Kajita K, Honda T, Amanuma R, Domon H, Okui T, Ito H, Yoshie H, Tabeta K, Nakajima T, Yamazaki K
Laboratory of Periodontology and Immunology, Department of Oral Health and Welfare, Niigata University Faculty of Dentistry, Niigata, Japan.
Oral Microbiol Immunol. 2007 Dec;22(6):398-402. doi: 10.1111/j.1399-302X.2007.00377.x.
In addition to bacteria, viruses have been reportedly implicated in periodontitis. However, the available data are confined to Toll-like receptor 2 (TLR2) and TLR4, which recognize bacterial products in periodontitis. In the present study, we investigated the expression levels of TLR5, -7, and -9 messenger RNAs (mRNAs) in addition to those of TLR2 and -4, and compared gingivitis and periodontitis. Interferon-alpha1 (IFN-alpha1), which is important for the antiviral response, was also compared.
Gene expression was analyzed using quantitative real-time polymerase chain reaction for 59 periodontitis and 27 gingivitis tissue samples together with viral serology in some patients. The presence of plasmacytoid dendritic cells (pDCs), a robust producer of IFN-alpha, was immunohistochemically analyzed in an additional seven periodontitis and two gingivitis specimens.
The expression levels of TLR2, -4, -7, and -9 were significantly higher in periodontitis lesions than gingivitis lesions. The expression level of TLR5 was comparable to levels of TLR2 and -4; however, no significant difference was found between gingivitis and periodontitis. Although the expression of IFN-alpha1 mRNA was higher in periodontitis lesions compared with gingivitis lesions, the level was quite low. Only a few pDCs were found in some periodontitis specimens. No difference was found for antibody-positivity between gingivitis and periodontitis.
This is the first study to show that a variety of TLRs are up-regulated in periodontitis lesions compared with gingivitis lesions, suggesting that diverse microbial and possibly viral antigens are involved in the pathogenic mechanisms for periodontal diseases. However, the ligands recognized by the various TLRs in periodontal lesions remain to be determined.
据报道,除细菌外,病毒也与牙周炎有关。然而,现有数据仅限于在牙周炎中识别细菌产物的Toll样受体2(TLR2)和TLR4。在本研究中,我们除了研究TLR2和TLR4的信使核糖核酸(mRNA)表达水平外,还研究了TLR5、TLR7和TLR9的表达水平,并比较了牙龈炎和牙周炎。还比较了对抗病毒反应很重要的α1干扰素(IFN-α1)。
使用定量实时聚合酶链反应分析59例牙周炎和27例牙龈炎组织样本的基因表达,并对部分患者进行病毒血清学检测。另外,对7例牙周炎和2例牙龈炎标本进行免疫组织化学分析,检测浆细胞样树突状细胞(pDC)(一种强大的IFN-α产生细胞)的存在情况。
牙周炎病变中TLR2、TLR4、TLR7和TLR9的表达水平明显高于牙龈炎病变。TLR5的表达水平与TLR2和TLR4的水平相当;然而,牙龈炎和牙周炎之间未发现显著差异。虽然牙周炎病变中IFN-α1 mRNA的表达高于牙龈炎病变,但其水平相当低。在一些牙周炎标本中仅发现少数pDC。牙龈炎和牙周炎之间的抗体阳性率没有差异。
这是第一项表明与牙龈炎病变相比,多种Toll样受体在牙周炎病变中上调的研究,提示多种微生物以及可能的病毒抗原参与了牙周疾病的致病机制。然而,牙周病变中各种Toll样受体识别的配体仍有待确定。