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!