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Osteoclasts are bone degrading cells, notorious for their role in osteoporosis (a bone disease characterized by decreased density and structural deterioration). However, complete absence of osteoclast activity can be lethal, and optimal bone health relies on remodeling, where osteoclasts resorb old bone and osteoblasts rebuild it. Osteoclasts are large multinucleated cells that form through cell-cell fusion of their precursors. This fusion process is crucial for osteoclast differentiation, but it is not completely understood. New insights into this process could enable development of advanced pharmaceuticals that can fine-tune osteoclast activity. Using mutants derived from a lethal genetic bone disease, we discovered a unique phenotype: osteoclasts that never stop fusing, creating huge cells that are also paradoxically inactive in resorbing bone. I will discuss the genes involved, and our recent results and hypotheses about this intriguing molecular mechanism.

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