Osteolysis, the most common expression of bone tumor, can cause pain, patho
logical fracture, epidural spinal cord compression and hypercalcemia. Multi
nucleated osteoclast-like cells, the main agents in bone resorption, are nu
merous in benign giant cell tumor of bone and can be recruited and activate
d by various carcinoma cell lines in vitro in animal models. Polykarion mac
rophages are also able to resorb bone matrix in a favourable tumoral enviro
nment. Direct bone resorption by tumor cells has recently been described in
vitro and in vivo in animals. The presence of diffusible substances such a
s hormones, cytokines and growth factors creates a favourable microenvironm
ent for stimulation of osteoclast-like cells and polykarion macrophages fun
ctional ability to resorb bone matrix. These mediators act within a complex
but still unelucidated network involving high cell production (tumor cells
, normal and reactional stroma as well as hematopoietic cells) and many tar
gets (tumor production (tumor cells, normal and reactional stroma as well a
s hematopoietic cells) and many targets (tumor cells, monocyte/macrophage l
ineage cells, and osteoclast-like cells). The presence in the same environm
ent of all these stimulating factors for tumor cell growth and resorbing ab
ility could explain the vicious circle of tumoral and osteolytic progressio
n. A better understanding of the complex mechanism of tumor induced osteoly
sis is essential for improving the conventional surgical approach to this p
athology.