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Osteomalacia and rickets
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Osteomalacia and rickets

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By: A.Taskin ( 4th year medical student at Sulaiman Al-rajhee colleges )

By: A.Taskin ( 4th year medical student at Sulaiman Al-rajhee colleges )

Published in Health & Medicine
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  • alkaline phosphatase, an enzyme produced by osteoblasts (bone-producing cells), is at a raised level in osteomalaciaparathyroid hormone, produced by the parathyroid gland, is raised as part of your body’s reaction to the condition.
  • narrow radiolucent lines – thought to be healed stress fractures or the result of erosion by arterial pulsation

Transcript

  • 1. OSTEOMALACIA & RICKETS Abdullah Taskeen
  • 2. DIFINATION : Rickets : osteopenia with disordered calcification leading to higher proportion of osteoid (unmineralized) tissue prior to epiphyseal closure (in childhood) osteomalacia : osteopenia with disordered calcification leading to higher proportion of osteoid (unmineralized) tissue after epiphyseal closure (in adulthood)
  • 3. BASIC: Bone consists of : A- a hard outer shell (cortex) made up of minerals, mainly calcium and phosphorus, B- a softer inner mesh (matrix) made up of collagen fibres.
  • 4. WHEN NORMAL BONE IS FORMED : A - these fibres are coated by mineral (this process is called mineralisation). B - The strength of the new bone depends on enough mineral covering the collagen matrix. The more mineral laid down, the stronger the bone.
  • 5. OSTEOMALACIA HAPPENS : A. if mineralisation doesn’t take place properly. B. bone is made up of collagen matrix without a mineral covering, C. so the bones become soft. D. These softened bones may bend and crack, and this can be very painful.
  • 6. AGAIN !! DIFINATION : Rickets : osteopenia with disordered calcification leading to higher proportion of osteoid (unmineralized) tissue prior to epiphyseal closure (in childhood) osteomalacia : osteopenia with disordered calcification leading to higher proportion of osteoid (unmineralized) tissue after epiphyseal closure (in adulthood)
  • 7. ETIOLOGY AND PATHOPHYSIOLOGY A. Vitamin D Deficiency B. Mineralization Defect C. Phosphate Deficiency
  • 8. CLINICAL PRESENTATION :
  • 9. INVESTIGATION :
  • 10. OTHERS : Serum 25OHD = low ( exept in V. D resistance rickets ) Serum fibroblast FGF-23 =  elevated in tumor associated osteomalcia
  • 11. RADIOLOGIC FINDINGS - pseudofractures, ‘Looser’s zones’ - Linear areas of low density surrounded scleroticborders. by - loss of radiologic distinctness of vertebral bod trabecula, - concavity of the vertebral bodies
  • 12. Looser Zones
  • 13. Looser Zones
  • 14. diffuse osteopenia and several insufficiency stress fractures of the bilateral ribs (arrows) and scapulae Stress fracture
  • 15. several insufficiency stress fractures in the right femoral lesser trochanter, both femoral necks (arrows), acetabula (arrowhead), and pubic rami (white arrow). Stress fracture
  • 16. GOLD STANDARD Bone biopsy : A. Increased osteoid width (> 15 μm), B. increased mineralization lag time, and C. lack of Uptake of double tetracycline
  • 17. ostoid ( pink ) > 80 % Ostoid thickness > 12 um Mineralization lag time > 100 days
  • 18. RX: - depends on the underlying cause • vitamin D supplementation • PO4 supplements if low serum PO4 is present • Ca supplements for isolated calcium deficiency • bicarbonate if chronic acidosis
  • 19. RX : calcitriol or alfacalcidol there is defective 1α-hydroxylation,  e.g. chronic kidney disease, vitamin D dependency and hypophosphataemic rickets with osteomalacia.
  • 20. REFERENCES : Kummar & clarck 7th edition MD- consult Good bye !!