Endocrinology for Dentistry

• Hormones are molecules secreted from endocrine glands into the blood with regulatory actions at distant sites. They act via cell surface receptors (eg insulin) or intracellularly (eg thyroxine, or steroid hormones). They are regulated by a feedback loop eg with pituitary gland.
• • Pituitary gland helps to control lots of other endocrine glands
  • Thyroid gland
  • In front of trachea and just below larynx - goes up and down when you swallow (can be seen when swollen - goitre)
  • 4 parathyroid glands within thyroid gland - control calcium
  • Adrenal gland
  • Has the adrenal cortex, which makes cortisol/hydrocortisone
  • Has the adrenal medulla, which makes adrenaline/epinephrine

  
• Pancreas

  • Main part is an exocrine gland - secretes digestive hormones into the duodenum (not into the bloodstream, therefore not endocrine)
  • Islets of Langerhans in pancreatic tissue - have beta cells, which make insulin, and alpha cells, which make glucagon

  Gonads - sex glands

  • Ovaries in women, testes in men

  
• Table shows how the pituitary hormones control the levels of the hormones of other glands elsewhere in the body - pituitary gland and hypothalamus (bottom part of the brain) together - hypothalamus releases a hormone which travels to the pituitary gland and triggers it to release the complementary one. Corticotrophin releasing hormone system is determined by negative feedback loop (the more cortisol in blood, the less CRH is released from hypothalamus).

  
• Not all endocrine glands are governed by the pituitary gland...

  
• Mechanisms of endocrine disease:

  • Autoimmune destruction of gland - lack the hormone that gland releases - e.g. Type 1 diabetes; destruction of beta cells of Islets of Langerhans leading to a lack of insulin
  • Autoimmune stimulation of gland - e.g. Graves diseases where a molecule mimics TSH to stimulate the thyroid gland
  • Other destruction of gland - surgery, cancer, tuberculosis
  • Tumour formation: effects of tumour = hypersecretion or mechanical pressure effects, which may lead to hyposecretion 
• Cushing's syndrome is hypercortisolism (too much cortisol/hydrocortisone released from the adrenal cortex) - causes:

  • Exogenous steroids - prescribed medications to suppress inflammation/immune system in pts with inflammatory conditions (eg arthritis, asthma or transplants) - most common cause nowadays
  • ACTH-secreting pituitary tumour - pituitary gland makes ACTH regardless of negative feedback loop, so too much cortisol is released from adrenal cortex
  • Cortisol-secreting adrenal adenoma (benign tumour) or carcinoma (malignant tumour) - makes too much cortisol directly at adrenal cortex
• Clinical features of Cushing's syndrome:

  • Moon face (because cortisol causes an increase in adipose tissue in certain parts of the body - gives you a round, swollen face due to fatty deposition under the skin - increased fatty deposition above the clavicles and in between the shoulder blades around the bottom of the neck "buffalo hump")
  • Buffalo hump
  • Abdominal obesity
  • Proximal muscle weakness (particularly the ones in the thighs and biceps and triceps) - round abdomen and thin limbs "lemon on sticks" appearance
• Clinical features of Cushing's syndrome:

  • Abdominal striae (stretch marks due to swelling of the abdomen)
  • Thin skin
  • Bruising
  • Osteoporosis - thinning and fragility of bones
  • Hirsutism (androgenic) - facial hair in women
  • Hypertension - mimics aldosterone therefore causes you to retain sodium - raises blood pressure
  • Oedema
  • Raised glucose

  
• Cushing's syndrome - investigation and treatment:

  • Raised urine or serum cortisol
  • Fails to suppress cortisol with dexamethasone
  • ACTH level - if ACTH level is high then cause is pituitary-driven (commonest), but if it's low then it's adrenal-driven; pituitary will be switched off
  • Imaging of pituitary/adrenals
  • Treatment usually surgical - adrenalectomy (to remove adrenal gland) or hypophysectomy (to remove adrenal tumour or pituitary gland) - may result in deficiency syndrome if whole gland has to be removed instead of just part of it
• Hypo-adrenalism:

  • Addison's disease = autoimmune destruction of adrenal cortex
  • Other causes:
  • Suppression of HPA (hypothalamic pituitary adrenal) axis following long-term steroid therapy - have to slowly take patients off long-term steroid therapy so that their HPA axis has time to "wake up" again
  • Adrenal metastases, TB, surgical removal
  • Pituitary failure (ACTH lack)
• Features of hypo-adrenalism:

  • Tiredness
  • Weight loss
  • Pigmentation (skin, palmar creases, buccal)
  • Hypotension
  • Hypoglycaemia
  • Addisonian crisis
• Features of Addisonian crisis:

  • Vomiting
  • Dehydration
  • Hypotension
  • Hypoglycaemia
  • Electrolyte disturbances
• Investigation of hypo-adrenalism:

  • Low cortisol levels
  • High ACTH - seen if it's primary adrenal failure - low ACTH if it's due to pituitary failure
  • Adrenal antibodies
• Treatment of hypo-adrenalism:

  • Hydrocortisone (= cortisol, the main glucocorticoid) - essentially replace the hormone
  • Fludrocortisone (synthetic mineralocorticoid) - equivalent to aldosterone, which is also missing
  • Increase hydrocortisone to cover illness; cortisol (hydrocortisone) is a stress hormone that goes up with illness or stress
  • Intravenous fluids/electrolytes/glucose and hydrocortisone for Addisonian Crisis
• Vitiligo goes alongside Addison's disease:

  • Autoimmune endocrinopathies, where you get an antibody against a particular endocrine gland, tend to group together and when you've got one you're at higher risk of getting another one - associated with those are one of two autoimmune conditions that are not strictly endocrine glands - one is an antibody against the melanocytes in the skin, leading to patchy depigmentation
  • So people with Addison's disease can get hyperpigmentation alongside vitiligo

  Subtle buccal mucosa pigmentation around the occlusal margin of the teeth

  
• Hyperthyroidism:

  • Excess thyroxine (T4) and tri-iodothyronine (T3)
  • T3 has less iodine attached compared to T4 (only has 3, whereas T4 has 4) but is the more active form
  • Thyroxine is converted to tri-iodothyronine in the tissues, but some tri-iodothyronine is secreted directly by the thyroid gland
• Causes of hyperthyroidism:

  • Graves disease (autoimmune stimulation - antibody that mimics the TSH receptor and switches the gland on through that receptor)
  • Multinodular goitre - lumpy swelling of the thyroid gland
  • Thyroid adenoma
  • (VERY rarely due to TSH excess)
• Features of hyperthyroidism - sped up metabolism:

  • Feels hot
  • Sweaty palms
  • Weight loss
  • Increased appetite
  • Poor sleep
  • Loose bowels
  • Tremor
  • Tachycardia/atrial fibrillation
  • Goitre
  • Graves eyes (exophthalmos, lip retraction/lag, eye movement restriction)
• Diagnosis and treatment of hyperthyroidism:

  • Raised T4 and T3
  • Suppressed TSH
  • Thyroid-stimulating antibodies
  • Thyroid scan
  • Radio-iodine - localised radiotherapy in thyroid gland to burn out the abnormal cells and suppress the thyroid gland because iodine is taken up by thyroid gland - one of the most commonly used treatments for an overactive thyroid gland
  • Surgical thyroidectomy (removing adenoma or some of thyroid gland - hopefully leaving enough for it to still be able to do its job)
  • Anti-thyroid drugs
  • Beta-blockers for symptom control - reduce heart tremor and sweating
• Features of hyperthyroidism:

  • Bulging eyes (exophthalmos)
  • Eyes looking in different directions
  • Eyelid slightly retracted - adrenaline stimulates the muscle that lifts the eyelids
  • Smooth goitre
  • Rarer features of Graves disease:
  • Curvature of the nails - resembles finger clubbing
  • Swollen feet and legs

  
• Hypothyroidism:

  • Lack of T4 (thyroxine) and T3 (tri-iodothyronine), high TSH
  • If not high TSH then there would be a problem with the pituitary gland
  • Causes:
  • Autoimmune destruction of thyroid
  • Surgical removal of thyroid
  • Radio-iodine treatment
  • Secondary to TSH lack in pituitary disease
• Features of hypothyroidism - slowing down:

  • Feels cold
  • Dry skin, thin hair
  • Slow, tired, confused
  • Slow pulse
  • Weight gain
  • Poor appetite
  • Sluggish bowels
  • Myxoedema - infiltration of interstitial tissues with proteinaceous fluid
  • Coarse facial features
  • Bags under eyes
  • Croaky voice
• Diagnosis and treatment of hypothyroidism:

  • Low T4 (thyroxine) and T3 (tri-iodothyronine), high TSH
  • Thyroid autoantibodies
  • Treatment is with thyroxine tablets
  • Example below of before and after pictures for pts on thyroxine tablets - thinning of the hair, puffy face, bags under eyes

  
• Acromegaly:

  • Growth hormone excess
  • Cause is pituitar tumour secreting growth hormone
  • Diagnosis/investigation:
  • High growth hormone level, that does not suppress with glucose (because glucose would normally suppress growth hormone levels)
  • Raised IGF-1
  • Pituitary MRI
  • Visual field testing (important for all pituitary tumours - eg non-secreting, prolactinomas)
  • Where possible, treatment is to remove the pituitary tumour
• Features of acromegaly:

  • Enlarged hands, feet, jaw (malocclusion), skull (change in hat, shoes, dentures, rings)
  • Coarse facial features - nose, brow, tongue
  • Thick skin
  • Arthritis - includes TMJ
  • Hypertension
  • Hyperglycaemia (insulin resistance)
  • Headache due to pituitary tumour
  • Bitemporal hemianopia due to compression of optic chiasm by the tumour

  
• Hyperparathyroidism causes hypercalcaemia. It is caused by parathyroid adenoma, sometimes hyperfunction of all 4 glands, but rarely carcinoma. Other causes of hypercalcaemia = vitamin D excess and cancers.
• Features of hypercalcaemia:

  • Often asymptomatic or non-specific
  • 'Stones, bones, abdominal groans and psychic moans'
  • Dry eyes and mouth
  • Thirst and polyuria, due to inability to concentrate urine

  Radiographic findings in hyperparathyroidism (which causes hypercalcaemia) below:

  
• Diagnosis and treatment of hyperparathyroidism:

  • High plasma calcium with raised PTH
  • Remember PTH will be low in other causes of hypercalcaemia
  • Imaging of parathyroids
  • Treatment usually surgical removal
• Hypoparathyroidism causes hypocalcaemia. It is caused by autoimmune destruction, or damage to parathyroids during thyroid surgery.
• Features of hypocalcaemia:

  • Tingling, paraesthesia
  • Cramps and tetany
• Diagnosis and treatment of hypoparathyroidism:

  • Low plasma calcium
  • Low PTH (should be high in other causes of hypocalcaemia eg vitamin D deficiency)
  • Treatment is with vitamin D analogues - PTH for replacement not available
• Dental relevance of endocrine disease:

  • Management of steroid replacement or therapy during illness/treatment
  • Acromegaly can present with TMJ arthritis, malocclusion or altered denture fit
  • Addison's disease - buccal pigmentation
  • Parathyroid bone disease can affect jaws - cysts and brown tumours
  • Ability to recognise other facial features