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下颌骨功能性后移位时大鼠颞下颌关节的改变。

Alterations of the rat temporomandibular joint in functional posterior displacement of the mandible.

作者信息

Cholasueksa Purisa, Warita Hiroyuki, Soma Kunimichi

机构信息

Orthodontic Science, Department of Orofacial Development and Function, Division of Oral Health Science, Graduate School, Tokyo Medical and Dental University, Tokyo, Japan.

出版信息

Angle Orthod. 2004 Oct;74(5):677-83. doi: 10.1043/0003-3219(2004)074<0677:AOTRTJ>2.0.CO;2.

Abstract

Functional malocclusion that induces posterior condylar displacement may affect the remodeling processes of the temporomandibular joint structures. We tested the hypothesis that intermittent posterior condylar displacement due to functional malocclusion traumatizes condylar cartilage and joint innervated nerve fibers. Thirty-nine eight-week-old Wistar rats were used. To induce functional posterior condylar displacement, guiding appliances were attached to maxillary incisors of 24 rats for four, seven, and 14 days. Fifteen normal rats served as controls. Sections were stained with hematoxylin and eosin or processed for immunohistochemistry of protein gene product 9.5 and growth-associated protein-43 (GAP-43). Functional posterior condylar displacement led to a diminution in proliferative cells, reduction in cartilage width, and re-expression of GAP-43-immunoreactive nerve fibers. These results indicate that intermittent posterior condylar displacement due to functional malocclusion causes dysfunctional remodeling of condylar cartilage and nerve injury.

摘要

导致髁突后移位的功能性错牙合可能会影响颞下颌关节结构的重塑过程。我们验证了这样一个假设,即功能性错牙合引起的间歇性髁突后移位会损伤髁突软骨和关节内的神经纤维。使用了39只8周龄的Wistar大鼠。为诱导功能性髁突后移位,给24只大鼠的上颌切牙安装引导装置,分别持续4天、7天和14天。15只正常大鼠作为对照。切片用苏木精和伊红染色,或进行蛋白基因产物9.5和生长相关蛋白43(GAP - 43)的免疫组织化学处理。功能性髁突后移位导致增殖细胞减少、软骨宽度减小以及GAP - 43免疫反应性神经纤维重新表达。这些结果表明,功能性错牙合引起的间歇性髁突后移位会导致髁突软骨功能失调性重塑和神经损伤。

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