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咬合过深刺激牙周膜中 XII 型胶原蛋白的表达。

Hyperocclusion stimulates the expression of collagen type XII in periodontal ligament.

作者信息

Tsuzuki Takashi, Kajiya Hiroshi, T-Goto Kazuko, Tsutsumi Takashi, Nemoto Tetsuomi, Okabe Koji, Takahashi Yutaka

机构信息

Department of Oral Rehabilitation, Fukuoka Dental College, Fukuoka 8140193, Japan.

Department of Physiological Science and Molecular Biology, Fukuoka Dental College, Fukuoka 8140193, Japan.

出版信息

Arch Oral Biol. 2016 Jun;66:86-91. doi: 10.1016/j.archoralbio.2016.02.009. Epub 2016 Feb 18.

Abstract

OBJECTIVES

It is known that excessive mechanical force exerted by hyperocclusion induces occlusal trauma. However, the mechanism of the process remains unclear. In the present study, we employed an in vivo hyperocclusion rodent model to examine morphological and biological mechanisms of occlusal trauma in periodontal ligament tissue.

DESIGN

To investigate alveolar bone resorption, tooth sections were stained to detect osteoclasts. To investigate the relationship between hyperocclusion and the regeneration of the cell matrix, we examined the effect of hyperocclusal force on the expression of collagens using immunohistochemistry and quantitative PCR methods.

RESULTS

The arrangement of collagen fibers in the furcation area of the teeth was undisturbed before hyperocclusion (control). Type I collagen was localized in the extracellular area at the furcation and there was faint expression and localization of type XII collagen in the periodontal ligament. The number of osteoclasts significantly increased in the furcation and lingual cervical regions on day 4 after hyperocclusion was induced. Type XII collagens were gradually up-regulated following the induction of hyperocclusion, in a time-dependent manner. Although type I collagen mRNA expression was stable before and after hyperocclusion, type XII collagen mRNA was significantly up-regulated on day 2 and day 4 after hyperocclusion treatment.

CONCLUSIONS

Our findings indicate that hyperocclusal force predominantly up-regulates the expression of type XII collagen in periodontal tissue, but not type I collagen, suggesting that there is a mechanism for regeneration of periodontal tissues as a response to occlusal trauma.

摘要

目的

已知咬合过深所施加的过度机械力会诱发咬合创伤。然而,该过程的机制仍不清楚。在本研究中,我们采用体内咬合过深啮齿动物模型来研究牙周韧带组织中咬合创伤的形态学和生物学机制。

设计

为了研究牙槽骨吸收情况,对牙齿切片进行染色以检测破骨细胞。为了研究咬合过深与细胞基质再生之间的关系,我们使用免疫组织化学和定量PCR方法检测咬合过深力对胶原蛋白表达的影响。

结果

在咬合过深(对照)之前,牙齿分叉区的胶原纤维排列未受干扰。I型胶原定位于分叉处的细胞外区域,牙周韧带中XII型胶原表达微弱且定位不明显。在诱导咬合过深后第4天,分叉区和舌侧颈部区域的破骨细胞数量显著增加。诱导咬合过深后,XII型胶原呈时间依赖性逐渐上调。尽管咬合过深前后I型胶原mRNA表达稳定,但在咬合过深处理后第2天和第4天,XII型胶原mRNA显著上调。

结论

我们的研究结果表明,咬合过深力主要上调牙周组织中XII型胶原的表达,而非I型胶原,这表明存在一种牙周组织对咬合创伤作出反应的再生机制。

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