Ricardo Lucilene Hernandes, do Prado Renata Falchete, Carvalho Yasmin Rodarte, da Silva Peralta Felipe, Pallos Debora
Periodontics Department, Department of Dentistry of Universiy of Taubaté, Taubaté, SP, Brazil.
Departament of Oral Biopathology of Institute of Science and Tecnology, São Paulo State University, São José Dos Campos, SP, Brazil.
J Oral Biol Craniofac Res. 2019 Jan-Mar;9(1):86-90. doi: 10.1016/j.jobcr.2018.10.004. Epub 2018 Oct 22.
The most important microscopic characteristic of Cyclosporine A-induced gingival overgrowth is fibroepithelial hyperplasia.
The objective was to investigate the influence of previous exposure to Cyclosporine A over gingival epithelium in experimental periodontitis in rats.
Twenty Wistar rats with 12 weeks-old were divided into four groups with 5 animals each: Control Group (CG); Cyclosporine Group (CsAG); Ligature group (LG) and Cyclosporine and Ligature Group (CsALG). Daily doses of CsA (10 mg/kg) were applied to CsAG and CsALG during 60 days since the beginning of the experiment and, a ligature was placed in LG and CsALG 30 days after the beginning of the experiment. After 60 days, animals were euthanized and gingival tissue was processed to histomorphometric analysis of epithelial thickness (mm), immunohistochemical expression of PCNA (%) and inflammatory response. Data were analyzed by Kruskal-Wallis and Mann Whitney at 0.05 significance level.
Considering epithelial thickness, CG was thinner than all groups, CsALG was the largest and CsAG and LG were similar between each other. Regarding the PCNA expression CG (16.46 ± 9.26) was similar to CsAG (34.47 ± 19.75) and, LG (59.02 ± 10.33) was similar to CsALG (40.59 ± 18.25). Significant difference (p < 0.05) occurred only in inflammation presence comparing CG/LG and CsAG/CsALG. A weak positive correlation between the number of PCNA+ and inflammatory cells (p = 0.001; r = 0.611) was observed.
Based on these results it was concluded that the enlargement of gingival epithelium observed in experimental periodontitis can be increased by previous exposition to CsA and inflammatory conditions enhanced proliferative activity of the keratinocytes.
环孢素A诱导的牙龈增生最重要的微观特征是纤维上皮增生。
研究既往接触环孢素A对大鼠实验性牙周炎牙龈上皮的影响。
将20只12周龄的Wistar大鼠分为四组,每组5只:对照组(CG);环孢素组(CsAG);结扎组(LG)和环孢素与结扎组(CsALG)。自实验开始后60天内,每天给CsAG和CsALG应用环孢素A(10mg/kg),实验开始30天后,在LG和CsALG中放置结扎线。60天后,对动物实施安乐死,并对牙龈组织进行处理,以进行上皮厚度(mm)的组织形态计量分析、PCNA免疫组化表达(%)和炎症反应分析。数据采用Kruskal-Wallis和Mann Whitney检验进行分析,显著性水平为0.05。
就上皮厚度而言,CG比所有组都薄,CsALG最大,CsAG和LG彼此相似。关于PCNA表达,CG(16.46±9.26)与CsAG(34.47±19.75)相似,LG(59.02±10.33)与CsALG(40.59±18.25)相似。仅在比较CG/LG和CsAG/CsALG的炎症存在情况时出现显著差异(p<0.05)。观察到PCNA+细胞数量与炎症细胞之间存在弱正相关(p = 0.001;r = 0.611)。
基于这些结果得出结论,实验性牙周炎中观察到的牙龈上皮增大可因先前接触环孢素A而增加,且炎症状况增强了角质形成细胞的增殖活性。