Abstract

The transcription factor nuclear factor (NF)-κB is well recognised as a pivotal player in osteoclastogenesis and inflammation induced bone loss. Here, the authors discuss their recent results, obtained using a genetic approach in mice, that indicate the importance of IKKβ, and not IKKα, as a transducer of signals from receptor activator of NF-κB (RANK) to NF-κB. Ablation of IKKβ results in lack of osteoclastogenesis and unresponsiveness of IKKβ deficient mice to inflammation induced bone loss. In the need of a more effective therapy for the treatment of inflammatory diseases causing bone resorption, specific inhibition of IKKβ represents a logical alternative strategy to the current therapies.