Monocytes and macrophages are capable of
degrading both the mineral and organic components of
bone and are known to secrete local factors which
stimulate host osteoclastic bone resorption. Recent
studies have shown that monocytes and macrophages,
including those isolated from neoplastic and
inflammatory lesions, can also be induced to
differentiate into cells that show all the cytochemical and
functional characteristics of mature osteoclasts,
including lacunar bone resorption. Monocyte/macrophage-
osteoclast differentiation occurs in the presence of
osteoblasts/bone stromal cells (which express osteoclast
differentiation factor) and macrophage-colony
stimulating factor and is inhibited by osteoprotegerin.
Various systemic hormones and local factors (eg
cytokines, growth factors, prostaglandins) modulate
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
generally contain a chronic inflammatory infiltrate in
which macrophages form a significant fraction. One
cellular mechanism whereby pathological bone
resorption may be effected is through generation of
increased numbers of bone-resorbing osteoclasts
from macrophages. Production of humoral factors
which stimulate mononuclear phagocyte-osteoclast
differentiation and osteoclast activity is also likely to
influence the extent of pathological bone resorption