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The present study investigated the effects of conditional deletion of ephrinB1 in osteoprogenitor cells driven by the  Osterix  ( Osx ) promoter, on skeletal integrity in a murine model of ovariectomy-induced (OVX) osteoporosis. Histomorphometric and μCT analyses revealed that loss of ephrinB1 in sham  Osx:cre-ephrinB1   fl/fl   mice caused a reduction in trabecular bone comparable to OVX  Osx:Cre  mice, which was associated with a significant reduction in bone formation rates and decrease in osteoblast numbers. Interestingly, these observations were not exacerbated in OVX  Osx:cre-ephrinB1   fl/fl   mice. Furthermore, sham  Osx:cre-ephrinB1   fl/fl   mice displayed significantly higher osteoclast numbers and circulating degraded collagen type 1 compared to OVX  Osx:Cre  mice. Confirmation studies found that cultured monocytes expressing EphB2 formed fewer TRAP +  multinucleated osteoclasts and exhibited lower resorption activity in the presence of soluble ephrinB1-Fc compared to IgG control. This inhibition of osteoclast formation and function induced by ephrinB1-Fc was reversed in the presence of an EphB2 chemical inhibitor. Collectively, these observations suggest that ephrinB1, expressed by osteoprogenitors, influences bone loss during the development of osteoporosis, by regulating both osteoblast and osteoclast formation and function, leading to a loss of skeletal integrity.

The osteoprogenitor-specific loss of ephrinB1 results in an osteoporotic phenotype affecting the balance between bone formation and resorption