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骨形态发生蛋白2在小儿颅骨缺损自行修复中的作用

Role of bone morphogenetic protein 2 in self-repair of pediatric cranial defects
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摘要 颅脑外伤在小儿各类外伤中占据首位。去骨瓣减压术为神经外科常见减少颅内压的手术方式,颅骨缺失会导致患儿脑组织缺少颅骨保护,颅骨作为脑组织最直接的保护屏障,若缺损不及时修补会因体位、情绪和腹压等会导致脑组织在颅内发生移动,从而造成脑穿通性畸形、癫痫发作和脑变性萎缩等疾病。小儿有好动、依从性差、自我保护能力差等特点,更容易形成二次伤害。小儿处于生长发育期,缺乏颅骨的保护,颅脑容易受到二次伤害,还会影响患儿神经系统的正常发育,造成患儿智力低下,神经系统发育不完善等相关并发症,所以重建颅骨的完整对患儿的生长发育至关重要。未成熟硬脑膜对颅骨的发育和缺损修复有重要作用,2岁以下的儿童能够修复巨大的颅骨缺损,而成年人则缺乏这种内源性能力。幼龄动物骨缺损中骨形态发生蛋白2(BMP2)上调,表明BMP2在骨组织再生中具有重要作用。许多生物调节因子可调控BMP2的活性。该综述就BMP2在小儿颅骨缺损修复中的研究现状做总结。 Craniocerebral trauma ranks first among all types of pediatric trauma.decompressive craniectomy is a common neurosurgical procedure to reduce intracranial pressure,and cranial bone loss will lead to a lack of cranial protection of brain tissue in children.The skull is the most direct protective barrier for brain tissue,and if the cranial defect is not repaired in a timely manner, movement of brain tissue in the skull may be caused by the factors such as body position,emotion, and abdominal pressure, thereby resulting in the disorders including brain penetrating malformations, epilepticseizures, and cerebral degeneration and atrophy. The active personality, poor compliance, and poor self-protection ofchildren may lead to secondary injuries. During the growth and development of children, the lack of cranial protectionmakes the skull vulnerable to secondary injuries and may affect the normal development of nervous system, resulting inmental retardation, poor development of the nervous system, and other related complications, and therefore, reconstructionof the integrity of the skull is essential for the growth and development of the child. The immature dura mater plays animportant role in cranial development and defect repair, and children within 2 years of age are capable of repairing largecranial defects, whereas adults lack such endogenous ability. Bone morphogenetic protein 2 (BMP2) is significantlyupregulated in bone defects in young animals, suggesting that BMP2 plays an important role in bone tissue regeneration.Many biological regulatory factors can modulate the activity of BMP2. This article reviews the current research status ofBMP2 in cranial defect repair in children.
作者 李政堂 郭雅鑫 邵国 张春阳 LI Zhengtang;GUO Yaxin;SHAO Guo;ZHANG Chunyang(Baotou Medical College,Inner Mongolia University of Science and Technology,Baotou,Inner Mongolia 014010,China;Department of Rehabilitation,Inner Mongolia Ordos Central Hospital,Ordos,Inner Mongolia 017000,China;Department of Neurosurgery,The First Affiliated Hospital of Baotou Medical College,Inner Mongolia University of Science and Technology,Baotou,Inner Mongolia 014010,China;Institute of Neurosurgical Diseases(Translational Medicine),Baotou Medical College,Baotou,Inner Mongolia 014010,China;Engineering and Technology Centre for Bone Tissue Regeneration and Damage Repair,Inner Mongolia Autonomous Region,Baotou,Inner Mongolia 014010,China;Centre for Translational Medicine,The Third People’s Hospital of Longgang District,Shenzhen,Guangdong 518100,China)
出处 《国际神经病学神经外科学杂志》 2024年第2期85-90,共6页 Journal of International Neurology and Neurosurgery
基金 国家自然科学基金(82160250、81960238) 国家临床重点专科建设项目经费资助。
关键词 颅骨 缺损修复 骨形态发生蛋白2 硬脑膜 skull defect repair bone morphogenetic protein 2 dura mater
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