Pöllänen M T, Overman D O, Salonen J I
Department of Periodontology, University of Turku, Finland.
J Periodontal Res. 1997 Apr;32(3):326-34. doi: 10.1111/j.1600-0765.1997.tb00541.x.
The structural and functional barrier preventing the free advancement of microbial plaque subgingivally along the tooth surface is formed by the junctional epithelial (JE) cells directly attached to the tooth (DAT cells). The mechanism leading to degeneration of the DAT cells is not known. In the present study we examined the possible role of short chain fatty acids (SCFAs) on epithelial cells by making use of 2 epithelial cell cultures (HaCaT and ERM) and an explant culture model of human JE. The SCFAs butyrate and propionate were used in concentrations found in human plaque and gingival crevicular fluid (0.25-16.0 mM). The SCFAs had no effect on primary cell adhesion nor on the epithelial attachment apparatus (EAA). By contrast, even 0.25 mM of butyrate significantly retarded epithelial cell growth. Similar effects with propionate were first observed at concentrations higher than 1.0 mM. The retardation of epithelial cell growth was found to be due to inhibition of cell division. Furthermore, after butyrate treatment dense accumulations of intermediate filaments and cytoplasmic vacuolization were characteristically seen in cells adjacent to cells of normal appearance. This suggests that some cells of the growing epithelial cell population are more sensitive to the SCFAs than others, and agrees with previous reports on the DAT cells of periodontally-involved teeth in vivo. The results suggest that SCFAs are microbial factors that play a role in the initiation and progression of periodontal pocket formation by impairing epithelial cell function rather than having a direct effect on the EAA.
防止微生物菌斑沿牙面在龈下自由进展的结构和功能屏障是由直接附着于牙齿的结合上皮（JE）细胞（DAT细胞）形成的。导致DAT细胞退变的机制尚不清楚。在本研究中，我们利用两种上皮细胞培养物（HaCaT和ERM）以及人JE的外植体培养模型，研究了短链脂肪酸（SCFA）对上皮细胞的可能作用。使用了在人菌斑和龈沟液中发现的浓度的SCFA丁酸和丙酸（0.25 - 16.0 mM）。SCFA对原代细胞黏附以及上皮附着装置（EAA）均无影响。相比之下，即使是0.25 mM的丁酸也能显著延缓上皮细胞生长。丙酸在浓度高于1.0 mM时首次观察到类似作用。发现上皮细胞生长的延缓是由于细胞分裂受到抑制。此外，在丁酸处理后，在外观正常的细胞相邻的细胞中典型地观察到中间丝的密集聚集和细胞质空泡化。这表明生长中的上皮细胞群体中的一些细胞比其他细胞对SCFA更敏感，这与先前关于体内牙周受累牙齿的DAT细胞的报道一致。结果表明，SCFA是微生物因子，通过损害上皮细胞功能而非直接作用于EAA，在牙周袋形成的起始和进展中发挥作用。
