physiology of bone formation and repair Flashcards
What do too much bone resorption and too much bone formation result in
osteoporosis and osteopetrosis respectively
What are the 2 main types of bone
long bone and flat bone
how are bones further classified
macroscopic
- cortical bone (thick hard bone on the outside)
- cancellous (spongy, inside), has spicules and trabeculae
microscopic
- lamellar (osteons)
- woven (immature and disorganised)
What composes the bone
living cells and acellular matrix 3 types of cells -osteoclasts (destructive part of bone, catabolic) -osteocytes (maintenance of bone) -osteoblasts (regulate bone growth)
How do osteocytes develop
Osteocytes arise from osteoblasts
describe osteoclasts
they can proliferate,
phagocytose bone matrix and crystals
secrete acids and proteolytic enzymes
What are the properties of the extracellular matrix in bone
70% minerals,
plus abundant proteins and sparse cells
high compressive strength and tensile strength
Where are glycosaminoglycans
primarily a sugar molecule which is found in bone and cartilage,
highly negative repels each other, attracts water and resists compression.
Where are growth factors found in the bone
They are suspended in the matrix, they are revealed by osteoclast action, which leads to proliferation and mineralisation.
bone remodelling= activation-resorption-formation sequence.
briefly outline the process of bone remodelling
osteoclasts resorb bone,
osteoblasts deposit bone and lays done bone (in different directions) and then
What are the 2 factors that determine remodelling
recurrent mechanical stress calcium homeostasis (plasma calcium is essential in maintaining the structural integrity of the skeleton)
How does mechanical stress strengthen bone
Inhibits bone resorption, promotes deposition
without weight-bearing, bone rapidly weakens.
What type of drugs are used for osteoporosis, give an example and how they work
e.g. bisphosphonates, alendronate inhibits osteoclast-mediated bone resorption
What are 2 meds apart from alendronate that is used for osteoporosis?
teriparatide encourages osteoblast formation of bone
denosumab, prevent osteoclast maturation.
describe the molecular mechanism of osteopetrosis
osteoblasts cannot remodel bone,
defective vacuolar proton pump or defective chloride channel.
What does osteopetrosis result in
Excess bone growth, at the foramina, may press on nerves
brittle (dense) bones
blindness
deafness
severe anaemia.
What hormones are involved in calcium regulation
PTH - parathyroid hormone, increases plasma calcium
Vit D- increases plasma calcium
calcitonin, made by thyroid c cells,
tones down blood calcium
What are some of the functions of vitamin D
increases intestinal calcium absorption
stimulates kidneys to reabsorb calcium
stimulates osteoclasts indirectly (via osteoblasts)
vit D facilitates bone remodelling.
What are some causes of low plasma calcium
loss
- pregnancy
- lactation
- kidney dysfunction
low intake
- insufficient ingestion of calcium
- rickets
parathyroid dysfunction
What does chronic hypocalcaemia result in
Skeletal deformities an increased tendency toward bone fractures impaired growth short stature dental deformities.