Oral Manifestations of Endocrinal Disorders / dental crown & bridge courses

Oral Manifestations of Endocrinal Disorders
Seminar on:
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INDIAN DENTAL ACADEMY
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Contents
Part-1
 Introduction
 Classification
 Growth hormone
 Thyroid hormones
 Gonadal hormones
 Radiographic features
 Oral manifestation & dental consideration
Part-2
 Parathyroid hormones
 Hormones of Adrenal gland
 Conclusion

What are hormones????
 Hormones are the substances released from the cells
that circulate and affect distant organs.
 The main physiologic function of hormones are
growth, maintenance of homeostasis and
reproduction.

Chemistry of hormones
Hormones are classified into three types depending on their
chemical nature.
1.Steroid derivative
These are the hormones derived from cholesterol or its
derivatives. Steroid hormones are corticosteroid and sex
hormones.
2.Protein derivative
These hormones are large or small peptides. Protein
hormones are, the hormones secreted by pituitary gland,
parathyroid gland, pancreas.
3.Derivative of amino acid- tyrosine
There are two types of hormones which are derivatives of the
amino acid called tyrosine. Thyroid hormones and adrenal
medullary hormones are derived from tyrosine.

Hormones secreted by major endocrine glands
Anterior pituitary
1.Growth hormone (GH)
2.Thyroid stimulating hormone (TSH)
3.Adrenocorticotropic hormone (ACTH)
4.Follicle stimulating hormone (FH)
5. Luteinizing hormone (LH)
6. Prolactin
7. Melanocyte stimulating hormone
Posterior pituitary
1. Antidiuretic hormone (ADH)
2. Oxytocin
Thyroid gland
1. Thyroxine
2. Triiodothyronine
3. Calcitonin www.indiandentalacademy.com

Parathyroid gland
Parathormone
Pancreas
1.Insulin
2.Glucagon
3.Somatostatin
Adrenal cortex
(i) Mineralcorticoids
1.Aldosterone
2.11 deoxycorticosterone
(ii)Glucocorticoids
1.Cortisol
2.Corticosterone

(iii) Sex hormone
1. Androgen
2. Estrogen
3. Progesterone
Adrenal medulla
1.Adrenaline (Epinephrine)
2.Noradrenaline (Norepinephrine)
3.Dopamine

Pituitary gland
 The pituitary gland is also known as hypophysis. It is small
gland with diameter of 1cm & weighs about 0.5-1 gm.
 Physiologically gland is divided into portions namely, the
anterior or adenohypophysis and posterior or
neurohypophysis.

Actions:
GH is responsible for growth of almost all parts of the body.
1) Metabolic effect:
a)Effect of GH on protein metabolism-
i)increases amino acid transport through cell membrane
ii)increases translation of RNA.
iii)increases the transcription of DNA to RNA.
iv)decreases catabolism of proteins.
b) Effect of GH on fat metabolism-
GH cause mobilization of fats from the adipose tissues, and thus
increase concentration of fatty acid in the body fluid. These
fatty acid are available for the production of energy. Thus, GH
spares proteins.
Growth Hormone

c) Effect of GH on carbohydrate metabolism-
The main action of GH on carbohydrate is conservation of
glucose-
i)Decrease the peripheral utilization of glucose
ii)Increase in deposition of glycogen in the cells.
iii)Decrease in the uptake of glucose by the cells.
iv)Diabetogenic effect of GH
2) Effect of GH on Bones:
GH is responsible for differentiation and development of bone. In
later stages increases growth of skeleton. It increases length as
well as thickness of the bone.

Antidiuretic hormone
 ADH is also called as vasopressin because it cause constriction of
blood vessels.
 The major function of ADH is retention of water by acting on
kidneys.
 Diabetes Insipidus is a syndrome of inability to hold on to free
water by kidneys. It can be caused by inadequate pituitary
production of ADH or resistance to ADH by the kidney.
 Excessive ADH- syndrome of inappropriate antidiuretic hormone
(SIADH) is a syndrome of too much total body water and manifest
as hyponatremia, that can lead to seizure and death if
undetected.
 Vassopressor effect of ADH is very much more than the amount
required to cause antidiuretic effect.

Disorders of Pituitary gland
 Gigantism
 Acromegaly
 Acromegalic gigantism
 Cushing disease
 Dwarfism
 Acromicria
 Simmond’s disease
 Diabetes Insipidus
 Syndrome of inappropriate hypersecretion of antidiuretic
hormone (SIADH).
 Dystrophia Adiposogenitalis

Oral manifestation of Pituitary disorders
 Patients with GH excess have characteristic coarse facial
appearance because of thick rubbery skin, enlarged nose and thick
lips.
 They have macrocephaly, macrognathia, disproportionate
mandibular growth and generalized diastema.
 Anterior open bite and malocclusion because of macrognathia and
tooth migration.
 Intraorally excessive soft tissue
growth usually presents as macroglossia
and hypertrophy of pharyngeal and
laryngeal tissues making the patient
susceptible to sleep apnea.

 GH deficiency presents with disproportionate growth of skull
and facial skeleton giving them small facial appearance for their
age.
 Tooth formation and growth of the alveolar regions of the jaws
are abnormal and may be disproportionately smaller than
adjacent anatomic structures, leading to crowding and
malocclusion.
 Crowding and malocclusion cause high tendency for plaque
accumulation and poor oral hygiene and hence may be prone for
gingivitis and periodontal disease.
 Eruption of primary and secondary dentition and shedding of
deciduous teeth is delayed.

Radiographic features
Hyperpituitarism
 General radiographic features:
-- The pituitary tumor responsible for hyperpituitarism often
produces enlargement (balloning) of the sella turcica.
--Skull radiograph may reveal enlargement of the paranasal
sinuses(especially the frontal sinus).
--Hyperpituitarism in adults also produces diffuse thickening
of outer table of skull.
 Radiographic features of the jaws
-- Enlargement of jaws most notably mandible. In acromegaly
the angle between ramus and body of the mandible may
increase.
--Macroglossia may result in flaring of teeth and this feature
is helpful in differentiation between acromegalic
prognathism and inherited prognathism.

Radiographic features associated with the teeth:
 Tooth crowns are usually normal in size, although the roots of
the posterior teeth often enlarge as a result of hypercementosis.
 Dental radiograph may demonstrate large pulp chambers
(taurodontism).
 Supraerruption of posterior teeth may occur in an attempt to
compensate for the growth of mandible.

Radiographic features of hypopituitarism:
 The crowns of the permanent form normally but their eruption
is delayed several years.
 The third molar buds may be completely absent.
 Jaws are small especially mandible; this results in crowding and
malocclusion

Dental management
 50% of the GH excess patient develop hypertension and 10%
develop cardiomegaly and over heart failure and 30% develop
insulin resistance or DM type 2.
 Henceforth dental management of these patients must consider
these complication and consultation with physician.
 Patients with GH deficiency require correction of dental and
skeletal malocclussion.
 If a DI patient require any dental treatment, under general
anesthesia, the anesthetist must monitor fluid and electrolyte
intake because the urine of DI patient is solute-free water.
 The clinician should also avoid or reduce the use of
glucocorticoids in DI patients, since glucocorticoids can increase
renal loss of water and can further complicate DI.

Thyroid gland
 Thyroid is endocrine gland situated at the root of the neck on
either side of the trachea.
 Normally it weighs about 20 to 40 gm. Thyroid has two lobes
connected in the middle by an isthmus.
 It is larger in females than in males.
 Diseases of thyroid gland are more common in females than in
males

Function of thyroid hormones
1) Effect on Basal Metabolic Rate:
Thyroxine increases BMR of almost all the tissues of the body.
2) Effect on Protein Metabolism:
Thyroxine increases the synthesis of protein by-
i)By increasing translation of RNA.
ii) By increasing the transcription of DNA to RNA.
iii) By increasing the activity of mitochondria.
iv)By increasing the activity of cellular enzyme.
3) Effect on fat metabolism:
Increases the free fatty acid level in the blood.www.indiandentalacademy.com

4) Effect on Carbohydrate metabolism:
Thyroxine stimulates almost all the process involved in metabolism
of glucose by-
i) increasing absorption of glucose from GIT.
ii) accelerates the transport of glucose through the cell membrane.
iii) increases the breakdown of glycogen into glucose.
iv) accelerates gluconeogenesis.
5) Effect on Plasma and Liver Fats:
Thyroxine also increases deposition of fats in liver leading to fatty
liver and decreases cholestrol level by increasing its excretion from
liver cells into bile.

6) Effect on Vitamin Metabolism:
Thyroxine increases the formation of enzymes and vitamins may be
utilized during the formation of the enzyme.
7) Effect on Body Temperature:
It increases the heat production in the body by accelerating the
various cellular metabolic processes and increasing BMR.
8) Effect on Growth:
Lack of thyroxine can arrest growth and increase in thyroxine can
accelerate the the growth of the body especially in children.
9) Effect on Body weight:
Increase in thyroxine secretion decreases the body weight and
decrease in thyroxine, increases the body weight.

10) Effect on Blood:
Thyroxine accelerates process of erythropoiesis.
11) Effect on Cardiovascular system:
i) it increases heart rate
ii) increases the force of contraction
iii) increases the blood flow
iv) increases the blood pressure
12) Effect on Respiration:
Increases rate and force of respiration indirectly by increasing
utilization of oxygen and formation of carbon dioxide.

13) Effect on GIT:
Increases the appetite & food intake. And also increases secretion
and movements of GIT.
14) Effect on Central Nervous System:
It is very essential for normal development and functioning CNS.
15) Effect on Skeletal Muscle:
Thyroxine is very essential for normal activity of skeletal muscles.
Slight increase in thyroxine can make muscle to work with rigor
and can produce weakness in muscle due to catabolism of
proteins, this condition is called as thyrotoxic myopathy.

16) Effect on Sleep:
Hypersecretion of thyroxine causes excessive stimulation of
skeletal muscle and CNS. So the person feels tired, exhausted and
feels like sleeping.
17) Effect on Sexual function:
Hyposecretion of thyroid hormone in men cause libido and in
women cause menorrhagia, polymenohorrhea & amenorrhoea
and hypersecretion causes leads to impotence in men and
oligomenorrhea.
18) Effect on other Endocrine gland:
Because of it effect on metabolism, thyroxine increases the
demand for secretion of other endocrine glands.

 Basal metabolic rate = measure energy of cells for
making its work = anabolism + catabolism.
 Its function determine by iodine level in blood:
↓ I- in blood:
 Regulate the gland to be functioning.
 Stimulate TRH Pituitary gland TSH stimulate
 thyroid gland thyroid hormones feed back inhibition.
↑ I- in the blood feed back mechanism no TRH no
TSH no T3 and T4.
 Feed back mechanism works normally during the disease
but the gland not responding to it.

Diagram showing the hypothalamic-pituitary-thyroid
axis involved in the control of thyroid secretion.
The secretion of thyroid-stimulating hormone (TSH) is regulated
by the interaction of thyroid-releasing hormone (TRH) and an
inhibitory factor (somatostatin).
Thyroid hormones (T3 and T4) act directly on the pituitary to
inhibit TSH secretion.
Thyroid hormones also act at the hypothalamic level to stimulate
somatostatin release. T4 is converted to T3 in the liver, kidney,
and heart and in the pituitary and hypothalamus. T3 is
more potent than T4 at all sites.

A, Thyroid enlargement in
hyperthyroidism; B, exophthalmos.
Disorders of thyroid gland
1.Hyperthyroidism
Graves disease
2.Hypothyroidism
Myxedema
Cretinism
3. Goiter
a. Toxic goiter
b. Nontoxic goiter
i) endemic colloid
ii) idiopathic nontoxic

Signs & symptoms of hyperthyroidism & hypothyroidism

Diagnosis
 Diagnosis begins with history and physical examination. In
patients with hyperthyroidism resulting from Grave’s disease the
classical signs and symptoms are unusually characteristic enough
to make diagnosis.
 In other patients laboratory studies become important. Serum
levels of T3 and T4 are elevated, and the most useful tests are
serum thyroxine or free thyroxine index, serum T3 and thyroidal
radioactive iodine uptake (RAIU).
 Cretinism is often suspected at birth however the typical
appearnce and behavioral changes may not become apparent
until the third to sixth month of life.

 It is important to determine whether the cause of hypothyroidism
is primary (i.e associated with decreased function of the thyroid
gland or secondary, involving of the hypothalamic-pituitary axis).
 Most sensitive test to is Radioimmunoassay for serum TSH. The
diagnosis of initial primary hypothyroidism is made if the serum
TSH levels are greater than two folds .
 When clinically hypothyroid patient presents with normal TSH
and T3 –resin uptake but a low serum T4 further studies must be
done to determine whether symptom are caused by pituitary or
hypothalamic failure.
 TRH stimulation test shows no TSH elevation with TRH injection,
whereas a definite rise is seen when cause is hypothalamic
failure, which is indicative of secondary hypothyroidism.www.indiandentalacademy.com

 As a part of a routine head & neck examination,
the oral health practitioner should palpate the
thyroid gland.
 Hyperthyroidism can exacerbate the patient’s response to dental
pain and anxiety.
 Signs of thyroid disease include changes in occulomotor function,
protrusion of eyes,excessive sweating, enlargement of thyroid,
tounge or lingual thyroid tissue and difficulty in swalllowing.
 Patients may have increased susceptibility to dental caries and
periodontal diseases.
 Accelerated dental eruption in children, maxillary or mandibular
osteoporosis.
Oral manifestation of thyroid gland disorder

 In hypothyroidism, orofacial findings include facial myxedema,
macroglossia, compromised periodontal health, delay tooth
erruption, delayed wound healing, a hoarse voice.
 Salivary gland enlargement, changes in taste, and burning
mouth syndrome and development of connective- tissue
diseases such as Sjogren sydrome SLE& have also been
reported.
 Hashimoto’s thyroditis have also been associated
with xerostomia and impaired salivary secretion.

Hyperthyroidism
 It results in advanced in an advanced rate of dental
development and early eruption, with premature loss of
primary teeth.
 Adult may show generalized decrease in bone density or loss of
some areas of edentulous alveolar bone.
Hypothyroidism
 In children there is delayed closing of epiphyses and skull
sutures with production numerous wormian bones(accessory
bone suture).
 Effect on teeth include delay eruption, short roots and
thinnning of the lamina dura.
 Maxilla and mandible are relatively small.

Dental considerations
 The most important concern in treating the patient with
hyperthyroidism is the risk development of thyrotoxicosis or a
“thyroid storm” which includes symptom of extreme irritability
and delirium, hypotension, vomiting and diarrhea. It can be
triggered by surgery, sepsis and trauma.
 Epinephrine is contraindicated and elective dental care should be
differed in patient.
 Patient who have hyperthyroidism are susceptible to
cardiovascular diseases, including atrial dysrhythmias,
tachycardia and hypertension.

 Certain analgesic must be used with caution in these patient.
Aspirin and NSAID’s may cause increased levels of T4, leading to
thyrotoxicosis. NSAID’s can also cause decrease effect of beta
blocker.
 Patients with hyperthroidism have elevated blood pressure and
may require increase attention and of longer duration to arrest
the bleeding

Hypothyroidism
 Lethargy is common finding in patient with uncontrolled
hypothyroidism and the oral health practitioner should be aware
of lethargy which could indicate poorly controlled condition.
 Lethargy could become a concern due to diminished respiratory
rate and increased risk of aspiration of dental material.
 These patients are susceptible to cardiovascular diseases,
therefore required consultation with medical provider.
 Antibiotic prophylaxis is required for the patient with atrial
fibrillation and cardiac valve pathology before invasive
pathology.

 Hypothyroidism patients are sensitive to Central nervous
system depressants and barbiturates so these medications
should be use cautiously.
 Patients with long-standing hypothyroidism may have
increased subcutaneous mucopolysaccharides .
 The presence of excess subcutaneous mucopolysaccharides
may decrease the ability of small vessels to constrict when cut
and may result in increased bleeding from the infiltrated
tissues, including mucosa and skin.
 Patients with hypothyroidism may have delayed wound
healing due to decreased metabolic activity in fibroblasts.

 Delayed wound healing may be associated with an increased risk
for infection because of the longer exposure of the unhealed
tissue to pathogenic organisms.
 Another cause of infection is as a result of drug side effect since
one of the most commonly used drug (propylthiouracil) can
cause agranulocytosis or leukopenia

Gonads and Gonadal dysfunction
 The gonads, like most other endocrine organs, are incorporated
into endocrine axis; the hypothalamic-pituitary-gonadal (HPG)
axis.
 The gonadal hormone released by pituitary are Follicle
stimulating hormone and Luteinizing hormone.
 In male, LH stimulates testosterone production from leydig cells
of testicles, and FSH stimulates sperm production by sertoli
cells.
 In females, FSH stimulates maturation of the follicle and LH
causes luteinization or maturation of follicle into corpeus
luteum as well as production of ovarian estradiol.

Oral manifestation of Gonadal disorders
 Hypersecretion of female sex hormone commonly occurs in
pregnancy.
 Hyposecretion of gonadal hormone occur during menopause.
Pregnancy
 Pregnancy cause physiologic changes throughout the body that are
relevance to dentist.
 In addition to hemodynamic and metabolic changes caused by
pregnancy may require special dental treatment planning
considerations for the protection of expectant mother and
developing fetus.

Medical aspects-
 The normal pregnancy lasts for 40 weeks. During pregnancy there
is a marked increase in cardiac output(30% to 50%), blood volume
increases to help sustain fetus and the plasma volume may
increase as much as 50%
 Other important physiologic changes of concern to dentist include
mild hypotension, dyspnea on exertion, fatigability and an
increase requirement for iron.
 The endocrine changes in pregnancy consits of increased
production of female sex hormones and glucocorticoids .

Oral Changes
 Several unusual oral manifestation that may occur in pregnant
woman such as melasma which disappears after delivery of new-
born baby.
 High levels of female sex hormone cause increased capillary
permeability, making susceptible to gingivitis (pregnancy gingivitis),
gingival hyperplasia and pyogenic grannuloma (pregnancy tumor).

 Increased angiogenesis, due to sex hormones coupled with gingival
irritation by local factors such as plaque, is believed to cause
pyogenic granuloma.
 It can happen at any time during pregnancy, but is reported to be
most common in first pregnancies, during the first and the second
trimesters.
 They are exuberant growths of grannulation tissue that develop in
interdental region, these lesions may regress following birth,
however surgical excison is usually warranted.
 The increased levels of female sex hormones during pregnancy are
responsible for altered gingival response.This theory is supported by
the fact that gingival inflammation tends to lessen in severity
postpartum and that meticulous plaque control during pregnancy
tends to minimize gingival inflammation during gestational period.

 Salivary estrogen level has been suggested as a screening test to
detect the risk potential for preterm labor. Salivary estrogen
levels are higher in the women destined to have preterm babies
than in women having normal term deliveries.
 Salivary estrogen also increases the proliferation and
desquamation of the oral mucosa and an increase in subgingival
crevicular fluid levels.
 The desquamating cells provide a suitable environment for
bacterial growth by providing nutrition predisposing the
pregnant woman to dental caries.

 Treatment of the pregnant patient must be structured in manner
that affords maximum protection to both mother and developing
fetus.
 The following recommendations should be regarded as general
guidelines that may modified based on patient’s medical or
dental status or by communication with patient’s physician.
 The specific dental management concerns in patients with
gonadal disorders are focused on the associated secondary
disorders.
 The pregnant patient is susceptible to gestation diabetes since
insulin action is antagonized by estrogen and progesterone.
 Patient education:- Explain need for good plaque control in view
of relationship between local irritants, hormonal changes and
gingival disease during pregnancy.
Dental management

 Elective and stressful procedure should be avoided during the
first trimester and the last half of the third trimester.
 The second trimester is the safest period to provide dental care
during pregnancy.
 Injudicious use of medications should be avoided during
pregnancy.
 Radiographs are not contraindicated during pregnancy but the
practioner should use good clinical judgement and limit the
number of x-rays.
Timing of dental treatment

First trimester (conception to 14th week)
 The most critical and rapid cell division and active organogenesis
occur between the second and the eighth week of postconception.
 Therefore, the greater risk of susceptibility to stress and
terratogens occurs during this time and 50% to 75% of all
spontaneous abortions occur during this period.
The recommendations are:
1. Educate the patient about maternal oral changes during
pregnancy.
2. Emphasize strict oral hygiene instructions and thereby plaque
control.
3. Limit dental treatment to periodontal prophylaxis and
emergency treatments only.
4. Avoid routine radiographs. Use selectively and when needed.
DENTAL MANAGEMENT GUIDELINES

Second trimester (14th to 28th week)
 Organogenesis is completed and therefore the risk to the fetus is
low. This is the safest period for providing dental care during
pregnancy.
1. Oral hygiene, instruction, and plaque control.
2. Scaling, polishing, and curettage may be performed if necessary.
3. Control of active oral diseases, if any.
4. Elective dental care is safe.
5. Avoid routine radiographs. Use selectively and when needed.
Third trimester (29th week until childbirth)
Although there is no risk to the fetus during this trimester, the
pregnant mother may experience an increasing level of discomfort.
Short dental appointments should be scheduled with appropriate
positioning while in the chair to prevent supine hypotension.www.indiandentalacademy.com

 It is safe to perform routine dental treatment in the early part
of the third trimester, but from the middle of the third
trimester routine dental treatment should be avoided.
1. Oral hygiene, instruction, and plaque control.
2. Scaling, polishing, and curettage may be performed
if necessary.
3. Avoid elective dental care during the second half of
the third trimester.
4. Avoid routine radiographs. Use selectively and when
needed.

Radiographs in Pregnancy
 X-rays are a type of electromagnetic radiation that have the
ability to ionize material through which it passes. Ionizing living
matter results in damage to cells or DNA.
 Depending on the amount of radiation and the stage of
pregnancy, damage to fetal cells may result in miscarriage, birth
defects, or mental impairment.
 Dental radiographs may be prescribed during pregnancy,
because radiation exposure to the fetus in utero is negligible.
 The dose to the fetus is about 1/50 000 of the direct exposure
to the head. As a consequence, the effective body dose from
the full mouth series of D speed films is less than 1x10-6 Gy .

 Teratogenecity of radiation depends on fetal age and the dose
of radiation. The greatest risk to the fetus for teratogenecity
and death is during the first 10 days after conception.
 The most critical period of fetal development is between 4 and
18 weeks after conception. The chance of fetal teratogenecity
with an exposure of 0.01Gy is about 0.1% and radiation doses
of up to 0.05 Gy or less are not associated with significant
increase in teratogenecity.
 Fetal exposure to radiation of more than 0.20 Gy will cause
microcephaly and mental retardation.

 Radiographs employed in dentistry such as the panoramic and
full mouth intraoral series are generally safe during pregnancy.
 The average radiation doses absorbed by the fetus in panoramic
and full mouth radiographs are 1.5x10-4 Gy and 10-5 Gy
respectively.
 The dental radiation received is also 40-fold less than the
naturally occurring background radiation.
 Although the risk of teratogenecity is exceedingly low with
dental radiographs, the amount of radiation exposure to the
pregnant mother and fetus can and must be minimized even
further by using bitewing radiographs instead of panoramic
radiographs, using high-speed films (E speed), the use of
rectangular collimation instead of circular collimation, properly
collimated beam, and lead aprons over the abdomen.

 The ADA endorses US Food and Drug Administration (FDA)
selection criteria for dental x-ray exposures, which states that
‘‘dental radiographs for pregnant patients may be prescribed
according to the usual and customary selection criteria.’’
 While considering potential risks of diagnostic imaging, the
potential benefits must be considered. Radiography
facilitates an accurate diagnosis. This in turn will lead to
maintenance of health or timely initiation of corrective
therapy when needed.
 Incomplete or inaccurate diagnosis delays appropriate
therapy and may lead to inappropriate management, and
further deterioration and complication become more likely.

Drugs
 Drugs are absorbed easily during pregnancy as the serum
concentration for drug binding is lower than in the nonpregnant
state.
 There is also a higher volume of drug distribution, lower maximum
plasma concentration, lower plasma half-life, higher lipid
solubility, and a higher clearance of the drugs.
 All these factors allow for easy transfer of an unbound drug across
the placenta exposing the fetus to the drugs.
 Certain drugs are known to cause miscarriage, teratogenecity, and
low birth weight of the fetus. Therefore, caution should be
exercised when prescribing drugs to a pregnant women.
 Most drugs are excreted in breast milk, exposing the newborn to
the drugs.
 Neonatal toxicity depends on the chemical properties, dose,
frequency, duration of exposure to the drugs, and amount of milk
consumed.

Menopause
 It represents decline of ovarian function and usually occurs
between age of 40 and 55 year. Artificial menopause occur if the
ovaries are removed or receive irradiation therapy.
 Signs and Symptom:
• Symptom that develop are due to deficiency of estrogen.
• Irritability, hot flashes, depression, paresthesias, insomnia,
nervousness.
• During advanced stages of menopause, osteoporosis resulting in
back or joint pain may occur.

Oral Changes
 Complaints of burning mouth and tongue, taste abnormalities
and dryness of the mucous membrane are not uncommon.
 Patients occasionally present with desquamative gingivitis. In this
condition there is atrophy and ulceration of the gingival tissues
that can produce extreme gingival pain and bleeding.
 Postmenopauasal women have increased susceptibility to
osteporosis, so dental radiograph may demonstrate hypocalcified
bone.
 These may predispose individual to dental caries, glossodynia,
dysgeusia, unpleasant metallic taste and oral candiasis.
 There is also an increase in the incidence of Sjogren’s syndrome,
pemphigus vulgaris, burning mouth syndrome and trigeminal
neuralgia.

References
 Burket’s textbook of oral medicine, eleventh edition.
 Differential diagnosis of Oral and Maxillofacial lesions, Wood &
Goaz, fifth edition
 White & Pharon, Textbook of Oral Radiology, fifth edition
 Essentials of Medical physiology, Sembulingam
 Dental management of patients with endocrine disorders-J Clin
Exp Dent. 2010
 Thyroid Disorders. Part I: Hyperthyroidism- J OOOE Vol. 101 No. 3
March 2006
 Pregnancy and Lactation - J ORAL SURGERY ORAL MEDICINE ORAL
PATHOLOGY ORAL RADIOL ENDOD June 2004, Vol. 97 No. 6

Thank you

Oral Manifestations of Endocrinal Disorders - II
Guided by-
Dr.S.S Degwekar
Presented by-
Neha Vyas
Seminar on:

Contents
Part-2
 Parathyroid hormones
 Hormones of Adrenal gland
 Conclusion
Part-1
 Introduction
 Classification
 Growth hormone
 Thyroid hormones
 Gonadal hormones

Parathyroid gland
 Normally there are four parathyroid gland, which are located
immediately behind thyroid gland at the upper and lower poles.
 Parathyroid glands are very small gland measuring about 6mm
long, 3mm wide and 2mm thick with dark brown color.
 Parathormone secreted by the parathyroid gland is essential for
the maintenance of blood calcium level within very narrow
critical level.

 Regulation of blood calcium level
- Calcium taken through dietary substances is absorbed from GIT into
blood and distributed to various parts of body.
- While passing through kidney large quantity of calcium is filtered in
the glomerulous.
- From the filtrate 98-99% of calcium is reabsorbed through urine.
- Depending upon the blood level the calcium may be deposited or
reabsorbed from bone.
- All these process are regulated by three hormone namely,
Parathormone, 1,25 Dihydroxy Cholecalciferal, Calcitonin.www.indiandentalacademy.com

I. Parathormone
- Secreted by chief cells of Parathyroid gland
- Main function is to increase level of blood calcium by
mobilizing calcium from bone.
II. 1,25 Dihydroxy Cholecalciferal
- Steroid hormone synthesized from vitamin D by means of
series of hydroxylation reaction in liver and kidneys.
- Action is to increase blood calcium by increasing calcium
absorption from intestine.
III. Calcitonin
- Secreted by parafollicular cells of thyroid gland.
- It is a calcium lowering hormone. It reduces blood calcium by
decreasing bone resorption.www.indiandentalacademy.com

Regulation of Blood Calcium level
Decreased blood calcium level Increased blood calcium level
Parathyroid Kidneys
Parathormone 1-25 Dihydroxy
Cholecalciferal
Bone Intestine
Reabsorption and
release of calcium
Absorption of
calcium
thyroid
Calcitonin
Bone
Deposition of calcium
Normal blood calcium levelwww.indiandentalacademy.com

Parathormone
Actions of PTH
Maintain blood calcium level (9-11 mg %) by following
mechanisms-
1)
PTH is responsible for resorption of bone by following phase
a) Rapid Phase
Occurs within minutes of release of PTH. PTH gets attached with
receptors of all membrane of osteoblast and osteocytes.
b) Slow Phase
Slow phase of bone resorption is by activation of osteoclasts.
Effect on Bones

2)
PTH increases the reabsorption of calcium from the renal
tubules.
3)
PTH increases absorption of calcium ions from GIT because
of formation of 1, 25 dihydroxy cholecalciferal from
vitaminD.
Effect on Kidneys
Effect on GIT

Role of PTH in activation of vitamin D
Vitamin D is essential for calcium absorption from GIT but it itself is
not active substance, it has to be converted into 1,25 Dihydroxy
cholecalciferal in liver and kidneys.
Activation of vitamin D
- There are various forms of vitamin D but important one is
vitamin D3 (cholecalciferol) which is synthesized in the skin 7
dehydroxy cholestrol by action of UV rays from sunlight.
- Activation of vitamin D3 occurs in following phase

Step 1.
- Cholecalciferol is converted into 25 hydroxy cholecalciferol in liver,
this process is limited and can be inhibited by 25, hydroxy
cholecalciferol itself , this is known as feedback mechanism.
- Inhibition is necessary for two reasons
-- Regulation of amount of active vitamin D.
-- Storage of vitamin D for months.
-- 25, hydroxy cholecalciferol can be stored in the body for 2-5
days while vitamin D3 can be stored in liver for months.
Step 2.
25 hydroxy cholecalciferol is converted into 1,25 dihydroxy
cholecalciferol in kidney and it requires presence of parathormone.

 Role of calcium in regulating 1,25 dihydroxy
cholecalciferol
- If more amount of calcium is present it then inhibits formation of
1,25 dihydroxy cholecalciferol in the following ways:
1) It directly supresses 25 hydroxy cholecalciferol conversion into
1,25 dihydroxy cholecalciferol , this effect is mild.
2)Increasing calcium ions causing decrease in PTH secretion hence
supressing the conversion of 25 hydroxy cholecalciferol into 1, 25
dihydroxy cholecalciferol.
-This makes calcium level in plasma to fall back to normal

Cholecalciferal (Vitamin D3)
(inactive form of vitamin D)
25- hydroxy cholecalciferol
1,25 Dihydroxy cholecalciferol
(active form of Vitamin D)
1,25 Dihydroxy cholecalciferol
Calcium
IntestineKidneyLiver
Parathormone
Inhibition
Activation of Vitamin Dwww.indiandentalacademy.com

Actions of 1,25 Dihydroxy Cholecalciferol
1. It increases absorption of calcium from intestine by formation of
calcium binding proteins, these proteins act as carrier protein for
facilated diffusion by which calcium ions are transported and
these proteins remain in the body even after removal of 1,25
dihydroxy cholecalciferol.
2. It increases the synthesis of calcium induced adenosine
triphosphate in intestinal epithelium.
3. It increases the synthesis of alkaline phosphate in intestinal
epithelium.

Regulation of Parathormone Secretion
- Parathormone secretion is inversely proportional to blood calcium
level. Increase in blood calcium level decreases PTH secretion.
- Condition in which secretion of PTH is decreased
1. Excessive quantities of calcium in the diet.
2. Increased Vitamin D in diet.
3. Increase resorption of calcium from the bones various diseases of
bone.
- Decrease in calcium ion concentration causing increase
Parathormone secretion as in case of rickets, pregnancy.

Calcitonin
Secreted by parafollicular cells of thyroid gland.
ActionsofCalcitonin
- Maintenance of blood calcium level along with PTH. It reduces
calcium level by acting on bones, kidney and intestine.
1. On Bones
Facilitates deposition of calcium on bones. It also suppresses the
activity of osteoclasts .
2. On Kidney
Calcitonin increases excretion of calcium through urine by inhibiting
the reabsoption of calcium from the renal tubules.
3. On Intestine
It prevents absorption of calcium from intestine into the blood.www.indiandentalacademy.com

Hypoparathyroidism
 Hypoparathyroidism causes hypocalcemia by decreasing the
resorption of calcium from bones.
 This causes neuromuscular hyperexcitability resulting in
hypocalcemic tetany.
 Normally, tetany occurs if the plasma calcium level falls below 6
mg% from its normal value of 9.4mg%.
 The four types of hypoparathyroidism are-
1.DiGeorge’s Syndrome
2.Postoperative hypoparathyroidism
3. Idiopathic hypoparathyroidism
4.Pseudohypoparathyroidism
Disorders of Parathyroid gland

Signs and symptoms of hypoparathyroidism
 Tetany is characteristic, as are paresthesias of the lips, tongue,
fingers & feet and myalgia and spasm of facial musculature.
 The neuromuscular instability associated with hypocalcemia can be
proved by tapping the facial muscles (Chvostek’s sign).
 Another useful test is Trousseau’s sign(carpodeal spasm) which
occurs when blood supply to the hand is reduced by application of a
blood pressure cuff above systolic pressure.
 Other symptoms include muscle weakness, cramps, heart
palpitation, and bizzare behaviour patterns.Abnormalties of skin,
nails, and teeth are common.The skin is coarse, scaly and dry and
the nail beds are deformed; hair is thin and alopecia may be
present.

Trosseau’s sign
Chvostek’s sign

Oral Manifestations
 Painful muscular spasms affect oral and laryngeal muscles.
 Despite low serum calcium levels, the maxilla and mandible are
abnormally dense with well-calcified trabeculae.
 If the hypoparathyroidism is part of autoimmune
polyendocrinopathy syndrome, oral mucocutaneous candiasis
may be present in acute or chronic form.
 If the hypoparathyroidism occurs in still developing teeth there
will be abnormalities in appearance and eruption pattern.

 There may be enamel hypoplasia, single or parallel horizontal
bands on enamel and poorly mineralized dentin.
 Other dental findings include malformed teeth, anodontia,
short blunt root apices, elongated pulp chambers, impacted
teeth and mandibular exostoses.
 If hypoparathyroidism occurs after dental development,
there are no abnormalities seen in erupted teeth.

Hyperparathyroidism
 Hyperparathyroidism is a disease in which there may be a complex
of biochemical, anatomic, and clinical abnormalities resulting from
the increased secretion of PTH.
 The primary clinical orofacial signs and symptoms of
hyperparathyroidism are reflections of the systemic effects of
hypercalcemia.
 This entity is the most common cause of a generalized rarefaction
of the jaws.
 Bones, stones abdominal groans, psychic moans with
fatigue overtones.
 Patient complains of weakness, anorexia, nausea, vomiting,
constipation, abdominal pains, muscular and joint pains, polyuria,
polydipsia and emotional instability

 Variety of osseous changes may be present these include
metastatic calcification, subperiosteal erosion, ostetis fibrosa
generalisata, disturbances in jaw bones, brown giant cell lesions
and rarely osteoscelrosis.
 Metastatic calcification: ectopic calcification in soft tissue is
most common cause of hyperparathyroidism. 45%-80% patient
reports nephrolithiasis and nephrocalcinosis.
Other soft tissues involved are subcutaneous tissues, walls of
blood vessel, articular cartilages and joint capsules.
 Subperiosteal erosion: especially of middle phalanges, is
considered hallmark of hyperparathyroid dysfunction. Loss of
lamina dura has been considered a type of subperiosteal
erosion, likening periodontal ligament to periosteum.

Osetitis fibrosa generalisata(cystica):
 The term osteitis fibrosa generalisata refers to pattern of
generalized rarefaction seen in skeletal as a late change in
primary, secondary, or tertiary hyperparathyroidism and
occasionally in pseudohyperparathyroidism.
 Early symptoms include vague aches and pains, which may be
uite disseminated later symptoms are severe bone pain and
tenderness followed by fractures and development of
deformities.
 On radiographs the bones may appear quite radiolucent with
thin cortices and hazy, indistinct trabeculae. Some bones may be
less homogenous, presenting a moth-eaten image. Regions in
which trabaculae are completely missing have a cystlike
appearance on radiographs.

Oral manifestation of hyperparathyroidism
 The primary clinical orofacial signs and symptoms of
hyperparathyroidism are reflections of systemic hypercalcemia.
 The lytic jaw lesions or jaw tumors can increase in size, causing
the bony cortex to expand, ultimately becoming destroyed.
 These tumors rarely expand into periosteum but can produce
gingival swelling.
 Due to bony changes teeth become mobile, drift and cause
malocclusion.
 With gradual loosening of the dentition periradicular
radiolucencies develop, with increased periodontal pocketing,
root resorption and dental pain.

Primary Hyperparathyroidism
 When excessive secretion arises from one or more parathyroid
gland it is referred as primary hyperparathyroidism.
 It is result of a primary hyperplasia or a benign or malignant
tumor of the parathyroid glands.
 Postmenopausal women are most commonly affected by
hyperparathyroidism.
 Pathologic hyperparathyroidism may affect one or more
members of the family, resulting in familial hyperparathyroidism.
This type may also be associated with MEN syndrome types1, 2A
& 2B or the hyperparathyroid jaw tumor syndrome(HPT-JT)
 In advanced cases the classic serum changes of increased levels
of calcium and alkaline phosphatase and decreased levels of
phosphorous are usually present.

Secondary Hyperparathyroidism
 Occurs when the parathyroid glands are stimulated to produce
increased amount of PTH to correct abnormally low serum
calcium levels.
 May also occur due to compensatory glandular enlargement in
response to unusual hypocalcemia induced by metabolic
disorders such as renal failure, deficiency of 1,25 dihydroxy
vitamin D or malabsorption of calcium found in rickets, and some
forms of osteomalacia.
 The low serum calcium levels stimulate increased production and
secretion of PTH, which then induce bone resorption with
liberation of calcium and phosphate ions.
 Contrary to the situation to primary hyperparathyroidism, in
secondary hyperparathyroidism there is an inverse relationship
between the levels of serum PTH and serum calcium.www.indiandentalacademy.com

Tertiary Hyperparathyroidism
 Parathyroid tumor develop due to long standing secondary
hyperparathyroidism this is known as tertiary
hyperparathyroidism.
 The increased PTH levels produced increased bone resorption
and a resultant hypercalcemia.

General radiographic features:
 Subtle erosion of bone from the subperiosteal surfaces of
phalanges of the hand.
 Demineralization of the skeleton results in an unusual
radiolucent appearnce.
 Osteitis fibrosa cystica resulting in apparent bone structure.
 Brown tumor are peripheral or central tumors of bone are
radiolucent.
 Pathologic calcifications of soft tissues is seen in kidneys and
joint.
 In prominent hyperparathyroidism, the entire calvarium has a
grannular appearance caused by the loss of central (diplopic)
trabaculae and thinning of cortical tables.

Radiographic features of the jaws
 Demineralization and thinning of cortical boundaries often
occur in the jaws in cortical boundaries such as inferior
border, mandibular canal and the cortical outlines of
maxillary sinuses.
 The density of the jaws is decreased.
 A change in the normal trabecular pattern may occur
resulting in a ground-glass appearance of numerous, small,
randomly oriented trabaculae.
 Brown tumors may appear in any bone but are more
common in facial bones and jaws, lesions may be multiple
within single bone.

Radiographic features of the teeth and associated structure
 Periapical radiographs reveal loss of lamina dura in patients
(only about 10%) with hyperparathyroidism.
 The loss of lamina dura may either be complete or partial
around a particular tooth.
 The result of loss of lamina dura may give the root a tapered
appearance because decreased image contrast.
 Fully developed teeth are not affected except that they appear
more radiopaque.

Fig 1. Photograph of the patient showing left palatal swelling
and temporary fillings in teeth #14 and #15.
Fig 2. A, Intraoral radiograph showing loss of lamina dura of
mandibular anterior teeth.

Radiographic features of hypoparathyroidism
 The principal radiographic change is calcification of basal
ganglia.
 On the skull radiographs this calcification appears flocculent
and paired within the cerebral hemispheres on the
posterioranterior view.
 Radiographic examination of the jaws may reveal enamel
hypoplasia, external root resorption, delayed eruption, or root
dilaceration.

Adrenal Gland
Adrenal cortex Adrenal medulla
Mineralcorticoid
Glucocorticoid
Sex steroid
Cortiosterone
11 Deoxycorticosterone
Cortisol
Aldosterone
Adrenaline
Non Adrenaline
Dopamine

Mineralcorticoids
 Secreted by Zona glomerulosa
 Aldosterone- life saving hormone
Glucocorticoids
 Secreted by Zona fascilulata
 Cortisol- life protecting hormone
Sex steroids
 Secreted by zona reticularis

Actions of Mineralcorticoids:
1) Effect on sodium reabsorbtion:
Acts on distal convulated tubule and collecting duct and increases
reabsortion of sodium .
2) Effect on extracellular fluid volume:
Hypernatremia may develop
Increased thurst
Increased intake of water
Increased ECF volume and blood pressurewww.indiandentalacademy.com

3) Effect on blood pressure:-
ECF volume blood volume
Blood pressure
Aldosterone escape or Escape phenomenon
This cause two reactions:-
a) Secretion of atrial natriuretic peptide(ANP)
b) Pressure diuresis

4) Effect on potassium ion:
Increases excretion of potassium ion through renal tubule.
decrease in aldosterone leads to hyperkalemia
Decrease
aldosterone
Hyperkalemia
Cardiac toxicity, weak
contraction of heart
Death
Development
of arrythmia
Increase
aldosterone
Hypokalemia Muscular weakness

5) Effect on hydrogen ion concentration:
Aldosterone cause sodium reabsorption from renal tubule
which causes excretion of hydrogen ion.
Aldosterone is essential for acid base balance.
6) Effect on sweat and salivary gland:
Sodium is reabsorbed from sweat glands and thus causes
conservation of sodium. It has similar effect on salivary gland.
7) Effect on intestine:
Aldsterone increases sodium reabsorption from intestine
especially colon.

Glucocorticoids
Actions:-
1) Effect on carbohydrate metabolism:
Increases the blood sugar level by two ways-
a) Promoting gluconeogenesis.
b) Inhibiting glucose uptake & utilization by peripheral cells
(anti-insulin action of glucocorticoid)
2) Effect on protein metabolism:
Glucocorticoids cause catabolism of proteins. They decrease
proteins in the cell and increase plasma amino acids and protein
content in the liver

4) Effect on mineral metabolism:
Glucocorticoids causes increase in retention of sodium & calcium.
And increases excretion of potassium.
Hypersecretion oedema, hypertension,
hypokalemia, muscular weakness
5) Effect on water metabolism:
It increases quantity of water intake and causes increases excretion
of water.
6) Effects on muscles:
It increases release of amino acid from muscle by catabolism of
proteins.
Hypersecretion muscular weakness & hypokalemiawww.indiandentalacademy.com

7) Effects on blood cells:
Decreases eosinophils, basophils & lymphocytes. And increases
neutrophils, RBC & platelets.
8) Effect on CNS:
Decrease in the hormone causes irritability and lack of
concentration.
9) Permissive action:
eg- calorigenic effect of glucagon
lypolytic
pressor effects of catecholamines
bronchodilator

10) Effects on resistance to stress:
Glucocorticoids provide increase in resistance to stress by:
i) release of amino acid
ii) release of fatty acid
iii) enhances vascular reactivity to catecholamines & fatty acid
iv) prevent severity of other changes in body due to stress.
11) Anti- inflammatory action:
i) prevent release of histamine and proteolytic enzyme
ii) decreases the permeability of capillaries
iii) inhibit migration of leukocytes into affected area

12) Anti-allergic action:
Prevents various allergic reactions.
13)Immunosuppressive effect:
Glucocorticoids suppress immune system by decreasing the
number of T lymphocytes and lymphoid tissue.
Regulation of secretion:
FEEDBACK CONTROL: regulates its own secretion through
negative feedback control by inhibiting release of CRF from
hypothalamus & ACTH from anterior puititary.
Cicardian Rhythm of ACTH:
ACTH and cortisol levels are high in the morning and low in the
evening.

Emotion , stress, trauma, and influence of cicardian rythm
Hypothalamus
Corticotropin Releasing harmone (CRF)
Anterior Pituitary
Adrenocorticotropic Hormone (ACTH)
Adrenal Cortex
cortisol
Inhibitionfeedback
Regulation of cortisol Secretionwww.indiandentalacademy.com

Disorders of adrenal cortex
Hyperactivity of adrenal cortex:
- Cushing syndrome
- Hyperaldosteronism
- Adrenogenital syndrome
Hypoactivity of adrenal cortex:
- Addison’s disease
- Addison’s crisis or Adrenal crisis
Congenital adrenal hyperplasia

Adrenal Medulla
 Medulla forms inner part of the gland and constitute 20% of
adrenal gland.
 Made up of interlacing cords of cells which contain fine granules
these are called as chromophil cells or chromaffin cells or
pheochrom cells.
 Hormones of adrenal medulla are amines derived from catechol
called catecholamines.
 Three catecholamines are secreted by adrenal medulla:
1. Adrenaline or Epinephrine
2. Noradrenaline or Norepinephrine
3. Dopamine www.indiandentalacademy.com

Actions :
1. Effect on Metabolism
Adrenaline influences metabolic function more than non-
adrenaline.
a) General Metabolism
Increases oxygen consumption, carbon dioxide removal and
basal metabolic rate. Hence called as Calorigenic hormone.
b) Carbohydrate Metabolism
- Increased blood sugar level
- Increased glycogenolysis in liver and muscle.
c) Fat Metabolism
- Adrenaline causes mobilization of free fatty acid from adipose
tissue.

2. Effect on Blood
- Reduces blood coagulation time
- Increases RBC and Hemoglobin content in blood by causing
contraction of spleen and release of RBC into Circulation.
3. Effect on Heart
- Adrenaline has stronger effect on heart than non-adrenaline.
- Increases overall activity of heart i.e. Heart rate (Chronotropic
effect), force of contraction (ionotropic effect) and excitability of
heart muscle (bathomotropic effect).

4.Effect on Blood vessel
- Non-Adrenaline has stronger effects on blood vessels.
- General Vasoconstrictors.
- Total peripheral resistance increases by non-adrenaline.
- Adrenaline also causes constriction of blood vessels it causes
dilation of blood vessel in skeletal muscle, Liver and heart through
beta-2 receptors.
- Hence total peripheral resistance is reduced by adrenaline.
5.Effect on Blood Pressure
-- Adrenaline
- Increases systolic and decreases diastolic blood pressure.
-- Non-Adrenaline
- Increases diastolic pressure & slightly increases systolic blood
pressure by action on heart.
Hypertension develops in excessive secretion of catecholamines.

6. Effect on Respiration
- Adrenaline increases rate and force of respiration.
7. Effect on Skin
- Increases secretion of sweat.
8. Effect on Skeletal Muscle
- Adrenaline causes severe contraction and quick fatigue of
skeletal muscle.
- Vasodilatation of skeletal muscle.

9. Effect on Smooth Muscle
- Cathecolamines causes contraction of smooth muscles in :
1. Splenic capsule
2. Arrector pili
3. Spincters of GIT
4. Uterus
5. Gall bladder
6. Dilator pupillae of iris.
- Cathecolamines causes relaxation of
1. Non spincteric part of GIT
2. Bronchioles
3. Urinary bladder.

10. Effect on CNS
- Increased activity of brain.
- Release of adrenaline during fight or flight reaction after
exposure to stress reaction .
11. Other Effects
-- On salivary glands
vasoconstriction in salivary gland causes mild increases in
salivary secretion.
-- Sweat Gland
-Increased secretion of apocrine sweat gland.
-- Lacrimal Gland
- Increased secretory activity of lacrimal gland.

-- Spleen
- causes contraction of smooth muscles of splenic capsule and
release of RBC.
-- ACTH
- Adrenaline increases ACTH
-- Nerve Fiber
- Adrenaline decreases latency of action potential in nerve fiber.
-- Renin Secretion
- Catecholamines increases secretion of renin from
juxtaglamerular apparatus of the kidney.

Pheochromocytoma
(primary adrenal medullary tumor).
 Clinical presentation:
- Episodic hypertension, headache, sweating, palpation and
flushing.
 It is of interest to dentist because reports have appeared in
literature describing patients with distinct symptom complex
charecterized by endocrine neoplasms (pheochromocytoma &
medullary carcinoma of thyroid gland) and multiple neuromas
involving lips, tongue layrnx and eyelids.
 This condition is referred to as multiple mucosal nervous system
or Sipple’s syndrome.www.indiandentalacademy.com

Oral manifestation of adrenal cortex
Hyperadrenocorticism (Glucocorticoid excess or
Cushing’s syndrome)
 Primary feature of Cushing’s syndrome is a round moon face due
to muscle wasting and accumulation of fat.
 Surface capillaries in face and other skin regions become fragile,
rendering them readily susceptible to haematomas after mild
trauma.
 Facial skin has ruddy color that stimulate glowing health, acne
and excessive facial hair are common.

 Long standing Cushing’s syndrome produces delayed growth and
development including skeletal and dental structures.
 Oral signs and symptoms of immunosuppression can be seen
including oral candidiasis, herpes labialis, herpes zoster
infections, gingival and periodontal diseases and impaired wound
healing.

Hypoadrenocorticism (Glucocorticoid deficency,
Addison’s disease)
 Primary orofacial feature is unusual skin pigmentation most
intensely on sun exposed areas.
 On face freckle and mole become more intense as well as tan-like
complexion.
 Mucocutaneous junction undergoes increased pigmentation
including lips, and can also occur on intraoral mucosal surfaces.
 Oral pigmentation appear as irregular spots from pale brown to
gray or black.

Dental management
 It is important to consider medical condition that include easy
bruising, impaired wound healing, osteoporosis, hypertension,
heart failure, DM, immunosuppression and depression and
psychosis.
 Assessment of the ability to withstand stress is essential
component.
 In adrenal insufficiency adrenal function is inadequate to produce
adequate cortisol in response to stress and patient may
experience severe hypotension, nausea, cardiovascular events,
stroke, trauma and death.

 Patients who are on chronic glucocorticoid therapy have decreases
in subcutaneous collagen and the production of other extracellular
proteins by fibroblast, so they may bleed and to bruise easily.
 There may also be related defects in the walls of small blood
vessels, resulting in defective constriction of these vessels during
bleeding.
 Wound healing is also impaired, and scar formation is less timely
and less vigorous than in a normal subjects.
 Patients who are on chronic glucocorticoid therapy are considered
to be immunocompromised and more than normally susceptible to
infection.
 Antibiotic prophylaxis is decided on the basis of the underlying
disease, however, and not on the basis of glucocorticoid therapy.

Hypoadrenocorticism
 Dental management is similar to that for patient who has taken
long-term moderate to high doses of glucorticoids since
Addison’s disease is frequently treated with exogenous
glucocorticoids.
 The oral health must be recognize and provide initial
management of an acute adrenal crisis (intramuscular or
intravenous hydrocortisone) when treating these patients.

Radiographic feature of Cushing’s syndrome
 The primary radiographic feature of Cushing’s syndrome is
generalized osteoporosis, which may have a granular bone
pattern.
 This demineralization may result in pathologic fracture.
 The skull can cause diffuse thinning accompanied by a mottled
appearance. The teeth may erupt prematurely, partial loss of
lamina dura may occur.

Dental and oral findings associated with endocrine disorder
Softtissueabnormalities:- Macroglossia
Abnormalpigmentationofskinandmucosa
Neckmasses(goiters,adenomas,carcinomas)
Salivaryglanddysfunction(xerostomia)
Ectopicglandulartissue(lingualthyroidgland)
Radiographicabnormalities:- lossoflaminadura
Delayedrootformation
Enlargementofparanasalsinuses
Abnormalcalcification
Osteolyticlesions(giantcelltumors)
Osteoporosis
Alteredtrabaculaepattern(groundglass
appearance)

Jaw and tooth abnormalities
Disproportionate jaw growth(prognathism,micrognathia)
Malocclusion
Tooth spacing and flaring
Retarded or accelerated eruption pattern
Defects in enamel and dentin formation

Conclusion
It is important for dentist to have
sufficient information with which to
suspect endocrinopathy, to describe
the clinical and radiographic oral
manifestation of various endocrine
disorder and to understand dental
management considerations in
patients with suspected or proven
endocrine dysfunction.

References
 Burket’s textbook of oral medicine, eleventh edition.
 Differential diagnosis of Oral and Maxillofacial lesions, Wood &
Goaz, fifth edition
 White & Pharon, Textbook of Oral Radiology, fifth edition
 Essentials of medical physiology, Sembulingam
 Oral manifestations established the diagnosis of
hyperparathyroidism: a rare case report- journal of indian
academy of oral madicine and radiology 2011
 Dental management of patients with endocrine disorders-J Clin
Exp Dent. 2010

Oral Manifestations of Endocrinal Disorders / dental crown & bridge courses

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