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Most therapeutics target inhibition of osteoclast-mediated bone resorption, but more recent attention in early drug discovery has focussed on anabolic targets in osteoblasts or their precursorsthat act at the cellular level, such as tyrosine kinase inhibitors or the anti-apoptotic proteins. These are not as common, but have much greater potential for the treatment of the disease, by enhancing bone regeneration.The mechanism of TNF production by osteoblasts depends on the expression of a target gene, TNF-β1 (TNF-β1), which is expressed in the majority of osteoblastic cells and induces apoptosis. In this regard, several factors mediate the apoptotic response to TNF-β1. TNF-α, a major circulating molecule, inhibits expression of the enzyme that metabolizes TNF-α in most cells, such as Bcl-Xl, but also in the bone marrow. Bcl-Xl expression is low in immature myoblasts of adults, but higher in osteoblasts, suggesting that some of the TNF-α mediated apoptosis involves Bcl-Xl. This may explain the difference between Bcl-Xl–positive osteoblast cells versus Bcl-Xl–negative cells.Another factor, which may be relevant in bone disorders and in other autoimmune diseases, is differentiation factor B (DFB). Fibrillogenic differentiation factor (DFG), also secreted by osteoblases and in osteoblastic cells, is known for its antifibrotic effects but also to mediate apoptosis. Although the mechanism for FGF-β induced apoptosis is not understood, it is thought to occur through FGF-β or FGF-β receptor. FGF-β acts by phosphorylation of FGF-β. B-Myc is also involved in bone remodeling, and its expression may also trigger bone apoptosis by interfering with G-protein coupled receptor-dependent signaling pathways. However, FGF-β may act via either or both of these processes.Several proteins that target inflammatory molecules also affect bone health. BACE1, Bcl-xl, Bax and CD31 target NF-κB, which is involved in mediating cell migration and migration-inducing signals. TNFα may also act through the NF-κB pathway in osteoporosis and other autoimmune diseases. The FGF-β pathway may also be involved in bone health in autoimmune diseases, since Bgfp, FGF-β2 and FGF-β3 can decrease bone density in humans, as measured by an MRI and an ileostomySimilar articles: