Osteoclast Multinucleation Mechanisms

Dear Colleagues,

Osteoclasts are specialized, multinucleated, and giant cells that resorb bone. Multinucleation is a hallmark of mature osteoclasts. The importance of multinucleation in osteoclast formation is demonstrated by the impaired bone-resorbing activity of osteoclasts that cannot achieve multinucleation. A functional defect in osteoclasts results in abnormal bone homeostasis. Therefore, it is important to understand the molecular signaling and genetic programs that control osteoclast multinucleation to improve our understanding of osteoclast biology and provide a molecular basis for designing therapeutic strategies for bone remodeling diseases.

Osteoclasts are hematopoietic in origin and are derived from myeloid precursors that also give rise to macrophages. In the past few decades, important advances have been made in molecular characterization of osteoclast multinucleation. To date, a number of molecules as well as cellular mechanisms (cell adhesion, the actin-based cytoskeleton, membrane-associated elements, irregular cell cycle, and cell fusion) have been revealed to be required for osteoclast multinucleation.

This Special Issue aims to cover a selection of recent research topics and current review articles related to osteoclast multinucleation. Since multinucleation is also observed in macrophages, and multinucleated macrophages have potential similarities to osteoclasts, we also welcome research and reviews characterizing the mechanisms of macrophage multinucleation, which will give us additional insights into the mechanisms underlying osteoclast multinucleation. Up-to-date review articles, commentaries, and experimental papers are all welcome.

Dr. Noriko Takegahara
Guest Editor

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