Mice lacking substance P have normal bone modeling but diminished bone formation, increased resorption, and accelerated osteopenia with aging

Regulation of Bone by Mechanical Loading, Sex Hormones, and Nerves: Integration of Such Regulatory Complexity and Implications for Bone Loss during Space Flight and Post-Menopausal Osteoporosis

“…Such a network of regulation could potentially explain the enhanced bone turnover during pregnancy and lactation versus the restoration of bone integrity in the post-lactation time frame. Interestingly, mice lacking the neurotransmitter substance P (SP) exhibit normal bone modeling when young but diminished bone formation and increased bone resorption with aging [77], which is somewhat consistent with a compromised neural system as described above. However, these mouse findings may indicate that there are additional regulatory factors operative when undergoing growth and maturation (i.e., anabolic factors) that decline with age allowing for the SP-deficiency to become evident.…”

“…However, these mouse findings may indicate that there are additional regulatory factors operative when undergoing growth and maturation (i.e., anabolic factors) that decline with age allowing for the SP-deficiency to become evident. In addition, these mice still retained CGRP, which also can exert effects on bone [77]. A limitation of this report is that the authors only used male mice for some experiments or did not report the sex of the animals used, so it is not known if any sex differences in the impact of the SP-deficiency was evident.…”

“…Recently, Liu et al [72] have reviewed the possibility of the "quaternary regulation" theory of a "peripheral nerveangiogenic-osteoclast-osteogenesis" network in a network mediated by neuropeptides. Thus, neuropeptides, such as neuropeptide Y (NPY), substance P, or calcitonin gene-related peptide (CGRP) released locally [73][74][75], could influence the metabolic activity of bone cells (i.e., osteoblasts, osteoclasts, osteocytes) [76][77][78][79]. Neuropeptides, such as CGRP, may have a role to play in bone remodeling [80], in the treatment of osteoporosis [81] or in fracture healing [82].…”

Single-cell atlas of craniogenesis uncovers SOXC-dependent, highly proliferative, and myofibroblast-like osteodermal progenitors

“…Accordingly, C3.1 and C3.2 weakly expressed proliferation and myofibroblast markers, and highly expressed osteogenic and hypodermal markers such as Aspn (asporin) and Thbs2 (thrombospondin-2). C3.1 was positive for Tac1 (tachykinin-1) expression, marking cells between periosteum and dura ( Kosaras et al, 2009 ; Wang et al, 2021 ). C3.2 surpassed C3.1 in expressing Col8a1 , Fbln2 (fibulin-2), Igfbp3 (insulin-like growth factor-binding protein-3), and other periosteal and neonatal suture markers ( Holmes et al, 2020 ).…”

Preparation of co-electrospinning membrane loaded with simvastatin and substance P to accelerate bone regeneration by promoting cell homing, angiogenesis and osteogenesis

“…who found that SP at different concentrations had a negligible effect on enhancing the osteogenic differentiation of MSCs [ 21 ]. However, upon reviewing the literature, inconsistent results were found, and clear evidence regarding the association between SP and the mechanisms involved in osteoblast differentiation is lacking [ 42 , 43 ]. These findings suggest that further investigations are necessary to gain a better understanding of the role of SP in osteogenic differentiation and bone reformation.…”