metabolic bone disease Flashcards
(14 cards)
macroscopically
Two patterns of organisation:
Cortical/compact bone
Releases mineral in response to significant or long lasting deficiency
Cancellous/trabecular/spongy bone
Releases minerals in response to acute deficiency
microscopically
Comprised of bone matrix and cells
By mass:
1/3 collagen fibres
2/3 calcium phosphate salt
hydroxyapatite (calcium phosphate and calcium carbonate combined)
Magnesium hydroxide, fluoride, sulphate
osteogenic cells
Develop into osteoblasts
Endosteum, cellular layer of periosteum
osteoblasts
Responsible for bone formation
At the end of bone remodelling cycle they remain as resting osteocytes.
osteocytes
dormant; sensitive to stimuli and communicate to osteoblasts
osteoclasts
Responsible for bone resorption.
Derived from monocyte precursors in marrow
RANK/RANKL/OPG system
M-CSF (expressed by osteocytes/osteoblasts) stimulates RANK expression
RANKL binds to receptor (RANK) on inactive osteoclasts
Results in osteoclast maturation and rapid bone resorption
Meanwhile, OPG is a “decoy receptor” for RANKL
Secreted by osteoblasts/osteocytes
Inhibits osteoclastic bone resorption
control of bone remodelling- PTH
Opposing effects related to duration of exposure
Continuous- bone resorption (cortical>trabecular)
Intermittent- enhances bone formation
control of bone remodelling- 1,25 OH vit D
(calcitriol)
Regulates calcium/phosphate absorption providing substrate for mineralisation
control of bone remodelling- calcitonin
hormone secreted by the thyroid gland.
Essentially opposite to PTH.
Evidence that it will increase BMD by inhibiting osteoclast formation and activity.
control of bone remodelling- hormones
Sex hormones
Oestrogen and androgens stimulate bone formation and inhibit resorption
Thyroid hormones
Directly stimulate osteoblast differentiation and mineralisation
Growth hormone and IGF1
Increase bone turnover
Stimulates osteoblastic bone formation > resorption
Small net increase in bone mass
management of osteoporosis- biphosphonates
e.g. Alendronic acid, Zoledronic acid
Work by inhibiting osteoclast activity
Potential complications:
Osteonecrosis of the jaw
Atypical femoral fracture
osteomalacia
Disorder arising from defective mineralisation of bone
If it occurs before bone growth is complete = Rickets
causes- decreased exposure to light/calcium intake/malabsorption
diagnosis- raised PTH, low vit D
paget’s disease
- increased osteoblast and osteoclasts activity
- results in disorganised bone tissue prone to fracture
clinical features- pain, deformities, deafness
