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目的:通过大鼠体内实验探讨种植体-基台界面细菌微渗漏现象以及软组织炎症情况。方法:无菌条件下在定制的种植体内部加入0.25 μl牙龈卟啉单胞菌（n Porphyromonas gingivalis，Pg）悬液（10n 9 CFU/ml），连接基台后置于含1 ml培养液的Ep（eppendorf）管中培养，7和14 d后取样接种于培养基，厌氧条件下继续培养，观察细菌生长情况。选用雄性SD大鼠6只，拔除上颌双侧第一磨牙1个月后分别于各拔牙窝内植入1枚种植体，分为空白对照组、阴性对照组和实验组（每组各4枚）。黏膜下愈合1个月后进行二期手术，清洁种植体内部后，实验组种植体内部加入0.25 μl Pg悬液（10n 9 CFU/ml），阴性对照组加入0.25 μl牛脑心浸液，空白对照组不加任何材料，各组均连接消毒后的穿龈基台。二期手术后28 d取样，实时荧光定量PCR检测各组种植体内细菌总量和Pg数量，对种植体周围黏膜的炎性渗出特征进行组织学观察和定量分析。n 结果:培养7和14 d后取样接种的培养基上均可见Pg生长。实验组种植体内部Pg的拷贝数为10n 2~10n 4，阴性对照组和空白对照组均未检测到Pg。同时，光学显微镜下可见实验组种植体微间隙周围结缔组织内存在炎性细胞聚集，从微间隙处向冠方和根方炎性细胞密度逐渐减少，而空白对照组和阴性对照组种植体周围结缔组织中仅存在散在炎性细胞。实验组冠方0.25~0.50 mm区域、冠方0.25 mm至微间隙处、微间隙处至根方0.25 mm区域、根方0.25~0.50 mm区域炎性细胞密度[中位数（四分位数间距）]分别为976（655）、1 673（1 245）、2 267（819）和895（162）个/mmn 2，均显著多于空白对照组相应位置[分别为201（180）、321（351）、309（236）和218（272）个/mmn 2]（n P<0.05）。n 结论:大鼠口腔种植体内部的Pg可发生微渗漏，引起种植体周围软组织炎性渗出，且该炎性渗出的分布具有一定特征。“,”Objective:To study the bacterial microleakage at the interface between dental implant and abutment in rats.Methods:Under aseptic conditions, suspension of 0.25 μl of n Porphyromonas gingivalis (Pg) (10n 9 CFU/ml) was added into the customized implant. After the abutment was connected, the suspension was cultured in an Ep (eppendorf) tube containing 1 ml brain heart infusion (BHI) culture medium. After 7 days and 14 days, the liquid in the Ep tube was taken and inoculated, and the growth of bacteria was observed. Six male SD rats with 12 implants were divided into experimental group (4 implants), negative control group (4 implants) and blank control group (4 implants). All 6 rats had two implants implanted in their bilateral upper jaws. During the second operation, suspension of 0.25 μl Pg (10 n 9 CFU/ml) was added to the inner part of the implant of the experimental group, culture solution of 0.25 μl was added to the control group and nothing was added to the blank control group. The amount of Pg and total bacteria in each group were evaluated by quantitative real-time PCR (qPCR). The inflammatory cell infiltrate in the peri-implant mucosa was evaluated histomorphometrically.n Results:The n in vitro model directly verified the presence of bacterial microleakage at implant-abutment interface (IAI), and the animal model confirmed the existence of microleakage through the infiltrate of inflammatory cells near the micro-gap in the experimental group indirectly. n In vitro experiments found that Pg had penetrated from the implant within a week by observation and culture. In animal study, the presence of 10n 2-10n 4 Pg was detected in the experimental group and it was not detected in the negative control group and the blank control group. At the same time, under the light microscope, in the experimental group, there were inflammatory cells aggregation in the connective tissue around the micro-gap and the density of inflammatory cells gradually decreased from the micro-gap to coronal and the apical of the connective tissue, while there were only scattered inflammatory cells in the connective tissue around the blank control group and the negative control group. In the experimental group, inflammatory cells density in area of 0.25-0.50 mm, 0-0.25 mm coronal to the micro-gap and 0-0.25 mm, 0.25-0.50 mm apical to the mico-gap was respectively, 976 (655), 1 673 (1 245), 2 267 (819) and 895 (162) cells/mmn 2,which was significantly more than the blank control group in the corresponding position [respectively 201 (180), 321 (351), 309 (236) and 218 (272) cells/mmn 2] (n P<0.05).n Conclusions:Pg in the dental implants of rats can be found in the microleakage through implant-abutment interface, and cause the soft tissue inflammation around the implant, and the inflammation has certain distribution characteristics.