2. INTRODUCTION
• HORMONES: Hormones are secretory products of
ductless(endocrine) glands released directly into the circulation in
small amounts in response to a specific stimulus and on delivery in
circulation produces response on the target cells or organs.
• Exocrine glands
• Which release their cellular secretions through a duct, which empties
to the outside or into the lumen of an organ.
• These include sweat glands, salivary and pancreatic glands, and
mammary glands.
6. Growth hormone:
• ROLE:
• Its excess causes gigantism, acromegaly.
• Its deficiency causes dwarfism.
• ACROMEGALY: If the increase occurs later in life, i.e.
after epiphyseal closure,
7. Clinical features:
• Thick lips, thick nose
• Arthropathy with joint swelling
• Myopathy
• Large spade like hands, thick wide fingers, large feet
• Prominent ridge and furrows
• Voice deepening
• Clubbing
8.
9. Oral manifestations
• Thickened oral mucosa
• Macroglossia
• Hypertrophy of soft palate
• Indentations on tongue
• Teeth in mandible tipped to buccal or labial side
• Mandible prognathic
10. Radiographic feature
• Prominence of supraorbital ridge
• Thickening of vault of skull
• Zygomatic arch thickenend
• Enlargement of paranasal sinus
• Unaffected lamina dura
• Hypercementosis
• Supraeruption of posterior teeth
11.
12. Investigation
• Normal GH level- 0.5-10 ng/ml
• Prolactin level are increased
• MRI
• DENTAL CONSIDERATION
• Orthognathic surgery
• Octreotide acetate supress levels in 70% of patients
13. • GIGANTISM – before epiphyseal closure of
long bones
CLINICAL FEATURES:
• Thick and furrowed oily skin
• Generalised excessive skeletal growth
• Increase in size of calvarium
• Mandible prominent and protruding
• Height affected
• Puberty delayed
14.
15. Oral manifestations
• Tooth size does not change
• Midline diastema
• Crown size normal
• Roots of posterior teeth enlarged due to secondary
hyperplasia
16. HYPOPITUITARISM
• Caused by compression or atrophy of anterior
pituitary cells by adenoma
• Growth hormone deficiency , before puberty-
Dwarfism
• After puberty or in adult – Simmond’s Disease
18. ORAL MANIFESTATIONS
• Mandible retarded- retrusion of chin
• Lack of condylar growth- short ramus
• Dental arch small
• Crowding, malocclusion
• Eruption and shedding of deciduous teeth – delayed
• Short root, apices wide opened with pulp canal
diverging toward apex
19. RADIOGRAPHIC FEATURES
• Deciduous teeth – delayed shedding
• Permanent tooth eruption delay
• Malocclusion
• 3 Molar tooth not formed
20.
21. SIMMOND’S DISEASE
• Decreased secretion of hormones
• LACK OF GONADOTROPIN (LH AND FSH)-
• Delayed puberty
• Small and soft testes
• Lack of beard
• Pubic hair
• amenorrhea
22. • LACK OF GROWTH HORMONE-
• Bone growth retardation
• Short stature
• LACK OF PROLACTIN-
• Absence or decrease in breast milk production
• LACK OF TSH-
• Fatigue, cold, dry skin
• LACK OF ACTH-
• Weakness, nausea, low blood pressure, low blood
sugar, pale skin
23. RADIOGRAPHIC FEATURES
• Skull and facial bone- small as same as in normal
children of 5-7 yrs of age
• Delay in maturation of skeleton remain un united
throughout the life
• Loss of alveolar bone due to marked resorption
24. INVESTIGATION
• Evoked GH is less than 0.3ng/ml
• MANAGEMENT
• replacement therapy – 0.15-0.3 mg/day, max 1.25
mg/day
25. HYPERPROLACTINEMIA
• Clinical features:
• In women – hypogonadism, oligomenorrhea,
amenorrhea, infertility, osteoporosis.
• In men – impotence, loss of muscle mass ,
osteoporosis, galactorrhea.
• TREATMENT:
• Medical- dopamine agonists.
26. DISORDERS OF ADH
• disorders of water
• Too little ADH is a syndrome of the inability to hold on
to free water by the kidneys.
• CLINICAL FEATURE- polyuria (> 3 L/d), and
resultant hypernatremia(high conc of sodium)
• Diagnosis of DI is made by a water deprivation test,
which should be done under appropriate medical
supervision.
27. • Excessive ADH - too much total body water and
manifests as hyponatremia.
• CAUSE- central nervous system disturbances such as
stroke, infection, trauma and hemorrhage.
• CLINICAL MANIFESTATION- is a change of mental
status that can lead to seizures and death is undetected.
• DENTAL CONCERN excessive polydypsia and polyuria
can lead to excessive consumption of optimally
fluoridated water to the point that affected individuals
can develop dental fluorosis and enamel defects.
29. TYPES
• GOITRE- diffuse hyperplasia of thyroid
• TOXIC ADENOMA – hyperfunction originates in
benign tumor of thyroid gland
30. CLINICAL FEATURES
• Symmetrical, diffuse nodular or smooth enlargement of thyroid
• Tender
• Heat intolerance
• Muscle weakness
• Losing weight
• Thin hair
• Fine tremor
• Widened pulse pressure ( increased systolic, decreased diastolic)
• Warm and smooth skin
31. • Ocular involvement – most striking feature
• Protusion of eyes
• Partial paralysis of ocular muscles
• Clubbing and lymphadenopathy
• Abdomen, liver and spleen may enlarge
• Excess sweating
• Difficulty in swallowing
32. ORAL MANIFESTATIONS
• Increased susceptibility to caries and periodontal
problems
• Premature exfoliation of deciduous tooth
• Rapid eruption of permanent teeth
• Osteoporosis of maxilla and mandible
• Burning tongue
33. INVESTIGATION
• Serum TSH (0.3-5.5 microg/l) suppressed by
hyperthyroidism
• Raised T4 ( 4.6- 12 microg/l) and T3 (0.7-2.04
microg/l)
34. DENTAL MANAGEMENT
• EPINEPHRINE is contraindicated and elective
dental care should be deferred
• Susceptible to cardiovascular disease
• PROPYLTHIOURACIL- cause leukopenia, sialolith ,
increase anticoagulant effect of warfarin
• ASPIRIN AND NSAIDS cause increase level of
circulating T4 – thyrotoxicosis
35. HYPOTHYROIDISM
• Decreased level of thyroid hormone
• Occur during infancy- CRETINISM
• In childhood – JUVENILE MYXEDEMA
• In adult- MYXEDEMA
36. TYPES
• PRIMARY HYPOTHYROIDISM- thyroid gland
itself is in some abnormal way
• SECONDARY HYPOTHYROIDISM- pituitary
gland does not produce an adequate amount of
thyroid stimulating hormone
37. CLINICAL FEATURES
• Hoarseness in voice
• Skin- cold and dry
• Gaining weight without eating more
• Lips- puffy, thickened and protruding
• Slowed reflexes
• Periorbital edema
• Base of skull – short
• Wide face
45. ORAL MANIFESTATIONS
• Brown tumor expand into periostium-gingival swelling
• Drifting of teeth ,
• malocclusion,
• gradual loosening of dentition ,
• periodontal pockets
• root resorption &
• dental pain
46.
47. RADIOGRAPHIC FINDINGS
• Osteoporosis
• thinning of cortical bone of maxilla & mandible,
Well-circumscribed unilocular or multilocular radiolucent lesions
known as "brown tumor" of hyperparathyroidism
contain abundant hemorrhagic tissue and hemosiderin, which
give it a characteristically dark reddish-brown color.
Degeneration of brown tumor leads to patchy osteoclastic bone
resorption, cystic lesions, and replacement of bone with abundant
vascular cellular fibrous tissue.
This transformation is referred to as "osteitis fibrosa cystica
51. HYPOPARATHYROIDISM
• deficiency in the production, secretion, or action of PTH and
the most common cause of hypocalcemia.
• CAUSE- when parathyroid glands are surgically removed to
correct primary hyperparathyroidism or during
thyroidectomy.
• Cell-mediated autoimmune glandular destruction associated
with mutations of the autoimmune regulator (AIRE) gene.
• Radiation to the neck, infection, and magnesium deficiency
52. CLINICAL MANIFESTATIONS
• paresthesia of hands, feet, and circumoral muscles;
• anxiety; confusion; and depression.
• A positive Chvostek's sign may be elicited if
tapping on the facial nerve in the preauricular
region causes twitching of the facial muscles.
• Tetany – involuntary contraction of muscles
56. Signs and symptoms
• Headache
• Palpitations
• face flushing
• Tremor
• Anxiety
• Weight loss
• Moon face
• Increased susceptibility to infection
57. • Fat deposition on face and back of shoulder
• Thin extremities
• Purple straie
• Bruises and petechiae
• Excess body and facial hair growth in women
• Mood swings
59. ADDISON’S DISEASE
• Adrenal insuffieciency, uncommon disorder that
occurs when body doesn’t produce enough of certain
hormones. (too little cortisol , too little aldosterone)