Bone 3.txt

  1. In response to low calcium, what are the combined effects of vitamin D and PTH?
    • Stimulate bone calcium mobilisation (osteoclasts)
    • Increase renal reabsorption of calcium in the distal tubule (mainly PTH)
    • Stimulate intestinal calcium and PHOSPHATE absorption (vitamin D)
  2. In response to high calcium?
    Osteoclast action is inhibited.
  3. Ricketts/osteomalacia (adults) causes failure of calcification due to?
    • Deficiency of or resistance to actions of Vit D.
    • Mineralisation of osteoid is not normal. (Dependant on Ca and PO4, which vit D maintains)
    • In growing children Ricketts can therefore cause deformaties.
  4. What are the causes of deficiency or resistance to vit D?
    • Lack of UV
    • Malabsorption (Coeliac)
    • Renal disease
    • Drugs e.g. phenytoin, degrades vit D into inactive form.
  5. Dental abnormalities of rickets?
    • Enamel hypoplasia
    • Increased width of predentine
    • Increased interglobular dentine
    • Deficient growth of condylar carlilage- lack of growth of vertical ramus
  6. Hyperparathyroidism leads to:
    • Increased osteoclastic activity
    • Increased absorption
    • Increase reabsorption
  7. Hyperparathyroidism can be primary or secondary, give an example of each:
    • Primary - hyperplasia of the gland
    • Secondary - Reactive hyperplasia due to persistent hypocalcaemia e.g chronic renal disease
  8. Clinical fts of hyperparathyroidism:
    • Generalised Osteoporosis
    • Bone lesions - Giant cell lesions (Brown Tumours) (epulis)
    • Metastatic Calcification- renal stones
    • Dental Rad - loss of lamina dura, ground glass
  9. Investigation findings for hyperparathyroidism:
    • Increased Calcium
    • Increased alkaline phosphatase
  10. What is osteoporosis?
    • Reduced bone density and mass, leading to increased risk of fracture.
    • Imbalance between bone formation and resorption.
    • Increased bone resorption due to osteoclasts activity compared to new bone formation.
  11. Risk factors for osteoporosis:
    immobilisation, post menopausal, steroids, age, smoking, alcohol.
  12. Clinical fts of osteoporosis:
    • Fractures in 3 common sites - Neck of femur, Ribs and sternum, lumbar vertebrae
    • Compression fractures in vertebra can slowly lead to deformity and distortion of skeleton, loss of height
    • Compression - lead to nerve problems, increased pain.
  13. Dental fts (osteoporosis):
    • Atrophic mandible/maxilla (edentulous)
    • Pathological fracture of jaw
  14. Tx (osteoporosis):
    • Assess predisposing factors
    • Prevention
    • Excercise
    • Ca intake
    • Bisphosphonates
    • OestrogenRT
  15. What hormone is in excess in acromegaly?
    Growth hormone. Due to hyperplasia or neoplasm of anterior pituitary.
  16. Clinical fts of acromegaly:
    • In adults, bone growth is reactivated. Large hands/feet/ears/nose
    • Prognathism, gaps in teeth
    • Macroglossia
    • Diabetes
    • Hypertension
    • Thick skin
  17. What is pagets disease?
    Chronic disorganised remodelling of bone unrelated to functional requirements. Bone is enlarged, abnormal, brittle. Older patients affected.
  18. Clinical fts (Pagets disease):
    • Progressive enlargement and deformity of affected bones (skull, femur, spine, pelvis, sternum, jaws)
    • Maxilla x2 than mandible. Spacing of teeth.
    • Narrowing of foramina can cause CN deficits.
    • Hypercementosis and ankylosis of teeth
    • Risk of malignancy (sarcomatous transformation) 0.1 percent.
  19. Radiographic features (Pagets):
    • Ground glass appearance of trabeculae.
    • Hypercementosis
    • Skull vault will show scalloped circumscribed zones of osteoporosis
    • Later, deposition of sclerotic bone - cotton wool appearance.
  20. Investigations (Pagets):
    Raised serum alkaline phosphatase level
  21. Histopathology (Pagets):
    • Osteolytic phase
    • Mixed phase
    • Osteosclerotic phase
    • Mosaic appearance
  22. Diff dx of radiographic appearance (Pagets):
    • Diffuse sclerotic OM
    • Osteosarcoma
    • FOD
  23. Treatment (Pagets):
    • Analgesia
    • Calcitonin
    • Biphosphonates
    • Mithramycin
  24. Dental problems (Pagets):
    • Endo, root canal may be decreased in size, or obstructed.
    • Extractions (hypercementosis, ankylosis)
    • Haemostasis (increased vasc. of pagetic bone)
    • Osteomyelitis may develop post XLA or surgery
    • Pros appliances remade.
  25. What is a central giant cell granuloma?
    A giant cell lesion in bone. Its aetiology unknown, possible haemodynamic disturbance in bone marrow.
  26. Who gets CGCG?
    • Younger people <30years
    • Mandible>maxilla
  27. Clinical features of CGCG:
    • Swelling of bone (rapid), can perforate soft tissue
    • Can get a peripheral version, primarily in soft tissue (epulis)
    • Asymptomatic
  28. Radiographic features of CGCG:
    • Demarcated Radiolucent Area
    • Thinning / Expansion of cortical plates
    • Multi/Unilocular
    • Teeth Displaced / Root Resorption
  29. Histology of CGCG:
    • Multinucleated Giant Cells (Osteoclast-like)
    • Vascular Stroma
    • Haemorrhage / Haemosiderin
  30. Treatment CGCG:
Card Set
Bone 3.txt
Metabolic disorders of bone - Miranda Pring