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  1. Metabolic Control of Calcium Metabolism
    Serum calcium is under regulation of vitamin D & parathormone (PTH)
  2. Vitamin D Metabolism
    Provitamin - D in skin 7- Dehydrocholesterol
    1. Provitamin D in diet Ergosterol
    2. Calciferol (Vit D2) in plan source
    3. Cholecalciferol (Vit D3) in animal Source
    4. Liver (Vit D 25 Hydroxylase) produces 25 (OH) Vit D3
    5. Kidney 25 (OH) D, lα Hydroxylase produces 1,25 (OH)2 Vit. D
      1. ↑ GI Ca++ absorption
      2. ↑ Renal tubule Ca++ resorption
      3. Bone calcification.
  3. Parathormone (PTH), Primary function is to maintain ECF Ca concentration. The hormone acts directly on bone & kidney and indirectly on intestine through 1,25 dihydroxy Vit D to increase. Ca concentration in turn PTH production is closely regulated by conc. of s. ionized calcium.
    1. Osteomalacia is a mineralization disorder, manifested by defects in mineralization of newly formed bone. It is characterized by
    2. Total amount of bone is normal but there is inadequate mineralization of newly formed bone.
    3. Osteoid matrix is secreted at normal rate but the mineralization is decreased (i.e. decrease in mineral apposition rate).
    4. This leads to increased osteoid maturation time. (Maturation of osteoid means mineralization of osteoid).
    5. Osteoid is increased in thickness, volume and total surface area.
  4. Rickets & Osteomalacia
    1. Are characterized by defective mineralization of bone. Bone tissue through out skeleton is incompletely calcified and therefore softened. Rickets refers to condition where it occurs before closure of growth plates so that abnormalities of skeletal growth are superimposed.
  5. Causes & Types (Mankin)
    1. Deficiency Rickets and Osteomalacia
      1. Vitamin-D deficiency
      2. Calcium deficiency
      3. Phosphorus deficiency
      4. Chelators in diet
    2. Absorptive Rickets and Osteomalacia
      1. Gastric abnormalities
      2. Biliary disease
      3. Enteric absorptive defects
    3. Renal Tubular Rickets and Osteomalacia
      1. Proximal tubular lesions
      2. Proximal and distal tubular lesions
      3. Distal tubular lesions (renal tubular acidosis)
      4. Primary ii. Secondary
    4. Renal Osteodystrophy
    5. Unusual Forms of Rickets and Osteomalacia
      1. Rickets with fibrous dysplasia
      2. Rickets with neurofibromatosis
      3. Rickets associated with soft-tissue and bone neoplasms
      4. Rickets due to anticonvulsant
  6. Pathology
    1. Primary disturbance in bone is failure of calcification of cartilage and osteoid tissue The chondrocytes multiply normally, but normal process of maturation of cartilage columns fails to place.
    2. The proliferative zone is as active as ever, but the cells pile up irregularly, entire physeal plate is increased in thickness, the zone of calcification is poorly mineralized & bone formation is sparse in zone of ossification.
    3. Endosteal & periosteal osteoblastic activity is normal, forming abundant osteoid. With defective mineralization, osteoclastic resorption of the uncalcified osteoid does not take place. Hence osteoid is laid down irregularly with widened osteoid seams and osteoid islets may even persist down into the diaphysis.
    4. The new trabeculae are thin & weak (as bundle of collagen fibers instead of running parallel to haversian canal, course perpendicularly) and with joint loading the juxtaepiphyseal metaphysis becomes broad and cup shaped
    5. Cortices are thin and may cause stress fracture or deformities.
    6. Clinical Features
  1. Generalized muscular weakness, lethargy arid irritability, listlessness, tetany or convulsions.
  2. Sitting, standing & walking are delayed.
  3. Protuberent abdomen with seperation of recti muscles ( muscular flaccidity)
  4. Large head, open fontanelles & craniotabes (box shaped head)
  5. Thickening of knees, ankle, & wrists physeal overgrowth (enlargement).
  6. Enlargement of costochondral junctions causing beaded ribs (rosary)
  7. Lateral indentation of chest due to pull of diaphragm on ribs -Harrson’s groove
  8. Pectus carinatum i.e. forward projection of sternum
  9. Short stature & bowing of long bones, with genu valgum, coxa vara.
  10. Delayed dentition with irregular soft decaying teeth (enamel defect).
  11. Pale skin, flabby subcutaneous tissue & typical widened look.
  1. Radiographic Findinges
    1. The characteristic feature of rickets are
      Thickening & widening of growth plate (physis).
      1. Indistinct and hazy metaphysis that is abnormally wide with cupping or flaring. (Brush like appearance)
      2. Bowing of diaphysis, with thinning of cortices.
      3. Looser’s zone in 20%
    2. Treatment is Stoss regimen.


  1. Pseudofracture / Increment Fracture / Milk man’s fracture / Osteoid seams/’Osteoid zones / Umbauzanones/ Looser’s zones / Looser’s lines
    These represent incomplete (insufficiency) stress fractures that have healed by callus consisting of osteoid tissue lacking calcium (i.e. unmineralized woven bone).
    1. Causes and Associations
      • It is caused by incomplete union (nonunion) of stress fracture or nutrient vessel pulsation injury by unmineralized woven bone. It is characteristically seen in
        - Osteomalacia and Rickets (most characteristic)
        - Vitamin D deficiency eg
        i. Chronic renal tubular disease (cause hypophosphatemia)
        ii. Phenobarbitones, diphenylhydantoin
        iii. Glomerular disease (cause PO4 retention and hyper phosphatemia)
        • Hereditary hyperphosphatasia
        • ii. Renal osteodystrophy
        • Vitamin A intoxication
        • iv. Cadmium poisoning
        • Congenital hypophosphatasia
  2. Common Locations
    1. Medial femoral neck
    2. Pubic and ischial rami
    3. Axillary edge of scapula immediately below the glenoid (typical location)
    4. Scapula lateral and superior border
    5. Ribs and clavicle
    6. Proximal (1/3) ulna & radius
    7. Phalanges, metacarpals & metatarsals.
    8. Ischial tubersity
  3. Typical Features - Thin (narrow) translucent band about 2-3 mm in width running per pendicular (at the right angle) to cortex
  4. Treatment of loosers zones is rest and treat the primary cause.
    1. Biochemical Abnormalities of Rickets
      Common changes to all types of rickets and osteomalacia are diminished levels of serum calcium and phosphate, increased alkaline phosphatase, dimished urinary excretion of calcium.
      1. The calcium phosphate product (normally 3) is diminished and value of < 2.4 are diagnostic.
      2. In vit D deficiency 25 -OH levels are also low.
    2. Nutritional (Vit D deficiency) Rickets
      Vit D deficiency results in inability to absorb calcium & phosphorus.
      PTH released in response to hypocalcemia, corrects S.Ca deficit but hypophosphatemia persists.
      So serum Ca++ level are normal to mildly decreased, phosphate levels are low and vitamin D levels are decreased, but PTH & alkaline phosphate levels are high.
  5. Vit D Resistant Rickets (Familial Hypophosphatemic Rickets)
    1. It encompasses a group of disorder in which normal dietary intake of vitamin D is insufficient to achieve normal mineralization of bone.
    2. The basic abnormality in X-linked dominant type is renal tubule’s inability to retain phosphate - phosphate diabetes and hypophosphatemia. Endrogen insensitivity to Vit. D is the cause in autosomal recessive type. Third type is failure of kidney to 2nd hydroxylation of Vit. D. In renal tubular acidosis kidney excretes fixed base & wastes bicarbonate - wasting of Ca++ & Na++ as well.

Extra Edge:


S. alkaline phosphatase is an index of osteoblastic activity.

Its levels are Increased In:

  1. Paget’s disease (Osteitis deformans)
  2. Rickets/Osteomalacia
  3. Primary Hyperparathyroidism
  4. Renal osteodystrophy (Renal failure in childhood)
  5. CRF with secondary hyperparathyroidism
  6. Lytic bone neoplasm (may be normal)
Normal –Osteoporosis/ Multiple myeloma /Hypoparathyroidism

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