Difference between revisions of "Bone Response to Damage"
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***Produced by <u>C-cells in the thyroid glands</u> in response to <u>increased</u> serum calcium | ***Produced by <u>C-cells in the thyroid glands</u> in response to <u>increased</u> serum calcium | ||
***Inhibits osteoclasts | ***Inhibits osteoclasts | ||
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Revision as of 10:30, 18 July 2008
Normal structure
- Damage to periosteum:
- Invokes a hyperplastic reaction of the inner layer
- Is painful
- Exostoses can remodel or remain
- Lifting of periosteum causes new bone formation below
- Circumferential incision (e.g. during fracture)
- Longitudinal bone growth results
- May be only on one side where periosteum is damaged
- Used by surgeons to treat angular limb deformities
- Damage to periosteum:
Physis (Growth plate)
- Site of many congenital or nutritional bone diseases in the growing animal
- Open in neonates and growing animals
- Chondrocyte proliferation balances cell maturation and death
- Closes and ossifies at maturity
- Regulated by androgens
- If growth teporarily stops -> layer of bone seals the growth plate -> moves into metaphysis when growth resumes -> forms Harris lines
Bone resorption
- Mediated by two hormones:
- Parathyroid hormone (PTH)
- Produced by chief cells in the parathyroid glands in response to decreased serum calcium
- In response, osteoclasts increase in number and resorb mineralised matrix - increase Ca in blood
- Calcitonin
- Produced by C-cells in the thyroid glands in response to increased serum calcium
- Inhibits osteoclasts
- Parathyroid hormone (PTH)