If signs of hypotension are evident, place the patient in a supine position with legs slightly elevated. However, in the absence of such signs, placing the patient in their preferred comfortable position is recommended.
  3. Provide basic life support and maintain proper circulation, airway and breathing.
  4. Provide definitive care that includes monitoring vital signs, activating emergency medical assistance, oxygen administration, if needed (5-10ml/min), and administration of glucocorticosteroids. In the case of a patient with chronic adrenal insufficiency, 50-100mg of hydrocortisone should be administered intravenously; re-administration should follow every 6-8 hrs.
  5. If the patient has no known history of adrenal insufficiency or gluococorticosteroid administration, but exhibits the diagnostic signs and symptoms of adrenal insufficiency, 4 mg dexamethasone phosphate (IV) should be administered immediately rather than waiting for the lab results (ACTH stimulation test). The drug should be re-administered every 6-8 hours, as needed.
  6. Additional management may include the administration of 1L of normal saline, and management of hypoglycemia by administration of 50-100 mL of 50% dextrose solution.

Unconscious patient:

  1. Determine the unconsciousness and place the patient in a supine position with legs elevated.
  2. Provide basic life support, maintain circulation, airway and breathing. Usually the pulse is rapid, weak and thready, but in rare circumstances the pulse might be absent, which warrants immediate initiation of external chest compressions.
  3. Definitive care includes the administration of oxygen and emergency medicines. Emergency medical assistance should be activated at this stage. If the patient’s medical history indicates the possibility of adrenal insufficiency, 100 mg hydrocortisone should be administered via IV or IM route. An additional 100mg of hydrocortisone should be administered by IV infusion (over 2 hrs.) or IM route. Further, management may include administration of 1ml of normal saline and 50% dextrose solution.
  4. If the cause of unconsciousness cannot be established, no drug administration is indicated, and basic life support (BLS) steps should be continued until the arrival of emergency medical assistance.
  1. Ara A, Denny C, Gajendra, Patil S, Vishwanath, Gummadapu S, Veena KM. Systemic Disorders and their Clinical Implications. RavikiranOngle, Praveen BN (ed).Textbook of Oral Medicine, Oral Diagnosis and Oral Radiology, 1st edition. New Delhi, Elsevior Inc., 2010;547-629.
  1. Human Physiology/The Endocrine System. [Online]. 2007 April 24 [updated 2014 Dec 8; cited 2015 May 21]; [1-18]. Available from: URL: https://www. saylor.org/site/wp-content/uploads/2010/11/The-Endocrine-System.pdf
  1. Sembulingam K, Sembulingam P. Endocrinology. In, Dr. TK ParthaSarthy (ed). Essentials of Medical Physiology, 5th edition. New Delhi, Jaypee Brothers Medical Publishers (P) Ltd, 2010;(351-97).
  1. White SC, Pharoah MJ. Systemic Diseases Manifested in Jaws. Oral Radiology: Principles & Interpretation, 6th New Delhi, Elsevier Inc.,2012;454-72.
  1. Hiller-Sturmhofel S, Bartke A. The Endocrine System- An Overview. Alcohol Health & Research Work 1998;22:153-64.
  1. Aparna M, Shenai P, Chatra L, Veena KM, Rao PK, Shahin KA. Endocrine Disorders in Head Neck Region: A Radiographic Perspective in Dental Clinic. Archives Medical Review Journal 2014;23:294-302.
  1. Gupta H Disorders of Pituitary Hormones. Available from: http://www.biology discussion.com/hormones/hormonal-disorders/disorders-of-pituitary-hormones/18694.
  1. Fraser LA, Uum SV What is your call? Work-up for Cushing syndrome CMAJ 2010;182-6.
  2. Buliman A, Tataranu LG, Paun DL, Mirica A, Dumitrache C. Cushing’s disease: a multidisciplinary overview of the clinical features, diagnosis, and treatment J Med Life. 2016; 9: 12–18.
  3. Castinetti F, Morange I, Devolx BC, Thierry Brue T Cushing’s disease Castinetti et al. Orphanet Journal of Rare Diseases 2012, 7:1-9.
  4. Hur KY, Kim JH, Kim BJ, Kim MS, Lee EJ, Kim SW Clinical Guidelines for the Diagnosis and Treatment of Cushing’s Disease in Korea Endocrinol Metab 2015;30:7-18.
  5. Larsen PR, Davies TF, Hay ID. The Thyroid. In: Williams RH, Wilson JD, Foster DW, Kronenberg HM, editors. Williams Textbook of Endocrinology. 9th ed. Philadelphia: Saunders; 1998. p. 389-416.
  6. Pyle MA, Faddoul FF, Terezhalmy GT. Clinical implications of drugs taken by our patients. Dent Clin North Am 1993;37:73-90.
  7. Klein I. Thyroid hormone and the cardiovascular system. Am J Med 1990;88:631-7.
  8. Pinto A, Glick M. Management of patients with the thyroid disease: Oral health considerations. J Am Dent Assoc 2002;133:849-58.
  9. Loevy HT, Aduss H, Rosenthal IM. Tooth eruption and craniofacial development in congenital hypothyroidism: Report of case. J Am Dent Assoc 1987;115:429-31.
  10. Young ER. The thyroid gland and the dental practitioner. J Can Dent Assoc 1989;55:903-7.
  11. Klein I, Levey GS. The cardiovascular system in thyrotoxicosis. In: Braverman LE, Utiger RD, editors. The Thyroid. 8th ed. Philadelphia: Lippincott-Raven; 2000. p. 596-604.
  12. Poumpros E, Loberg E, Engstrom C. Thyroid function and root resorption. Angle Orthod 1994;64:389-94.
  13. Little JW. Thyroid disorders. Part I: Hyperthyroidism. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2006;101:276-84.
  14. Silverton SF. Endocrine disease. In: Greenberg MS, Glick M, editors. Burket’s Oral medicine Diagnosis and treatment. 10th ed. Hamilton, Ontario : BC Decker Inc; 2003. p. 578-91.
  15. Muzyka BC. Atrial fibrillation and its relationship to dental care. J Am Dent Assoc 1999;130:1080-5.
  16. Malamed SF. Thyroid gland dysfunction in medical emergencies in the dental office. 5th ed. St. Louis: Mosby; 2000. p. 275-86.
  17. Sherman RG, Lasseter DH. Pharmacologic management of patient with disease of the endocrine system. Dent Clin North Am 1996;40:727-52.
  18. Carlos-Fabue L, Jimenez-Soriano Y, Sarrion-Perez MG. Dental management of patients with endocrine disorders. J Clin Exp Dent 2010;2:196-203.
  19. Huber MA, Terezhalmy GT. Risk stratification and dental management of the patient with thyroid dysfunction. Quintessence Int 2008;39:139-50.
  20. Barron J. The Endocrine System: Thyroid & Parathyroid Gland. About Thyroid & Parathyroid Dysfunction— Natural Health Remedies Newsletter. Endocrine System & amp; Thyroid, Part-2 available from: URL:https://jonbarron. org/diet-and-nutrition/endocrine-system-thyroid-and-parathyroid-gland.
  21. Carl W. Chronic renal disease and hyperparathyroidism: Dental manifestations and management. Compendium 1987;8:697-9, 702, 704.
  22. Silverman S Jr, Ware WH, Gillooly C Jr. Dental aspects of hyperparathyroidism. Oral Surg Oral Med Oral Pathol 1968;26:184-9.
  23. Bissada NF, el-Mostehy MR. Hyperparathyroidism. Pathogenesis, diagnosis and oro-dental manifestations. Egypt Dent J 1968;14:226-34.
  24. Silverman S Jr, Gordan G, Grant T, Steinbach H, Eisenberg E, Manson R. The dental structures in primary hyperparathyroidism. Studies in forty-two consecutive patients. Oral Surg Oral Med Oral Pathol 1962;15:426-36.
  1. Bridge AJ. Primary hyperparathyroidism presenting as a dental problem. Br Dent J 1968;124:172-6.
  1. Venkatesh KV, Nandini VV. Periapical radiolucency not requiring endodontic therapy: An unusual case. Indian J Dent Res 2009;20:126-8.
  2. Loushine RJ, Weller RN, Kimbrough WF, Liewehr FR. Secondary hyperparathyroidism: A case report. J Endod 2003;29:272-4.
  3. Frankenthal S, Nakhoul F, Machtei EE, Green J, Ardekian L, Laufer D, et al. The effect of secondary hyperparathyroidism and hemodialysis therapy on alveolar bone and periodontium. J Clin Periodontol 2002;29:479-83.
  4. Michiwaki Y, Michi K, Yamaguchi A. Marked enlargement of the jaws in secondary hyperparathyroidism — A case report. Int J Oral Maxillofac Surg 1996;25:54-6.
  5. Bakathir AA, Margasahayam MV, Al-Ismaily MI. Maxillary hyperplasia and hyperostosis cranialis: A rare manifestation of renal osteodystrophy in a patient with hyperparathyroidism secondary to chronic renal failure. Saudi Med J 2008;29:1815-8.
  6. Vigneswaran N. Oral and maxillofacial pathology case of the month. Renalosteodystrophy induced macrognathia. Tex Dent J 2001;118:570-1, 582.
  7. Antonelli JR, Hottel TL. Oral manifestations of renal osteodystrophy: Case report and review of the literature. Spec Care Dentist 2003;23:28-34.
  1. Dinkar AD, Sahai S, Sharma M. Primary hyperparathyroidism presenting as an exophytic mandibular mass. Dentomaxillofac Radiol 2007;36:360-3.
  2. Parbatani R, Tinsley GF, Danford MH. Primary hyperparathyroidism presenting as a giant-cell epulis. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1998;85:282-4.
  3. Padbury AD , Tözüm TF, Taba M, Ealba EL, West BT, Burney RE, et al. The impact of primary hyperparathyroidism on the oral cavity. J Clin Endocrinol Metab 2006;91:3439-45.
  4. Prado FO, Rosales AC, Rodrigues CI, Coletta RD, Lopes MA. Brown tumor of the mandible associated with secondary hyperparathyroidism: A case report and review of the literature. Gen Dent 2006;54:341-3.
  5. Nair PP, Gharote HP, Thomas S, Guruprasad R, Singh N. Brown tumour of the jaw. BMJ Case Rep 2011;pii: bcr0720114465.
  6. Rai S, Bhadada SK, Rattan V, Bhansali A, Rao DS, Shah V. Oro-mandibular manifestations of primary hyperparathyroidism. Indian J Dent Res 2012;23:384-7.
  7. Andreades D, Belazi M, Antoniades D. Diagnosis of a maxillary brown tumor associated with hyperparathyroidism secondary to chronic renal failure — A case report. Oral Health Prev Dent 2004;2:143-7.
  8. Angadi PV, Rekha K, Shetty SR.An exophytic mandibular brown Tumor : An unusual presentation of primary hyperparathyroidism. Oral Maxillofac Surg 2010;14:67-9.
  9. Vardhan BG, Saraswathy K, Koteeswaran D. Primary hyperparathyroidism presenting as multiple giant cell lesions. Quintessence Int 2007;38:342-7.
  10. Sagliker Y, Acharya V, Ling Z, Golea O, Sabry A, Eyupoglu K, et al. International study on Sagliker syndrome and uglifying human face appearance in severe and late secondary hyperparathyroidism in chronic kidney disease patients. J Ren Nutr 2008;18:114-7.
  11. Asaumi J, Aiga H, Hisatomi M, Shigehara H, Kishi K. Advanced imaging in renal osteodystrophy of the oral and maxillofacial region. Dentomaxillofac Radiol 2001;30:59-62.
  12. Scutellari PN, Orzincolo C, Bedani PL, Romano C. Radiographic manifestations in teeth and jaws in chronic kidney insufficiency. Radiol Med 1996;92:415-20.
  13. Ganibegovic M. Dental radiographic changes in chronic renal disease. Med Arh 2000;54:115-8.
  14. Carlos FL, Jimenez SY, Sarrion PMG. Dental Management of patients with endocrine disorders. J Clin Exp Dent. 2010;2:196-203.
  15. Worth HM, Metabolic and Endocrine Changes in Teeth and Jaws. Principles and Practice of Oral Radiologic Interpretation. Year Book Medical Publishers, 1963;353-66.
  16. The Endocrine System. [Online]. 2007 Dec 12 [cited 2015 May 14]; [206-30]. Available from: URL: http://www.highered.m com/sites/dl/free/007 3525626830198/Ch10.pdf.
  17. Sarkar PK, Shinton RA. Hutchinson-Guilford progeria syndrome. Postgrad Med J 2001;77:312-17.
  18. Sarkar SB, Sarkar S, Ghosh S, Bandyopadhyay S. Addison’s disease Contemporary Clinical Dentistry 2012;3:484-86.
  19. Lanza A, Heulfe I, Perillo L, Dell’Ermo A, Cirillo N Oral Pigmentation as a Sign of Addison’s Disease: A Brief Reappraisal The Open Dermatology Journal 2009;3: 3-6
error: Content is protected !!