Inflammatory osteolysis: a conspiracy against bone

Inflammatory osteolysis: a conspiracy against bone.

There are many causes of inflammatory osteolysis, but regardless of etiology and cellular contexts, the osteoclast is the bone-degrading cell. Thus, the impact of inflammatory cytokines on osteoclast formation and function was among the most important discoveries advancing the treatment of focal osteolysis, leading to development of therapeutic agents that either directly block the bone-resorpt...

Osteoclasts; culprits in inflammatory osteolysis

Periarticular osteolysis, a crippling complication of rheumatoid arthritis, is the product of enhanced osteoclast recruitment and activation. The osteoclast, which is a member of the monocyte/macrophage family, is the exclusive bone resorptive cell, and its differentiation and activation are under the aegis of a variety of cytokines. Receptor activator of NF-kappaB ligand (RANKL) and macrophage...

M-CSF mediates TNF-induced inflammatory osteolysis.

TNF-alpha is the dominant cytokine in inflammatory osteolysis. Using mice whose BM stromal cells and osteoclast precursors are chimeric for the presence of TNF receptors, we found that both cell types mediated the cytokine's osteoclastogenic properties. The greater contribution was made, however, by stromal cells that express the osteoclastogenic cytokine M-CSF. TNF-alpha stimulated M-CSF gene ...

Bone implant interface, osteolysis and potential therapies.

Tumor cell p38 MAPK: A trigger of cancer bone osteolysis.

Osteolytic bone destruction is a hallmark of bone-metastatic cancers. Current therapy is unable to completely cure or prevent this disease in patients. The p38 mitogen-activated protein kinase (MAPK) affects a diverse range of intracellular responses with well-known roles in development, cell-cycle and differentiation, inflammation, apoptosis, senescence, and tumorigenesis. This article is an o...