Department of Periodontology, School of Dental Medicine, University of Bern, Bern, SwitzerlandPrince Philip Dental Hospital, The University of Hong Kong, Hong Kong SAR PR China.
Clin Oral Implants Res. 2012 Feb;23(2):182-190. doi: 10.1111/j.1600-0501.2011.02220.x. Epub 2011 Aug 2.
To monitor clinical, microbiological and host-derived alterations occurring around teeth and titanium implants during the development of experimental gingivitis/mucositis and their respective healing sequence in humans.
Fifteen subjects with healthy or treated periodontal conditions and restored with dental implants underwent an experimental 3-week period of undisturbed plaque accumulation in the mandible. Subsequently, a 3-week period with optimal plaque control was instituted. At Days 0, 7, 14, 21, 28, 35 and 42, the presence/absence of plaque deposits around teeth and implants was assessed, (plaque index [PlI]) and the gingival/mucosal conditions were evaluated (gingival index[GI]). Subgingival/submucosal plaque samples and gingival/mucosal crevicular fluid (CF) samples were collected from two pre-determined sites around each experimental unit. CF samples were analyzed for matrix-metalloproteinase-8 (MMP-8) and interleukin-1beta (IL-1β). Microbial samples were analyzed using DNA-DNA hybridization for 40 species.
During 3 weeks of plaque accumulation, the median PlI and GI increased significantly at implants and teeth. Implant sites yielded a greater increase in the median GI compared with tooth sites. Over the 6-week experimental period, the CF levels of MMP-8 were statistically significantly higher at implants compared with teeth (P<0.05). The CF IL-1β levels did not differ statistically significantly between teeth and implants (P>0.05). No differences in the total DNA counts between implant and tooth sites were found at any time points. No differences in the detection frequency were found for putative periodontal pathogens between implant and tooth sites.
Peri-implant soft tissues developed a stronger inflammatory response to experimental plaque accumulation when compared with that of their gingival counterparts. Experimental gingivitis and peri-implant mucositis were reversible at the biomarker level. Clinically, however, 3 weeks of resumed plaque control did not yield pre-experimental levels of gingival and peri-implant mucosal health indicating that longer healing periods are needed.
监测在实验性牙龈炎/黏膜炎发展过程中牙齿和钛种植体周围出现的临床、微生物和宿主来源的变化，以及人类相应的愈合顺序。
15 名具有健康或牙周治疗条件且植入物修复的受试者在下颌进行了为期 3 周的未经干扰的菌斑积累实验。随后，进行了为期 3 周的最佳菌斑控制。在第 0、7、14、21、28、35 和 42 天，评估牙齿和种植体周围菌斑沉积的存在/不存在情况，（菌斑指数[PlI]）和牙龈/黏膜状况进行评估（牙龈指数[GI]）。从每个实验单位的两个预定部位采集龈下/黏膜下菌斑样本和牙龈/黏膜沟液（CF）样本。CF 样本用于分析基质金属蛋白酶-8（MMP-8）和白细胞介素-1β（IL-1β）。使用 DNA-DNA 杂交技术分析微生物样本，以确定 40 个种。
在 3 周的菌斑积累期间，种植体和牙齿的 PlI 和 GI 中位数显著增加。与牙齿部位相比，种植体部位的 GI 中位数增加更大。在 6 周的实验期间，CF 中 MMP-8 的水平在种植体部位显著高于牙齿部位（P<0.05）。CF 中 IL-1β 的水平在牙齿和种植体部位之间没有统计学上的显著差异（P>0.05）。在任何时间点，种植体和牙齿部位之间的总 DNA 计数均无差异。在种植体和牙齿部位之间，未发现假定的牙周病原体的检测频率存在差异。
与牙龈相比，种植体周围软组织对实验性菌斑积累表现出更强的炎症反应。在生物标志物水平上，实验性牙龈炎和种植体周围黏膜炎是可逆的。然而，临床上，经过 3 周的重新控制菌斑，并没有恢复到实验前的牙龈和种植体黏膜健康水平，这表明需要更长的愈合时间。
