Homeostasis of bone metabolism and function depends upon bone remodeling, a coordinated, closely coupled process of resorption and formation of new bone. A variety of cell types and functions, hormones (steroid, polypeptide and thyroid hormones), as well as autocrine and paracrine growth factors and cytokines, act in concert to rebuild the skeleton while maintaining its structural and biomechanical properties (1). The two major players involved in bone remodeling, osteoblasts and osteoclasts, are of different origin: osteoblasts derive from pluripotent mesenchymal stem cells of the bone marrow, whereas osteoclasts originate from the hematopoietic granulocyte-macrophage colony-forming units (GM-CFU) (1). Thus, their differentiation to mature bone cells differs substantially with respect to their cytokine requirements and subsequent events of signal transduction.
In addition to their phenotypic markers, collagen type I and alkaline phosphatase, osteoblasts produce a variety of cytokines that are crucial for their maturation, including interleukin 6 (IL-6), IL-11, granulocytemacrophage colony-stimulating factor