METABOLIC BONE

DISORDERS
By:
Dr.Shaheen Ahmed
Dept of Oral Surgery
 Metabolic bone disease effects the skeleton in two ways:

-there is either too much

-or more commonly there is too little calcified bone.
OSTEOPOROSIS
 Osteoporosis is a progressive bone disease characterized by a
decrease in bone mass and density which can lead to an
increased risk of fracture.

 Bone mineral density (BMD) is reduced and bone

microarchitecture deteriorates.

 Most common metabolic bone disease.

Types:
Primary Type 1
 Most common in women after menopause.

Primary Type 2/Secondary/Senile osteoporosis 

 After age 75.

 Seen in both females and males at a ratio of 2:1.

 Results from chronic predisposing medical problems, or

prolonged use of medications such as glucocorticoids.

Causes:
Primary:
 Age.
 Estrogen deficiency.
 Family history.

 
Secondary:
 Drugs: steroids!
 Systemic disease.
 Malabsorption.
 Poor diet.
 Smoking.
 Excess alcohol.
 Sedentary lifestyle.

 
Clinical Features:
 Osteoporosis is itself asymptomatic, but it
increases the likelihood of pathological fractures.

 It may be associated with enhanced atrophy of the mandible and

tooth loss.

 Bone pain and tenderness.

 Cramps in legs at night.

 Fatigue.
Treatment:
General
 Treat any underlying conditions.

 Lifestyle factors- stop smoking, reduce alcohol, lose weight

and exercise.

Pharmacological
 Bisphosphonates. They reduce bone resorption and increase

bone formation.
HYPER-PARATHYROIDISM
 Over production of parathyroid hormone due to hyperplasia or
adenoma of parathyroid glands.

 Effects of PTH include stimulation of intestinal absorption of

Ca, reabsorption of Ca from renal tubules and bone resorption
by osteoclasts.
Clinical features:
 Fragile bones that easily fracture (osteoporosis).

 It may present as a giant cell lesion of the jaw.

 Kidney stones.

 Hypercalcemia and hypercalciuria.

 Polyuria and polydipsia.

 Weakness and fatigue.

 Bone, joint and abdominal pain.

 Muscle soreness (myalgias).

Histopathology:
 Focal areas of bone resorption results in formation of lesions
called brown tumour which consist of large number of
multinucleate, osteoclast like giant cells.

 There is much haemosiderin pigment present, hence the name.

Treatment:
 Surgery is the most common treatment for primary
hyperparathyroidism.

 Treatement of underlying cause in secondary hyperparathyroidism.

 Bisphosphonates prevent the loss of calcium from bones and may

lessen osteoporosis caused by hyperparathyroidism. 

 Calcimimetics: Drug that mimics calcium circulating in the blood.

The drug may trick the parathyroid glands into releasing less
parathyroid hormone. This drug is sold as cinacalcet (Sensipar).
RICKETS AND OSTEOMALACIA
 These are disorders caused by insufficient levels of vitamin D
in the body.

 This can be due to deficiency of or resistance to the action of

vitamin D.

 Rickets is the name used when it occurs in children whereas

Osteomalacia is the term used for adults.
Causes:
 Insufficient exposure to sunlight and nutritional deficiency.

 Gastrointestinal malabsorption.

 Liver disease

 Renal disease causing defective 1,25-dihydroxyvitamin D

synthesis.

 Drug causes include anticonvulsants.

 Severe dietary calcium deficiency can cause rickets despite

adequate vitamin D.
Clinical Features:
Others include:

 Increased incidence of dental caries.

 Impaired growth; short stature.

 Bone pain.

 Delayed walking or a waddling gait.

 Fractures may occur without recognised trauma.

Clinical Features:
 Muscular weakness and paraesthesia.

 Spinal curvature and signs of hypocalcaemia (eg tetany,

carpopedal spasm).

 Multiple fractures which are often bilateral and symmetrical. 

 Skeletal deformity can occur in the vertebral bodies and skull.

 There may be forward projection of the breastbone (pigeon chest)

and deformities of the spine, including scoliosis or kyphosis.
Treatment:
General management

 Education: dietary advice

 Encourage exposure to sunlight.

 Vitamin D supplementation.

 Treatment of any underlying condition.

 Treatment of pain.

 Orthopaedic intervention may be required.

Specific Management

 Children:
◦ Oral calciferol in the form of either Ergocalciferol
or colecalciferol is the treatment of choice for children with
rickets.
◦ Children <6 months should be treated with 3000 IU of
calciferol daily, increasing to 6000 IU daily after 6 months of
age.
◦ Aged 12-18 years should be given 10,000 IU.

 Adults:
Calciferol treatment, in a daily dose of 10,000 IU or a weekly
dose of 60,000 IU
ACROMEGALY
 Disease caused by prolonged and excessive secretion of
growth hormone.

 It is due to a secreting adenoma of the anterior lobe of the

pituitary after epiphyses have closed.

 There is renewed growth of the bones of the jaws, hands, and

feet with overgrowth of some soft tissues.
Treatment:
Somatostatin analogues
 The primary current medical treatment of acromegaly is to use

somatostatin analogues – octreotide (Sandostatin) or

lanreotide (Somatuline).

 These somatostatin analogues are synthetic forms of a brain

hormone, somatostatin, which stops GH production.

Growth hormone receptor antagonists

 The latest development in the medical treatment of acromegaly is

the use of growth hormone receptor antagonists. 

 Administered subcutaneously by daily injections.

THANKYOU!