• Osteomalacia is the general term for the

softening of the bones due to defective bone

mineralization.
Rickets & Osteomalacia
• Osteomalacia in children is
known as rickets, and because of
this, it is often restricted to the
milder, adult form of the disease.
• It may show signs as diffuse body
pains, muscle weakness, and
fragility of the bones.
 General characteristics
• Osteomalacia is derived from Greek:
– osteo bone
– malacia softness
• most commonly found in:
– dark-skinned
– diet-disbalanced subjects (mainly lactating females).

• Age: adults
• Site: WEIGHT-BEARING BONES such as vertebral
bodies and femoral neck
 Physiology
Normal bone metabolism: CA

• CALCIUM  99% in bone.

• Main functions muscle /nerve function, clotting.
• Plasma calcium 50% free, 50% bound to albumin.
• Dietary needs:
– Kids: 600mg/day
– Adolescent 1300mg/day,
– Adult: 750mg/day
– Pregnancy: 1500mg/day,
– Breastfeeding: 2g/day,
– Fractures: 1500mg/day
• Absorbed in duodenum (active transport) and jejunum
(diffusion), 98% reabsorbed in kidney prox. tubule, may be
excreted in stool.
Normal bone metabolism: PHOSPHATE

• PHOSPHATE  85% in bone.

• Functions: metabolite and buffer in enzyme systems.
• Plasma phosphate mainly unbound.
Daily requirement: 1-1.5g/day
Regulation of Calcium & Phosphate Metabolism:
Peak bone mass at 16-25 years.
Bone loss 0.3- 0.5% per year (2-3% per year after 6th decade).
1. Parathyroid Hormone (PTH)
2. Vitamin D3
3. Calcitonin
4. Other Hormones:
Estrogen: Prevents bone loss
Corticosteroids: Increases bone loss
Thyroid hormones: Leads to osteoporosis
Growth hormones: Cause positive calcium balance
Growth factors
 Mineralization of osteoid is reduced while bone mass remains
normal.

Responsible metabolic disturbances are vitamin D deficiency,

phosphate deficiency, and mineralization defects.

Adults with osteomalacia experience only mild bowing of long

bones; however, stress resistance of bones is reduced, and gross or
microscopic fractures
• Serum Ca & Phosphate in equilibrium with Ca & Phosphate
in bone.

Constant
Ca Phosphate
Product
 Kidney disease 

Defect in phosphate No hydroxylation 

execration of Vit.D3 
 Hypocalcaemia So, 
Stimulation of PTH 

Bone..  Kidney 
Relase of Ca. Ca absorption 
 Etiology
• Calcium deficiency
– Hypo-phosphataemia
– Defect in Vitamin D metabolism
• Nutritional
– Diet: oily fish, eggs, breakfast cereals
– Antacid abuse, causing reduced dietary phosphate
binding

• underexposure to sunlight
– Elderly individuals with minimal sun exposure
– Dark skin, skin covering when outside
• Calcium deficiency
– Hypo-phosphataemia
– Defect in Vitamin D metabolism
• intestinal mal-absorption
– Coeliac
– Intestinal bypass
– Post-Gastrectomy
– Chronic pancreatitis
– Biliary disease (reduced absorption of Vitamins)
– Small bowel disease
• Calcium deficiency
– Hypo-phosphataemia
– Defect in Vitamin D metabolism
• liver & kidney diseases
– Fat mal-absorption syndromes
– Kidney failure: RTA, Renal osteodystrophy

• Epilepsy: phenytoin, phenobarbitorate

• Genetic disease
• Other Etiologies:
– Receptor Defects
– Altered phosphate homeostasis
Sufficient
osteoid

Poor
mineralization
 Symptoms & Signs
• Bone pain , backache
• Muscle weakness
• Vertebral collapse: kyphosis
• loss of height
• Deformities & stress fractures
• Osteomalacia in adults starts insidiously as aches and pains in
the lumbar region and thighs, spreading later to the arms and
ribs.
• Pain is non-radiating, symmetrical, and accompanied by
tenderness in the involved bones.
• Proximal muscles are weak, and there is difficulty in climbing
up stairs and getting up from a squatting position
• Physical signs include deformities like lordosis.
• Pathologic fractures due to weight bearing may develop.
• Most of the time, the only alleged symptom is chronic and
bony ache which is only revealed by pressure or shocks.
• Rickets
– Tetanus , convulsions, failure to thrive
– restlessness, muscular flaccidity
– Flattening of skull (craniotabes)
– Thickening of wrists from epiphyseal overgrowth, Stunted growth,
Rickety rosary, spinal curvature, Coxa vara, bowing,
– Fx of long bones
• Osteomalacia
– Aches and pains
– muscle weakness loss of height
– stress fx
 biochemistry

1.Hypo-calcaemia
2.Hypo-calcuria
3.High alkaline phosphatase
Work up for Osteomalacia
 Ca , P , Alk ph
 24 h urinary Ca
 25 (OH) Vit-D
 1 , 25 (OH) Vit-D
 PTH
 Bone Biopsy
1- ca P = Nl Alk ph
2- ca = Nl P Alk ph
3- ca P Alk ph

24 h Urinary ca < 100 mg / 24 h

24 h Urinary Hydroxyproline Excretion
 X-ray
*Rickets
- Growth plate widening & thickening
- Metaphyseal cupping
- Diaphyseal deformities
*Osteomalacia
- Looser zone , biconcave vertebra , protrusio acetabuli
- Spontaneous fractures
*Signs of secondary hyperparathyroidism
Loosers zones
– incomplete stress Fx with
healing lacking calcium, on
compression side of long
bones.
Codfish vertebrae due to
pressure of discs
Trefoil pelvis, due to
indentation of acetabulae
stress fx
Loosers zones
 Treatment
Depends on the cause
Nutritional
Vitamin D deficiency
Dietary chelators of calcium
Phytates
Oxalates
Phosphorus deficiency (unusual)
Antacid abuse
Depends on the cause
Gastro-intestinal absorption defects
Post-gastrectomy
Biliary disease
Enteric absorption defects
Short bowel syndrome
Rapid onset (gluten-sensitive enteropathy)
Inflammatory bowel disease
Crohns
Celiac
Depends on the cause
Renal tubular defects
Vitamin D dependant
type I
type II
Treatment; High levels of vit D

Vitamin D resistant (familial hypophosphatemic rickets)

Treatment; Phosphate 1-3 gm daily, Vit D3 high dose
Fanconi syndrome I, II, III
Renal tubular acidosis
Depends on the cause
Renal Osteodystrophy – in chronic renal failure
Miscellaneous
Hypophosphatasia
Anticonvulsant therapy

SURGERY
For deformities
 Osteomalacia Treatment

Calcium Correct
Vitamin D Fracture
supplements deformity if
(5000u) management
(3g/day) needed
• Natural sources cheese, sardines, salmon, dark leafy
vegetables & sesame seeds.