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  1. According to WHO, it is defined as a bone density that falls 2.5 standard deviation (SD) below the mean for roung healthy adults of same race and gender also referred to as a T score less than -2.5.
  1. The fractures that are most common (in decreasing order) are — vertebral crush fracture, hip (neck femur) and lower end radius fractures.

1. Spine

2. Hip

3. Wrist
Three common sites of Osteoporotic Fractures

It is a condition of quantitative decrease in bone mass. (Not qualitative like in osteomalacia where the ratio of unmineralized bone matrix to bone mass is increased, making it a qualitative defect)

Etiology: few important causes are

  1. Type-1: post menopausal
  2. Type-2: senile(age related)
  1. Endocrinopathy (hyperthyroidism, cushing's disease
  2. Immobility
  3. Drugs (heparin, cytotoxic drugs, phenytoin)
  4. Inflammatory arthritis (ankylosing spondylitis, rheumatoid arthritis)
Clinical Features:
  1. Most of cases of osteoporosis are asymptomatic. They presents to clinician as insufficiency fracture,
  2. Over all most common site of osteoporotic fracture is spine.
  3. Colle's fracture is most commonly seen in 50-60 yrs
  4. Spine fracture is most commonly seen in 60-70 yrs
  5. Hip fracture is most commonly seen in age above 70 yrs
  6. Hip fractures are either intertrochanteric femur fracture (more common) or fracture neck of femur (less common)
  7. Laboratory: normal calcium,phosphate, and alkaline phosphatase. Few markers are used during treatment of osteoporosis.
  8. Bone formation: alksline phosphatase, osteocalcin.
  9. Bone resoption: TRAP, telopeptide, deoxypyridinoline.
  10. X ray: poor test for osteoporosis. Its evident on x ray only when 30% of bone loss is there. cod fish mouth vertebra. Singh and Maini index is the index used for osteoporosis based on x ray of hip joint.
  11. Dexa scan: Investigation of choice. Value is given as T-score (most commonly used, compares BMD with 25 year male, lumbar spine BMD) or Z score (age and sex matched)
  12. Three sites choosen: Hip, spine, wrist. Value of one site only give bone mineral density (BMD) and prediction fracture of that site only.
  13. WHO defines osteopenia as T score between -1 and -2.5 and osteoporosis as score below -2.5.
Medications are broadly divided into two categories
  1. Drugs that decreases bone resoption (antiresoptive)
  2. Drug that increases bone stock (anabolic)
  1. Bisphonates: is most commonly used drugs for osteoporosis. It is antiresoptive (alendronate given either daily or weekly, risodronate (weekly), ibondronate (monthly, zolendronate (intravenous, yearly)
    Disadvantage of this class of drug is esophagatis and it makes bone much rigid if taken for many years. Bones are prone to fracture without significant injury (called fosavance fracture or alendronate fracture) most commonly seen in subtrochanteric femur, visible on plainn x ray.
  2. Calcitonin: given intrnasal or subcutanous route. It isantiresoptive drug. It also acts as analgesics.
  3. Teriparatide: PTH analogue, given daily subcutaneous route. It is anabolic drug that is used in severe osteoporosis.
  4. Strontium: It has dual action.Strontium ranelate is characterized by a unique mode of action, concomitantly decreasing bone resorption and stimulating bone formation. Strontium This treatment appears to reduce fractures at all skeletal sites, including the hip in osteoporotic patients most at risk. Strontium ranelate, with its antifracture efficacy demonstrated up to 5 years, may now be considered as a first-line treatment of osteoporosis.
    Future Drugs
    1. Sodium fluoride is mitogenic for osteoblasts. Low dose with calcium produced gain in bone density. Higher doses leads to production of abnormal unmineralized bone with decreased bending strength (fluorosis)
    2. RANKL - Inhibiton
      1. RANKL (receptor activator of nuclear factor - K β ligand) a protein expressed by osteoblastic stromal cells, binds to RANK (receptor activator of nuclear factor KB) and is primary mediator of osteoclast differentiation, activation & survival. So RANKL is responsible for osteoclast mediated bone resorption.
      2. Osteoprotegrin, a soluble RANKL receptor, is a key regulator of RANKL - RANK pathway of osteoclastic resorption.
      3. Denosumab (AMG 162, Amgen) is a fully human monoclonal antibody (Ig C2) that binds RANKL (mimicking osteoprotegerin) and blocks interaction of RANKL with RANK.

Extra Edge
Biochemical abnormalities for diagnosis of metabolic bone disorders.

  1. Osteoporosis
    1. Quantitative decrease of bone units with maintenance of qualitative characterstics i.e. normally mineralized osteoid of decreased volume is present
    2. Normal Ca++, PO3-4, S. alkaline phosphate and PTH.
  2. Osteomalacia
    1. Mineralization of osteoid is poor i.e. bone units are normal in number but less mineralized
    2. Due to dietary deficiency S. Ca++ & S. PO43- levels are low with resultant increase in s. alkaline phosphatase and PTH.
  3. Multiple Myeloma
    1. It has osteolysis thus increasing S. Ca++ and & serum phosphate.
    2. S. alkaline phosphate and PTH levels are normal
  4. Hyperparathyroidism
    PTH and S. alkaline phosphate are raised
    1. Primary
      PTH is increased - parathyroid adenoma thus ↑Ca++ and ↓PO3-4 levels
    2. Secondary
      PTH is increased - disease that causes ↓Ca++ & ↑PO3-4 levels So Ca++ & P levels may be variable.

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