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