Resumen de Human osteoclast ontogeny and pathological bone resorption
Monocytes and macrophages are capable of degrading both the mineral and orga ni c components of bone and are know n to secre te loca l fac to rs w hi c h stimul a te host osteoclasti c bone resorp ti o n. Rece nt studi es have shown that monocytes and macrophages, including th ose iso la ted from neo pl asti c and inflammatory lesio n s, ca n a lso b e indu ced to differentiate into cells that show all the cytochemical and fun c ti o na l c h a rac te risti cs of mat ur e osteoclasts, including lacun ar bone resorption. Mo nocyte/macrophage-osteoclast differentiation occurs in the presence of osteoblastslbone stromal cells (whic h express osteoclast differentiation facto r) a nd m ac rop hage-co lony stimul ating factor and is inhibited by osteoprotegerin.
Vario us systemic ho rm o nes a nd loca l factors (eg cy tok in es, growth factors, prostaglandin s) mod ul ate osteoclast formation by controlling these cellular and humoral elements. Various pathological lesions of bone and joint (eg carcinomatous metastases, arthritis, aseptic loosening) are associated with osteolysis. These lesions genera ll y co nta in a chro ni c infl ammatory infiltrate in which ma c rophages form a sig nifica nt fract io n. One ce llul a r m ec h a nis m whereby p a thol og ica l bone reso rption may be effected is through ge nerati on of in creased numb ers of bo ne -reso rbin g osteoc lasts from macrop hages. Prod ucti o n of hum ora l factors w hi c h stimul a te mono nu c lear ph agocy te -osteoc last differentiation and osteoclast activity is also likely to influence the extent of pathological bone resorption.
