Yoon JP, et al. Clin Orthop Surg. 2015 Mar;7(1):97-103. https://doi.org/10.4055/cios.2015.7.1.97

Many reports have revealed the importance of the sympathetic nervous system (SNS) in the control of the bone marrow environment. However, the specific role of neuropeptide Y (NPY) in this process has not been systematically studied. Here we show that NPY‐deficient mice have significantly reduced hematopoietic stem cell (HSC) numbers and impaired regeneration in bone marrow due to apoptotic destruction of SNS fibers and/or endothelial cells. Furthermore, pharmacological elevation of NPY prevented bone marrow impairments in a mouse model of chemotherapy‐induced SNS injury, while NPY injection into conditional knockout mice lacking the Y1 receptor in macrophages did not relieve bone marrow dysfunction. These results indicate that NPY promotes neuroprotection and restores bone marrow dysfunction from chemotherapy‐induced SNS injury through the Y1 receptor in macrophages. They also reveal a new role of NPY as a regulator of the bone marrow microenvironment and highlight the potential therapeutic value of this neuropeptide. Synopsis Neuropeptide Y maintains hematopoietic stem cells in the bone marrow by instructing the stromal microenvironment. NPY deficiency causes impairment of HSC survival and bone marrow regeneration. Bone marrow dysfunction by NPY deficiency is due to the destruction of SNS nerve fibers and/or EC reduction. NPY mediates Y1 receptor activation in macrophages, contributing in turn to HSC survival. Treatment with NPY or Y1 agonists prevents cisplatin‐induced bone marrow nerve injury.

Background: This study was performed to evaluate the results of negative pressure wound therapy (NPWT) in patients with open wounds in the foot and ankle region. Materials and methods: Using a NPWT device, 16 patients were prospectively treated for soft tissue injuries around the foot and ankle. Mean patient age was 32.8 years (range, 3–67 years). All patients had suffered an acute trauma, due to a traffic accident, a fall, or a crush injury, and all had wounds with underlying tendon or bone exposure. Necrotic tissues were debrided before applying NPWT. Dressings were changed every 3 or 4 days and treatment was continued for 18.4 days on average (range, 11–29 days). Results: Exposed tendons and bone were successfully covered with healthy granulation tissue in all cases except one. The sizes of soft tissue defects reduced from 56.4 cm² to 42.9 cm² after NPWT (mean decrease of 24%). In 15 of the 16 cases, coverage with granulation tissue was achieved and followed by a skin graft. A free flap was needed to cover exposed bone and tendon in one case. No major complication occurred that was directly attributable to treatment. In terms of minor complications, two patients suffered scar contracture of grafted skin. Conclusion: NPWT was found to facilitate the rapid formation of healthy granulation tissue on open wounds in the foot and ankle region, and thus, to shorten healing time and minimize secondary soft tissue defect coverage procedures.