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Osteoclasts are the cells responsible for bone resorption in steady state and bone destruction in chronic inflammatory diseases and osteoporosis.  Up to recently, they have been considered only as a single population of bone-resorbing cells whose differentiation and activity are increasing in pathologies associated with bone destruction. However, recent data demonstrated that besides bone resorption, osteoclasts are innate immune cells. In particular, they present antigens and activate T cell responses towards tolerance in steady state. Moreover, they are also able to stimulate inflammatory T cells in the context of chronic inflammation. Using RNAseq on purified mature osteoclasts, we showed that these divergent immune effects are related to functionally and transcriptionally distinct subsets of osteoclasts. Therefore, bone destruction not only relies on an increased number of osteoclasts but also on the emergence of different osteoclast subsets having opposite immune outcomes. Taking advantage of the immune characteristics of these different subsets and in particular their different capacity to respond to danger signals arising from gut dysbiosis, we could specifically block the differentiation of inflammatory osteoclasts and reduced bone destruction in ovariectomized mice. These new data on the diversity and innate immune

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