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脑源性神经营养因子(BDNF)在下牙槽神经横断后牙周鲁菲尼终末再生中的作用。

The involvement of brain-derived neurotrophic factor (BDNF) in the regeneration of periodontal Ruffini endings following transection of the inferior alveolar nerve.

作者信息

Harada Fumiko, Hoshino Natalia, Hanada Kooji, Kawano Yoshiro, Atsumi Yukako, Wakisaka Satoshi, Maeda Takeyasu

机构信息

Division of Oral Anatomy, Department of Oral Biological Science, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan.

出版信息

Arch Histol Cytol. 2003 May;66(2):183-94. doi: 10.1679/aohc.66.183.

DOI:10.1679/aohc.66.183
PMID:12846558
Abstract

The present study employed immunohistochemistry for protein gene product 9.5 (PGP 9.5) to examine the regeneration process of Ruffini endings, the primary mechanoreceptor in the periodontal ligament, in heterozygous mice with targeted disruption of the brain-derived neurotrophic factor (BDNF) gene and their littermates, following transection of the inferior alveolar nerve. When immunostained for PGP 9.5, periodontal Ruffini endings appeared densely distributed in the periodontal ligament of the heterozygous mice, but the density of the positively stained nerve fibers in the ligament was 20% lower than that in the control littermates. At 3 days after surgery, the PGP 9.5-positive neural elements had disappeared; they began to appear in the periodontal ligament of both animals at 7 days. However, the recovery pattern of the PGP 9.5-positive nerves differed between heterozygous and wild type mice, typical periodontal Ruffini endings morphologically identical to those in the control group appeared in the wild-type mice at 7 days, whereas such Ruffini endings were detectable in the heterozygous mice at 28 days, though much smaller in number. On day 28, when PGP 9.5-positive nerves were largely regenerated in wild type mice, their distribution was much less dense in the ligament of the heterozygous mice than in the non-treated heterozygous mice. The density of PGP 9.5-positive nerve fibers was significantly lower in the heterozygous mice than in wild type mice at any stage examined. These data showing that a reduced expression of BDNF causes delayed regeneration of the periodontal Ruffini endings suggest the involvement of BDNF in the regeneration process of these mechanoreceptors.

摘要

本研究采用免疫组织化学方法检测蛋白基因产物9.5(PGP 9.5),以观察在脑源性神经营养因子(BDNF)基因靶向破坏的杂合小鼠及其同窝对照小鼠中,切断下牙槽神经后牙周膜主要机械感受器鲁菲尼终末的再生过程。用PGP 9.5进行免疫染色时,牙周鲁菲尼终末在杂合小鼠的牙周膜中呈密集分布,但该韧带中阳性染色神经纤维的密度比对照同窝小鼠低20%。术后3天,PGP 9.5阳性神经元消失;术后7天,二者的牙周膜中均开始出现PGP 9.5阳性神经元。然而,杂合小鼠和野生型小鼠中PGP 9.5阳性神经的恢复模式不同,野生型小鼠在术后7天出现形态上与对照组相同的典型牙周鲁菲尼终末,而杂合小鼠在术后28天才能检测到此类鲁菲尼终末,但其数量要少得多。在术后28天,当野生型小鼠中PGP 9.5阳性神经大量再生时,其在杂合小鼠韧带中的分布密度远低于未处理的杂合小鼠。在任何检测阶段,杂合小鼠中PGP 9.5阳性神经纤维的密度均显著低于野生型小鼠。这些数据表明BDNF表达降低会导致牙周鲁菲尼终末再生延迟,提示BDNF参与了这些机械感受器的再生过程。

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