DISORDERS OF THE ENDOCRINE SYSTEM AND

DENTAL MANAGEMENT.

DEPARTMENT OF ORAL MEDICINE/ ORAL PATHOLOGY, LASUTH.

DR DAWODU S.
3RD JUNE, 2019.
 OUTLINE
• INTRODUCTION.
• TYPES OF ENDOCRINE DISORDERS.
• ORAL MANIFESTATION OF ENDOCRINE DISORDERS.
• DENTAL MANAGEMENT OF PATIENTS WITH ENDOCRINE DISORDERS.
• CONCLUSION
• REFERENCES.
INTRODUCTION
• The endocrine system is essential for hormonal secretion and It controls
many physiological processes and maintains homeostasis.
• There are many endocrine diseases which may include Diabetes
mellitus, Addison disease, Cushing disease, Hyperthyroidism, and
Hypothyroidism.
• The major endocrine glands are :
• Pineal gland, pituitary gland, Thyroid gland, Thymus, Adrenal gland
Pancreas, Ovaries, Testes.
 TYPES OF ENDOCRINE DISORDERS.
Glucose homeostasis disorder – Diabetes, Hypoglycemia.
Thyroid disorders – Goitre, Hyperthyroidism, Hypothroidism.
Calcium homeostasis disorders and Metabolic bone diseases:
- Parathyroid gland disorders ; Hyperthyroidism ( primary, secondary,
tertiary) and Hypoparathyroidism.
- Osteoporosis, Paget’s disease (osteitis deformans).
Pituitary gland disorders – Hypopituitarism, Acromegaly, Cushing’s
disease, tumors, Gigantism, Dwafism.
Sex hormone disorders.
THYROID GLAND DISORDERS.
• The thyroid gland secretes three hormones: thyroxine (T4), tri-
iodothyronine (T3) and calcitonin.
• T4 and T3 are hormones that affect metabolic processes throughout the
body.
• Thyroid stimulating hormone (TSH or thyrotropin), produced by the
pituitary gland, regulates the secretion of thyroid hormones (T4 and T3)
through a negative feedback mechanism.
• Calcitonin is involved, with parathyroid hormone and vitamin D, in
regulating serum calcium and phosphorus levels and in the skeletal
remodeling.
• Thyroid hormones influence the growth and maturation of tissues, energy
metabolism and turnover of both cells and nutrients
 THYROID GLAND DISORDERS.

HYPERTHYROIDISM
• Hyperthyroidism or thyrotoxicosis is defined by overproduction of the
thyroid hormones T3 and T4 thyroid gland function.
• It is caused by ectopic thyroid tissue, toxic thyroid adenoma, toxic
multinodular goiter, factitious thyrotoxicosis and Graves’ disease and
diffuse toxic goiter, being the most common cause of hyperthyroidism
• Clinical manifestations include: weight loss, increased appetite,
nausea, vomiting, thin and brittle hair, soft nails, warm and moist
skin, increased skin pigmentation and heat intolerance.
• Others are; bilateral exophthalmos, ptosis, periorbital edema,
retraction of the upper and lower eyelid due to muscle contracture
and conjunctival injection).
THYROID GLAND DISORDERS.

Treatment includes :
• Antithyroid agents : propylthiouracil, carbimazole, and methimazole)
which block hormone synthesis;
• Iopanoic acid and ipodate sodium that are inhibitors of the peripheral
conversion of T4 to T3;
• Beta-blockers (propanolol) that slow the adrenergic activity and eliminate
the tachycardia, anxiety, nervousness, tremors and sweating;
• Glucocorticosteroids, such as dexamethasone, that decrease the secretion
of thyroid hormone and iodine that inhibits the release of preformed
hormone.
THYROID GLAND DISORDERS.

HYPOTHYROIDISM.
• It is defined by a deficiency of the thyroid hormone. It can be
acquired or by congenital defects.
• When it is present in infancy, it is manifested as cretinism and if it
occurs in adults (especially in middle-aged women) it is known as
myxedema.
• Characteristic signs of cretinism include mental retardation,
developmental and growth delay, marked disproportion between the
head and body (wide head), lack of muscle tone, overweight, less
expressive face with a broad and flat nose, hypertelorism, short neck ,
pale, dry and wrinkled skin.
 THYROID GLAND DISORDERS.

HYPOTHYROIDISM CONT’D.
• Myxedema is characterized by widespread metabolic slow-down,
depression, overweight, diminished cardiac output and respiratory
rate, decreased pulse, generalized edema (especially in face and
extremities),
• hoarseness because the edema affects the vocal cords, sinus
bradycardia,
• swollen nose, ears and lips, thickened and dry skin, scalp brittleness,
thin or absent eyebrows and decreased sweating.
ORAL MANIFESTATIONS OF PATIENTS WITH THYROID GLAND
DISORDERS
• HYPERTHYROIDISM
1. Accelerated dental eruption in children
2. 2. Maxillary or mandibular osteoporosis
3. Enlargement of extra-glandular thyroid tissue (mainly in the lateral
posterior tongue)
4. Increased susceptibility to caries
5. Periodontal disease
6. Burning mouth syndrome
7. Development of connective-tissue diseases like Sjögren’s syndrome or
systemic lupus erythematosus.
 ORAL MANIFESTATIONS OF PATIENTS WITH THYROID GLAND
DISORDERS CONT’D.
HYPOTHYROIDISM
1. Delayed eruption
2. Enamel hypoplasia in both dentitions, (being less intense in the
permanent dentition).
3. Anterior open bite
4. Macroglossia
5. Micrognathia
6. Thick lips
7. Dysgeusia
8. Mouth breathing
DENTAL MANAGEMENT OF PATIENTS WITH THYROID GLAND
DISORDERS.
• Dental management of the patient with hyperthyroidism:
• Before dental treatment is planned, we must a detailed general clinical
history, Clinical examination, and if possible a confirmatory test.
• Consultation with the specialist is recommended, to discuss the overall
condition of the patient.
• In controlled patients, the same dental management as in healthy
patients is carried out . Reduction of stressful situations and the spread
of infectious foci.
• In uncontrolled cases, the use of epinephrine or other pressor amines in
local anesthetics of the retraction cords should be restricted because the
myocardium of these patients is sensitive to adrenaline and may lead to
arrhythmias, palpitations and chest pain.
Dental management of the patient with hyperthyroidism cont’d
• Surgical procedures must be avoided because presence of acute oral
infection and severe stress may precipitate thyroid storm crisis.
• These symptoms include tachycardia, irregular pulse, sweating,
hypertension, tremor, nausea, vomiting, abdominal pain and coma.
• If an emergency dental treatment is required, consultation with the
patient’s endocrinologist is advisable because a conservative
treatment is preferable.
• Treatment should be discontinued if signs or symptoms of a
thyrotoxic crisis develop, and access to emergency medical services
should be readily available.
Dental management of the patient with hyperthyroidism cont’d
• People who have hyperthyroidism and are treated with
propylthiouracil must be monitored for possible agranulocytosis,
hypoprothrombinemia or bleeding, and a complete blood count
including prothrombin time done before performing any invasive
procedures is usually recommended.
• In these patients proper analgesia is indicated and nonsteroidal anti-
inflammatory drugs (NSAIDs) and aspirin should be used with caution.
• One way the dental professional can protect the thyroid gland is to
use thyroid collar while taking patient X-rays. The thyroid gland is
extremely sensitive to radiation as a radiation exposure is a known
risk factor.
Dental management of the patient with hypothyroidism.
• Consulting the patient’s physician and carrying out a detailed
general clinical history before performing dental treatment is
indicated.
• In controlled patients we must avoid oral infection.
• In uncontrolled patients, oral infection, central nervous depressants
such as narcotics and barbiturates should be avoided because they
may cause an exaggerated response.
• The presence of oral infection, central nervous depressants and
surgical procedures can precipitate a myxedematous coma. Surgery
procedures should also be avoided in these patients.
• 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.
Dental management of the patient with hypothyroidism
cont’d
• These patients are susceptible to cardiovascular disease, therefore
they may be on anticoagulation therapy.
• Antibiotic prophylaxis must be assessed in valvular pathology and
atrial fibrillation.
• Before dental treatment is carried out, a complete blood count is
required to evaluate coagulation factors.
• We must avoid the use of epinephrine in local anesthetics or
retraction cords.
• Patients are treated with synthetic preparations containing sodium
liothyronine, sodium levothyroxine.
• Hormone replacement therapy based on thyroid hormones can be
prescribed in cases of severe deficiency of thyroid hormones.
PARATHYROID GLAND DISORDERS
 PARATHYROID GLAND DISORDERS
• Parathyroid glands secret parathyroid hormone (PTH) involved in
regulating the metabolism of calcium and phosphorus.
• It plays an important role in tooth development and bone
mineralization and increases bone resorption.
• In the kidneys, it stimulates formation of active metabolite of vitamin
D, which promotes the intestinal absorption of calcium and decreases
renal reabsorption of phosphate.
Disorders : Hyperparathyroidism
Hypoparathyroidism.
PARATHYROID GLAND DISORDERS

• Hyperparathyroidism
• It is characterized by hypersecretion of parathyroid hormone which
occurs in three categories :
- Primary: occurs with a hyperfunction of one or more parathyroids,
usually caused by a tumour (adenoma in 85% of all cases) or
hyperplasia of the gland that produces an increase in PTH secretion
resulting in hypercalcemia and hypophosphatemia.
- Secondary : normally related to patients with intestinal malabsorption
syndrome or chronic renal failure, Occurring in a decrease of vitamin
D production or with hypocalcemia causing the glands to produce a
high quantity of PTH. There is also hyperphosphatemia.
PARATHYROID GLAND DISORDERS

• The PTH-related signs are brown tumors and osteitis fibrosa cystica,
which is referred as renal osteodystrophy or Von Recklinghausen’s
disease.
• The diagnosis of HPT is suspected by an increase in serum calcium
and it is confirmed by the increase in PTH.
• One of the main clinical manifestations of hyperparathyroidism is
bone disease. The ribs, clavicles, pelvic girdle and mandible are the
bones most involved.
PARATHYROID GLAND DISORDERS

• Brown tumor presents itself as a friable red-brown mass. Its name is

due to color that it takes from the haemorrhagic infiltrates and
haemosiderin deposits that are often found inside.
• It presents as osteolytic lesion that develops due to changes in bone
metabolism caused by high serum concentration of PTH.
• It is mainly due to secondary HPT in patients with renal insufficiency,
but it has also been described as a rare manifestation of calcium
malabsorption
PARATHYROID GLAND DISORDERS

• It is an extremely rare manifestation of primary HPT, in these cases it

is usually a result of the overproduction of the parathyroid hormone
by a parathyroid tumor. ( adenoma/carcinoma).
• Mandible involvement is common, especially in the area of premolars
and molars, and it is rare in maxilla.
• Radiographically, lesions are characterized as well-defined radiolucent
areas( unilocular or multilocular).
• Presence of loss of the lamina dura, and changes in the pattern of
the trabecular bone of the jaws.
PARATHYROID GLAND DISORDERS

• Long-term injures commonly produce a significant expansion of

cortical, root resorption and displacement of roots can appear.
• Histologically, it is characterized by an abundant stroma, consisting of
bundles of spindle or oval cells, and several multinucleated
osteoclast-like giant cells.
• Calcified material can be found, as well as areas with extravastion of
red blood cells and pigmentation by haemosiderin.
A panoramic radiograph od a patient with Browns tumor showing loss of the lamina
dura surrounding the roots of the teeth
• decrease of trabecular density
PARATHYROID GLAND DISORDERS.
• These findings are not pathognomonic, making it necessary to
perform a differential diagnosis with other lesions such as an
aneurismal bone cyst, cherubism and central giant cell granuloma.
• Dental management of the patient with hyperparathyroidism
• The clinical management of these patients does not require any
special consideration.
• There is a higher risk of bone fracture, hence precautions must be
taken during surgical treatment.
• On the other hand, it is important to recognize the presence of
brown tumor and to perform a correct differential diagnosis in order
to give appropriate treatment.
ORAL MANIFESTATIONS OF PATIENTS WITH PARATHYROID
GLAND DISORDERS
HYPOPARATHYROIDISM
HYPERPARATHYROIDISM 1. Dental abnormalities:
1. Dental abnormalities: • Enamel hypoplasia in horizontal lines
• Widened pulp chambers • Poorly calcified dentin
• Development defects • Widened pulp chambers and pulp
• Alterations in dental eruption calcifications
• Weak teeth • Shortened roots
• Maloclusion • Hypodontia
2. Brown tumor • Delayed dental development
3. Loss of bone density 2. Mandibular tori
4. Soft tissue calcifications 3. Chronic candidiasis
4. Paresthesia of the tongue or lips
PARATHYROID GLAND DISORDERS

• HYPOPARATHYROIDISM
It is a metabolic disorder characterized by hypocalcemia and
hypophosphatemia due to a deficiency or absence of parathyroid
hormone secretion.
It may also develop as an isolated entity of unknown etiology
(idiopathic hypoparathyroidism), or in combination with other
disorders such as autoimmune diseases or developmental defects.
It can cause hypocalcemia with consequent paresthesia, tetany and
seizures.
Disorders of ectodermal tissues are also common in these patients.
PARATHYROID GLAND DISORDERS

• This pathology is diagnosed on the basis of measurements of serum

calcium and parathyroid hormone levels.
• The main treatments available for these patients is vitamin D or its
analogues, calcium salts and drugs that increase renal tubular
resorption of calcium, to obtain adequate, but low, normal serum
calcium levels.
PARATHYROID GLAND DISORDERS.
Dental management of the patient with hypoparathyroidism
• These patients have more susceptibility to caries because of dental
anomalies.
• Management includes; the prevention of caries with periodic reviews,
dietary counselling and oral hygiene instructions in a diagnosed patient.
• Before performing dental treatment, serum calcium levels should be
determined. It must be above 8mg/100ml to prevent cardiac arrhythmias,
seizures, laryngospasms or bronchospasms.
• If a suspicion arises, for an undiagnosed patient, dental treatment should
be suspended until a complete medical evaluation is performed.
 ADRENAL GLAND DISORDERS.

• Adrenal hormones
• The adrenal glands are located on the upper pole of each kidney. They
are composed of the adrenal medulla, which produce adrenaline,
noradrenaline, dopamine and progesterone
• Cortex, which is responsible for the production of steroid hormones,
such as: glucocorticoids (cortisol and cortisone), mineralocorticoids
(aldosterone and deoxycorticosterone), and androgens
(dehydroepiandrosterone).
ADRENAL GLAND DISORDERS.
 ADRENAL GLAND DISORDERS

The corticosteroids are classified according to their effects:

•Mineralocorticoids, produced in the zona glomerulosa, help in the
regulation of blood pressure and electrolyte balance.
• Glucocorticoids such as cortisol, are synthesized in the zona fasciculata
and their functions include
- regulation of glycogen and lipid metabolism
- immune system suppression.
- Carbohydrate, protein and fat, mineral, and water metabolism.
• The innermost layer of the cortex produces Androgens (testosterone
and estrogen hormones).
ROLE OF SUBSTANCES SECRETED BY THE CORTEX
Regarding the role of substances that are secreted by the cortex, Cortisol is
involved in the
• mechanisms of adaptation of the organism to stress maintaining
homeostasis;
• it has anti-inflammatory and immunosuppressive effect,
• it is responsible for mobilizing fatty acids from adipose tissue, it maintains
vascular response,
• it promotes the liver’s protein synthesis via glycogenesis,
• it inhibits bone formation and delays healing.
• Anti-allergic actions.
Regulation of secretion of corticosteroids.
• Corticosteroid production and release from the adrenal cortex is in
turn regulated by adrenocorticotropic hormone (ACTH), which is
synthesized and secreted in the anterior hypophysis
(adenohypophysis).
• In accordance to the circulating glucocorticoid concentrations, a self
regulating or negative feedback mechanism is established at
hypothalamic and hypophyseal level.
• ACTH is in turn controlled by a series of factors such as corticotropin
releasing hormone (CRH), which is secreted by the hypothalamus
through the hypothalamo-hypophyseal portal vessels.
Regulation of secretion of corticosteroids.
• CRF stimulates the corticotropes of anterior pituitary and causes the
synthesis and release of ACTH.
• factors such as emotion, stress, trauma, and circadian rhythm causes
release of ACTH, which induces glucocorticoid secretion.
• Cortisol regulates its own secretion through negative feedback control
by inhibiting the release of CRF from hypothalamus and ACTH from
anterior pituitary.
• ACTH secretion follows circadian rhythm (sleep-wake cycle.
Mineralocorticoids
• Aldosterone is called the life saving hormone. Total loss results to
death within 3 days to 2 weeks.
• It is necessary for maintaining sodium and extracellular fluid balance,
resulting in resorption of sodium in exchange with the potasium and
hydrogen ions in the distal tubule of the nephron and in other tissues
such as salivary glands, sweat glands and colon.
• It helps in the conservation of sodium in the body.
• It makes up to renin-angiotensin-aldosterone axis.
Mineralocorticoids
• Kidneys, in response to low blood volume, Increase in potassium ion
concentration , decrease in sodium ion concentration, real or
perceived (heart failure), secrete an enzyme called Renin, which acts
in the general circulation on angiotensinogen produced by the liver
and converts it into angiotensin I.
• Angiotensin I, under the action of the angiotensin converting enzyme
(ACE), converts it in angiotensin II.
• Angiotensin II is a potent arteriolar vasoconstrictor and the primary
regulator of aldosterone secretion, which maintains blood volume by
retaining sodium.
 ADRENAL GLAND DISORDERS

• Adrenal gland disorders include :

• Hyperactivity of the adrenal cortex (HYPERADRENOCORTICISM)
• Cushing’s syndrome
• Hyperaldosteronism
• Adrenogenital syndrome
• Hypoactivity of the adrenal cortex. (HYPOADRENOCORTICISM)
• Addison’s disease or chronic adrenal insufficiency.
• Congenital adrenal hyperplasia.
HYPOADRENOCORTICISM
• Addison’s Disease (hypocortisolism) is a rare, chronic disorder in
which the adrenal glands do not produce sufficient steroid hormones
(glucocorticoids and often mineralocorticoids).
• It is associated with idiopathic, surgical, or infectious destruction or
tumor of parenchyma of the adrenal gland or infiltration of the cortex
by sarcoidosis, tuberculosis or amyloidosis.
• Cortisol deficiency clinically manifests as hypoglycemia, hypotension,
muscle weakness, anorexia, nausea, weight loss and diminished
resistance to infections and stress.
ORAL MANIFESTATION OF PATIENTS WITH ADRENAL GLAND
DISORDER
• The oral mucosa can in turn develop black-bluish plaques, mainly
affecting buccal mucosa, gingivae, palate, tongue and lips.
• Possible oral infection.
• Delayed wound healing.
• Dental management of the patient with Addison’s disease
• Most of these patients are treated with corticosteroids.
• Conducting treatment in the morning when cortisol level is highest.
• Control of anxiety and emotional stress.
• Use long-acting anesthetics e.g Bupivacaine to minimize pain.
 HYPOADRENOCORTICISM
Dental management of the patient with Addison’s disease
cont’d.
• Treatment of postoperative pain.
• Prevention of iatrogenic fracture during surgery in patients with a
long history of continuous corticotherapy.
• Blood loss should be reduced because it increases the risk for
hypotension and patient placed in a supine position.
• Untreated adrenal insufficiency should be referred for medical care
and dental treatment postponed.
• Blood pressure should be taken before the dental procedure and
repeated every 5mins during the procedure.
• Dental procedure should be performed under good glycemic control.
TREATMENT PLAN FOR PATIENTS WITH ADRENAL INSUFFICINECY ON
CORTICOSTEROID
PROCEEDURE PRIMARY ADRENAL INSUFFICIENCY SECONDARY ADRENAL INSUFFICIENCY.

Routine dentistry No supplementation required. No supplementation required

25mg Hydrocortisone, Daily therapeutic dose.

Minor surgery
preoperatively on the day of
procedure.
Moderate Daily therapeutic dose.
surgical stress 50-75mg on the day of surgery and
up to 1 day and return to normal
dose on day 2.
Major surgical Daily therapeutic dose
stress 100-150mg of hydrocortisone per
day for 2-3 days before procedure.
50mg is given IV 8hly for 2-3 days.
HYPOADRENOCORTICISM

Different stages of adrenal suppression in patient undergoing

corticosteroid therapy.
• Stage I: doses of corticosteroids do not produce adrenal suppression.
• Stage II: the glucocorticoids in blood inhibit the hypothalamic
hypophyseal-adrenal axis, and the body stops producing cortisol
physiologically.
• This stage is therefore characterized by adrenocortical suppression,
though the administered corticoid dose is still insufficient to cover the
organic needs in the event of stress inducing situations.
• Stage III: the administered corticoid dose is sufficiently high to
continue suppressing the adrenal cortex but also to cover the body
needs in the event of stress.
HYPOADRENOCORTICISM
• Addisonian Crises /Adrenal crisis.
• Addisonian crises or acute adrenococortical insufficiency is a rare but
serious complication in patients with primary Addison’s disease.
• It is more likely to be attributable to administration of high-doses of
exogenous corticosteroids therapeutically.
• The reason for this is the sudden withdrawal of exogenous corticoids,
or the existence of situations requiring greater amounts of corticoids
than those afforded by replacement therapy.
• It could also be precipitated by stressful situation such as surgery.
HYPOADRENOCORTICISM
• It presents as a sudden failure of the adrenal cortex function. The
resulting clinical picture compromises shock with nausea, vomiting,
abdominal pain and hypotension. Fever and hypothermia may be
observed and can lead to coma and death.
Dental management of the patient with Addisonian Crises
• Prevention is the best management approach for Addisonian crises.
• A detailed clinical history and a consultation with the specialist is
recommended. However, if crisis takes place, we should interrupt dental
procedure, place the patient in dorsal decubitus and contact with the
corresponding medical emergency service.
 HYPOADRENOCORTICISM
Dental management of the patient with Addisonian Crises
• Until medical help arrives, oxygen should be administered to the
patient (5-10 liters/min).
• If the patient is unconscious, he should be placed in dorsal decubitus
with the legs raised, and then notify the emergency service to arrange
transfer of the patient to the hospital. Basic vital support should be
provided in accordance to the patient’s condition.
• If an adrenal cause is suspected, 100 mg of hydrocortisone should be
administered intravenously or intramuscularly, within 30 seconds if
possible, and two hours later, another 100 mg of hydrocortisone
dissolved in saline for intravenous or intramuscular injection should
be given.
HYPER-ADRENOCORTICISM
• Hyperadrenocorticism (Cushing’s syndrome) refers to manifestations
induced by chronic exposure to excess glucocorticoids produced by the
adrenal cortex.
• It most commonly arises from iatrogenic causes due to administration of
exogenous glucocorticoids.
• Signs and symptoms may include:
• High blood pressure, Abdominal obesity but with thin arms and legs,
reddish stretch marks, a round red face “moon face”, buffalo hump on
the back, weak muscles, weak bones, acne, and fragile skin that heals
poorly.
• Women may have more hair and irregular menstruation.
• Occasionally there may be changes in mood, headaches and fatigue.
 HYPER-ADRENOCORTICISM
• “CUSHINGOID MAP" is an acronym to consider the complications and
symptoms of Cushing's syndrome:
• Cataracts, Ulcers, Skin (striae, thinning, bruising), Hypertension/
hirsutism/ hyperglycemia,
• Infections, Necrosis (avascular necrosis of the femoral head),
Glycosuria, Osteoporosis/ obesity,
• Immunosuppression, and Diabetes
• Muscle weakness/ moon facies, Amenorrhea, Peptic ulcer/ purpuria
HYPER-ADRENOCORTICISM
Dental management of the patient with hyperadrenocorticism
• Prevention of infections, pathological fractures during surgical treatments
and complications such as hypertension, hyperglycemia, depression and
delayed healing.
• In patients on steroids we must evaluate the need to administer additional
corticosteroid.
• Patient are usually prone to hypertension, delayed wound healing,
osteoporosis, and peptic ulcer. This should be managed separately if
present.
• Aspirin and NSAIDs should be avoided for patients on long term use of
corticosteroid as it could aggravate peptic ulcer.
 DIABETES MELLITUS.
• It is caused by an underproduction of insulin, a resistance of insulin
receptors in end organs to the effects of insulin, or both.
• Insulin-dependent (type I) and non–insulin-dependent (type II) and
gestational diabetes.
• It is a metabolic disease characterized by dysregulation of carbohydrate,
protein, and lipid metabolism.
• The primary feature of this disorder is elevation in blood glucose levels
(hyperglycemia), resulting from either a defect in insulin secretion from the
pancreas, a change in insulin action, or both.
• Symptoms include; Excessive thirst, urination and hunger (the three “P”)
• Sudden weight loss, Increased fatigue, Increased susceptibility to infections
due to lowered immunity.
ORAL MANIFESTATION OF DIABETES MELLITUS
• Burning mouth.
• Altered wound healing and an increased incidence of infection.
• Enlargement of the parotid glands
• Xerostomia.
• Compromised periodontal health
• Oral candidiasis.
Dental Management of Patient with Diabetes
• Defer surgery until the diabetes is well controlled; consult the patient’s
physician.
• Schedule an early morning appointment; avoid lengthy appointments.
• Use an anxiety-reduction protocol, but avoid deep sedation techniques in
outpatients. Conscious sedation should be considered for extremely anxious
patients.
• Monitor pulse, respiration, and blood pressure before, during, and after
surgery. Maintain verbal contact with the patient during surgery.
• If the patient must not eat or drink before oral surgery and will have difficulty
eating after surgery, instruct him or her not to take the usual dose of regular
or NPH insulin; start intravenous (IV) administration of a 5% dextrose in water
drip at 150 mL per hour.
Dental Management of Patient with Diabetes
• If allowed, have the patient eat a normal breakfast before the dental
procedure and take the usual dose of regular insulin.
• Consult the physician if any questions concerning modification of the
insulin regimen arises.
• Watch for signs of hypoglycemia. Diabetic patients should be
encouraged to bring their glucometer with them to the dental office.
• Treat infections aggressively with the use of antibiotics.
• If the clinician suspects an undiagnosed diabetic state, the patient
should be questioned to elicit a history of polydipsia, polyuria,
polyphagia, or unexplained weight loss.
Dental Management of Patient with Diabetes.
• The most common diabetic emergency in the dental office is
Hypoglycemia, a potentially life-threatening complication that must be
managed accordingly.
Signs and symptoms include:
• confusion, sweating, tremors, agitation, anxiety, dizziness, tingling or
numbness, and tachycardia.
• Severe hypoglycemia may result in seizures or loss of consciousness.
• As soon as a patient experiences signs or symptoms of possible
hypoglycemia, he or she should check the blood glucose with a glucometer.
If a glucometer is unavailable, the condition should be treated
presumptively as a hypoglycemic episode.
• The dental practitioner should give the patient approximately 15 g of oral
carbohydrate in a form that will be absorbed rapidly.
Treatment of Hypoglycemia
1. If patient is awake and able to take food by mouth, give 15 g oral
carbohydrate in one of the following forms:
• 4–6 oz fruit juice or soda
• 3–4 tsp table sugar
• hard candy
• cake frosting
2. If patient is unable to take food by mouth and IV line is in place, give
• 25–30 mL D50 ( 50% dextrose soln) or 1 mg glucagon .
3. If patient is unable to take food by mouth and IV line is not in place, give 1 mg
glucagon subcutaneously or intramuscularly.
Treatment of Hypoglycemia cont’d
• The patient should be observed for 30 to 60 minutes after recovery.
• Evaluation by glucometer can ensure that normal blood glucose levels
have been achieved before the patient is discharged.
• Diabetic ketoacidosis and hyperosmolar nonketotic acidosis require
immediate medical evaluation and treatment.
• The dentist should be able to perform BLS (basic life support ) and
then call for emergency care.
 Recommendations
• Dental professionals should have a thorough understanding of current
medical treatment regimens and the implications of diabetes on
dental care are able to help their diabetic patients achieve and
maintain the best possible oral health.
• Diabetic status of all new dental patients should be ascertained and a
full periodontal examination should be recommended.
• Periodontal treatment should be regarded as a possible way of
improving glycemic control.
SUMMARY
• Endocrine disorders of particular importance to dentistry include the
disorders of pancreas, adrenal glands, parathyroid gland and thyroid
gland.
• This presentation focuses on the these disorders majorly.
• The brief pathophysiology, oral manifestations, and dental
management of the disorders was discussed.
CONCLUSION

• It is essential for dental practitioners to recognize these disorders and

to properly manage patients with endocrine disorders
• Appropriate precaution and care should be instituted by dental
personnel in treating patients with endocrine disorders.
 REFERENCES.
• Lorenzo-Calabria J, Grau D, Silvestre FJ, Hernández-Mijares A. Management of
patients with adrenocortical insufficiency in the dental clinic. Med Oral.
2003;8:207-14.
• Pinto A, Glick M. Management of patients with thyroid disease: oral health
considerations. J Am Dent Assoc. 2002;133:849-58.
• Woeber KA. Update on the management of hyperthyroidism and
hypothyroidism. Arch Fam Med. 2000;9:743-7.
• T Hougardy DM, Peterson GM, Bleasel MD, Randall CT. Is enough attention being
given to the adverse effects of corticosteroid therapy? J Clin Pharm Ther.
2000;25:227-34.
• Sutbeyaz Y, Yoruk O, Bilen H, Gursan N. Primary hyperparathyroidism presenting
as a palatal and mandibular brown tumor. J Craniofac Surg. 2009;20:2101-4
• Laura Carlos Fabue, Yolanda Jiménez Soriano, Mª Gracia Sarrión Pérez. Dental
management of patients with endocrine disorders. J Clin Dent. 2010;2(4):196-
203.
Thank you for listening.