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Low‐Intensity Pulsed Ultrasound Accelerates Traumatic Vertebral Fracture Healing by Coupling Proliferation of Type H Microvessels
Author(s) -
Wu Suiyi,
Xu Ximing,
Sun Jingchuan,
Zhang Yao,
Shi Jiangang,
Xu Tianming
Publication year - 2018
Publication title -
journal of ultrasound in medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.574
H-Index - 91
eISSN - 1550-9613
pISSN - 0278-4297
DOI - 10.1002/jum.14525
Subject(s) - medicine , low intensity pulsed ultrasound , bone healing , intensity (physics) , x ray microtomography , ultrasound , anatomy , radiology , therapeutic ultrasound , physics , quantum mechanics
Objectives Patients with traumatic vertebral fractures often have major associated postoperative morbidities such as healing failure and kyphosis. Low‐intensity pulsed ultrasound (US) has been found to promote bone fracture healing. The objectives of our study were to determine whether low‐intensity pulsed US could promote traumatic vertebral fracture healing and to explore its inner mechanisms. Methods A rat model of traumatic vertebral fracture was created and treated with low‐intensity pulsed US after surgery. At 4 weeks after surgery, radiographic, micro‐computed tomography, and 3‐dimensional reconstruction were used to assess the radiologic healing status; a histologic analysis was performed to evaluate the pathologic process and relationship between osteogenesis and type H microvessels. Results Well‐remodeled trabecular meshworks were found in the low‐intensity pulsed US treatment group compared to the control group. Micro‐computed tomography and 3‐dimensional reconstruction revealed more and thicker trabeculae after low‐intensity pulsed US treatment. Abundant chondrocytes, a newly formed bone marrow cavity, trabeculae, and microvessels were formed at the fracture sites. More osterix‐positive osteoblasts were circling the newly formed bone meshwork and were situated at the interface of chondrocytes in the low‐intensity pulsed US treatment group. Type H microvessels were spreading around the newly formed trabecula, bone marrow cavity, osteoblasts, and interface of chondrocytes, with a larger mean vascular density in the low‐intensity pulsed US group. Conclusions Low‐intensity pulsed US could accelerate traumatic vertebral fracture healing by temporally and spatially increasing chondrogenesis and osteoblast‐induced osteogenesis coupled with angiogenesis of type H microvessels in a rat model of traumatic vertebral fracture.