Endocrine disease in dentistry /certified fixed orthodontic courses by Indian dental academy
Endocrine disease and
INDIAN DENTAL ACADEMY
Leader in continuing dental education
Mechanism of hormone action
TSH, PTH, ADH, FSH, LH
H + R→ ATP→cAMP→increased
protein kinase activity.
increase intracellular Ca from
EC/ER/mitochondria; combines with
calmodulin which alters str and fn of
Mechanism of hormone action
H enters the cell, combines with R; H+R
combine with acceptor site on human
index of suspicion necessary
Peak incidence 30-50 years.
Causes- acidophil tumor of anterior
Acromegaly – clinical features
Acro-megaly- oral features
Prognathism, mal-occlusion – class II.
Acromegaly- X- Ray Skull
III, IV and VI th cranial nerves.
Investigations- IGF-1 assay
- CT scan.
- GH levels after 75 g. oral glucose.
loss, heat intolerance,muscle
increased systolic BP.
Lid retraction, lid lag and exophthalmos
Hashimoto’s thyroiditis,Radioiodine therapy,surgery,Iodine deficiency
drugs like amiodarone,lithium etc.
-Hashimoto’s thyroiditis- common in
middle age, presents with goitre and
Thyroid- dental implications
visible to dentist
Hyperthyroidism- pain, anxiety and
Hypothyroidism- avoid sedation
Treated patients are normal.
Zona fascicularis- Cortisol
Zona reticularis-Adrenal androgens
Actions of Cortisol
diffuse passively through the
cell membrane and bind to intracellular
The steroid-receptor complex is
transported to the nucleus, where it
binds to specific sites on steroidregulated genes, altering levels of
Action on CHO metabolism
raise the blood glucose
level by acting as an insulin antagonist
and by suppressing the secretion of
insulin, thereby inhibiting peripheral
glucose uptake, which promotes
The actions on protein metabolism
Mainly catabolic in effect, resulting in an
increase in protein breakdown and nitrogen
Mobilization of glycogenic amino acid
precursors from peripheral supporting
structures, such as bone, skin, muscle, and
connective tissue, due to protein breakdown.
Hyper aminoacidemia also facilitates
Actions on fat metabolism
Glucocorticoids regulate fatty acid
mobilization by enhancing the activation of
The actions of cortisol on protein and adipose
tissue vary in different parts of the body.
Cortisol depletes the protein matrix of the
vertebral column (trabecular bone), not long
bones. Peripheral adipose tissue mass
decreases, whereas abdominal and interscapular fat expand.
on the microvasculature and to
suppression of inflammatory cytokines.
Cortisol maintains vascular
responsiveness to circulating
vasoconstrictors and opposes the
increase in capillary permeability during
depletion of circulating eosinophils
and T cells. Thus, cortisol impairs
also inhibit the
production and action of the mediators
of inflammation, such as the
lymphokines and prostaglandins.
Glucocorticoids inhibit the production
and action of interferon by T
lymphocytes and the production of IL-1
and IL-6 by macrophages.
inhibit the production
and inflammatory effects of bradykinin,
platelet-activating factor, and serotonin.
Antibody production is reduced and
lysosomal membranes are stabilized,
Actions of cortisol-contd.
Glucocorticoids also have weak mineralocorticoid-like properties, and high doses
promote renal tubular sodium re-absorption
and increased urine potassium excretion.
Glucocorticoids also can influence behavior;
emotional disorders may occur with either an
excess or a deficit of cortisol.
LABORATORY EVALUATION OF
Urinary excretion of free cortisol, 17
Plasma levels of cortisol, aldosterone- max
values in morning, low levels in evening.
Stimulation tests ( for detecting hypofunction)
25 units of Cosyntropin i.v./i.m., measure
plasma cortisol levels before, 30 minutes
after and 60 minutes after inj.If stimulated
level >7 microgm/dl- normal
Tests of Mineralocorticoid Reserve
These tests use protocols designed to create
a programmed volume depletion, such as
sodium restriction, diuretic administration, or
A simple, potent test consists of severe
sodium restriction and upright posture. After 3
to 5 days of a 10-mmol/d sodium intake, rates
of aldosterone secretion or excretion should
increase two- to threefold over the control
values. Supine morning plasma
LABORATORY EVALUATION OF
Suppression test for hyper-functionOral dexametasone 1 mg at midnight of
previous day, 8 a.m. plasma cortisol should
be < 5 microgm/dl in normal persons.
Definitive test- 0.5 mg Dexa-methasone 6
hrly for 2 days, plasma cortisol < 5
microgm/dl, urinary excretion of cortisol in
24 hrs < 30 microgm.
Tests of Mineralocorticoid
tests rely on an expansion of
extra-cellular fluid volume, which should
decrease circulating plasma renin
activity and decrease the secretion
and/or excretion of aldosterone.
TESTS OF PITUITARY-ADRENAL
Insulin-induced hypoglycemia –
In this test, regular insulin (0.05 to 0.1 U/kg
body weight) is given intravenously as a bolus
to reduce the fasting glucose level to at least
50% below basal. The normal cortisol
response is a rise to more than 500 nmol/L
Other tests are metyrapone test and CRH
stimulation with ACTH
Serum sodium, chloride, and
bicarbonate levels are reduced, and the
serum potassium level is elevated.
Normocytic anemia, a relative
lymphocytosis, and a moderate
Hydrocortisone (cortisol) is the mainstay of
treatment. The dose for most adults
(depending on size) is 20 to 30 mg/d. To
simulate the normal diurnal adrenal rhythm,
two-thirds of the dose is taken in the morning,
and the remaining one-third is taken in the
Fludrocortisone-0.05 to 0.1 mg per day by
Treatment of Addison’s disease
vomiting for > few hours- iv fluids and
If significant infection- double the dose
of cortisol during illness.
For GA- IV Hydrocortisone 100mg
before induction, repeat every 8 hrs.
Halve every 24 hrs till 5th day.
Cushing’s syndrome- Causes
Defect in hypothalamus- increased CRH
Ectopic ACTH from primitive small cell (oat
cell) type of bronchogenic carcinoma,tumors
of the thymus, pancreas, or ovary; medullary
carcinoma of the thyroid,bronchial adenomas,
carcinoid tumors or pheochromocytomas
20 to 25% of patients with Cushing's
syndrome have an adrenal neoplasm.
Evaluation of patient
Signs and symptoms
Screening test ( 1mg DXM previous MN)
Dexa-methasone suppression test
0.5 mg DXM 6hrly for 2 days
increased u. 17 ketosteroid
increased u. DHEA.
Iatrogenic Cushing’s syndrome
and urinary cortisol reduced
because of suppression of HPA axis by
Treatment for Adrenal Neoplasm
When an adenoma or carcinoma is
diagnosed, adrenal exploration is performed
with excision of the tumor. Adenomas may be
resected using laparoscopic techniques.
The principal drug for the treatment of
adrenocortical carcinoma is mitotane< 6gm/d.
This drug suppresses cortisol production and
decreases plasma and urine steroid levels
ACTH producing tumors
Whether pituitary or ectopic- treatment is
excision. Radio-therapy can also be tried.
If inoperable ACTH producing tumors
present, bilateral adrenalectomy with lifelong
steroid supplement is the treatment.
Steroidogenesis can be inhibited by
ketoconazole 600 mg.
Dental aspects of Adrenal
Liaise with physician
Oral candidiasis in Cushing’s syndrome
Oral pigmentation in Addison’s disease.
Managing a patient on steroids
Minor surgery and GA- The usual oral dose of
steroid is given on the morning of surgery,
and the usual dose of oral steroid after
Moderate or major surgery and GA-Usual oral
dose of steroid on the morning of surgery. +
Hydrocortisone 25-50 mg at the time of
induction + HCHS 25mg 3 times daily after
surgery or for 72 hrs after major surgery.
Usual steroid dose after stopping injection
Steroids and Dentistry
pt. is on >10mg Prednisolone daily,
no need to increase the dose.
If pt. is receiving 1-10 mg Prednisolone
cover with double dose if required.
If pt has stopped steroids for last 3
months highest risk. Pre-operative day
+ day of surg + 2 post-op days
Parathormone binds to the receptors on
osteoblast cells, and cytokines are released
which stimulate osteoclast cells; causing
PTH decreases renal clearance of Ca,
increases intestinal absorption,and causes
Released in response to low Ca, Mg levels.
-chief cell hyperplasia,
- Carcinoma parathyroid and
-MEN I and II.
Hydration, increased salt intake,mild
and forced diuresis.
In young patients, surgery.
Acquired- due to surgery/radiotherapy
for thyroid; auto-immune failure.
Ineffective PTH- CRF,Vitamin D
deficiency and Pseudo-hypoparathyroidism.
Vitamin D3 500 – 3000 micrograms/day
or Calcitriol 0.25 –1 micrograms/day.
• Calcium 2-3 gm/day.
• Thiazide diuretics with salt restriction.
The magnitude of the problem- 3.5 crore diabetics in India.
- 14% of the urban population.
- Estimated to be 5.72 crore by 2025.
- Only 10-12% of diabetics receive
modern pharmacologic treatment.
Diabetes Mellitus- definition
A syndrome characterized by chronic
hyperglycemia and disturbances of
carbohydrate, fat and protein
metabolism associated with absolute or
relative deficiency of insulin secretion
2 hours after 75 g oral glucose
Type 1 Insulin deficiency
Type 2 Insulin resistance but can progress to
insulin def.- lean type,obese type & MODY.
Drugs and chemicals
Insulin receptor abnormalities
Genetic syndromes- Myotonic dystrophy,
Type 1 DM
Childhood/Adolescence or adult onset.
Childhood type- higher ICA and IAA more
Adult onset-Latent auto-immune diabetes in
GAD (Glutamic acid decaroboxylase)
associated,lower antibody levels
May masquerade as non-obese type 2.
Type 2 DM
Diagnosed by excluding type1.
Most common form of DM( 90%
Strongly associated with obesity and
Usually > 40 yrs but MODY type
Strong family history.
Encourage regularity in meal timing and
consistency about quantity of each meal.
Calorie intake 1500 kcal/day in males and
1200 kcal/ day in females
-Avoid refined CHO and alcohol
-Encourage high fiber food.
-Reduce saturated fat,Sodium 2.4-3 gm/day.
DM – Role of Exercise
Check-up for BP, CVS, CNS, eyes, feet and
renal function before starting exercise.
Tailor exercise to the patient’s needs and as
per his limitations.
Benefits of exercise- reduces insulin
resistance, improves lipid profile, corrects
Aerobic exercise with a warm-up of 3-5
Type 2 DM-management
Oral hypoglycemic drugs
1) Insulin secretagoguesa) Sulfonylureasglibenclamide, gliclazide,glipizide
b) Metiglinide deivatives- Repaglinide.
2) Insulin sensitizers
a) Biguanides- Metformin.
b) Thiozolidinedone- Pioglitazone,Rosiglitazone
3) Drugs delaying CHO absorption- Acarbose
Insulin in type 2 DM
Not controlled with diet,exercise and
Given pre- prandial with basal cover.
Sources of InsulinHuman,porcine and bovine.
Duration of ActionRapid acting –onset ½ hr; duration 8 hrs.
Intermediate- NPH onset 1.5 hrs,duration 24 h
Insulin delivery systems (Insulin pens,
Chronic-Atherosclerosis of large
-retinopathy, maculopathy, early cataract.
Diabetes and dentistry-1
Wear and tear of gingival tissues due
to dentures more in uncontrolled
diabetes; chances of oral candidiasis.
Delayed healing and chances of
infection after invasive dental
Diabetes and dentistry- 2
High risk patients1) Poor metabolic control- FPG > 250 mg
%, HbA1c > 9%.
Frequent episodes of hypoglycemia or
3) Multiple complications.
Diabetes and dentistry-3
For type II – VI procedures, defer
treatment until metabolic control is
Palliative rather than extensive
restorative surgery preferred.
Aggressive control of oral infection – a
Diabetes and surgery
Metabolic changes during surgery-Hormone changes which aggravate DMAdrenaline,GH,cortisol.
-More glucose production less muscle uptake.
- metabolic acidosis likely.
Increased insulin requirements in type 1 DM
Type 2 DM may require insulin cover perioperatively.
DM and Surgery-plan
Target glucose level 7-11 mmol/lit
IV fluids should not contain glucose.
Monitor electrolytes frequently (K +)
Ensure good analgesia- reduce stress.
GKI infusion10% Dextrose, 10 mmol K+,10 U actrapid.