Abstract
Extracellular vesicles (EVs), including exosomes, microvesicles, and apoptotic bodies, play an important role in cellular communication during skeletal growth and homeostasis. Bioactive molecules carried by EVs are transported to neighboring and distant cells to trigger a series of signaling cascades influencing bone homeostasis. The bioactive activities of osteoclast-derived EVs include regulation of osteoclastogenesis and osteoclast–osteoblast communication. As osteoclast-derived EVs have the potential to regulate osteoclasts and osteoblasts, their application in osteoporosis and other bone metabolic disorders is currently under investigation. However, very few reviews of osteoclast-derived EVs in bone remodeling regulation have yet been published. This article aims to review recent advances in this field, summarizing a new regulator of osteoclastogenesis and osteoclast–osteoblast communication mediated by osteoclast-derived EVs. We will analyze the major challenges in the field and potential for the therapeutic application of EVs.
Highlights
Bone is a dynamic, living tissue continually undergoing modeling and remodeling
Intercellular communication between osteoblasts and osteoclasts plays an important role in the regulation of bone homeostasis (Cao, 2011; Deng et al, 2015), as maintenance of bone requires careful balancing of resorption and formation processes (You et al, 2013)
Overexpression of miR-214-3p expression in osteoclasts inhibited osteoblast activity in this co-culture system. These findings suggest that exosomal miR-214-3p could be transferred from osteoclasts to osteoblasts to inhibit osteoblast activity in vitro
Summary
Bone is a dynamic, living tissue continually undergoing modeling and remodeling. Many factors, including hormones, growth factors, physical activity, and drugs, can influence bone homeostasis (Xiao et al, 2016; Delgado-Calle et al, 2017; Li X. et al, 2017). Intercellular communication between osteoblasts and osteoclasts plays an important role in the regulation of bone homeostasis (Cao, 2011; Deng et al, 2015), as maintenance of bone requires careful balancing of resorption and formation processes (You et al, 2013). Huynh et al (2016) demonstrated that RANKL rich osteoclast-derived EVs inhibit 1,25-dihydroxyvitamin D3 (1,25(OH)2D3)-induced formation of osteoclast-like multinucleated cells in mouse marrow by inhibiting the interaction of RANKL-RANK, and the interaction between osteoblasts and osteoclasts.
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
