It has previously been demonstrated that impaired angiogenesis is associated with metabolic abnormalities in bone in addition to osteoporosis (including postmenopausal osteoporosis). Enhancing vessel formation in bone is therefore a potential clinical therapy for osteoporosis. The present study conducted an in-depth investigation using desferrioxamine (DFO) in an ovariectomy (OVX)-induced osteoporotic mouse model in order to determine the time frame of alteration of bone characteristics and the therapeutic effect of DFO. It was demonstrated that OVX induced instant bone mass loss 1 week following surgery, as expected. In contrast, DFO treatment protected the mice against OVX-induced osteoporosis during the first week, however failed to achieve long-term protection at a later stage. A parallel alteration for cluster of differentiation 31/endomucin double positive vessels (type H vessels) was observed, which have previously been reported to be associated with osteogenesis. DFO administration not only partially prevented bone loss and maintained trabecular bone microarchitecture, however additionally enhanced the type H vessels during the first week post-OVX. The molecular mechanism of how DFO influences type H vessels to regulate bone metabolism needs to be further investigated. However, the findings of the present study provide preliminary evidence to support combined vascular and osseous therapies for osteoporotic patients. Pharmacotherapy may offer a novel target for improving osteoporosis by promoting type H vessel formation, which indicates potential clinical significance in the field of bone metabolism.