osteoclasts

pagets presentation

areas of hyperactive resorption with compensatory increased formation

what hormones increases osteoclast formation

- 1, 25 OH vit D increases: MCSF RANKL -glucocorticoids: increase RANKL -PTH: increase RANKL

requirements for osteoclast formation

- MCSF from osteoblasts -RANKL from stromal cells

how do osteoclasts cause bone resorption

- bind to bone via integrin -carbonic andhydrase II produces H+ -H+ is pumped into resorption pit via ATPase pump - lysozymes release enzymes into pit -they are activated by H+ - MCSF and RANKL activate function -calcitionin and INF inhibit function

what hormones decreases osteoclast formation

- estradiol - TGF increase OPG

pagets disease pathogenesis

- increased vit D receptors -increased RANKL by stroma cells = increase osteoclast number and activity

steroid induced osteoporosis pathogenesis

- inhibits OPG (osteoclast inhibitor) -increases PTH and RANKL -inhibits osteoblast number and activity

consequence of metabolic bone disease in malignancy

1) tumor -> PTHrp 2) tumors -> cytokines = increase number and activity

what inhibits osteoclasts

OPG

oestopetrotic model

osteoclasts arent activated or dont function normally characterized by net accumulation of bone mass. can decrease marrow cavity