Yu Z, Feng Y, Kong H, Xiao Y, Li Y, Wang J, Cao Y Z, Li D H
Department of Oral Implants, School of Stomatology, The Fourth Military Medical University & State Key Laboratory of Military Stomatology & National Clinical Research Center for Oral Diseases & Shaanxi Engineering Research Center for Dental Materials and Advanced Manufacture, Xi'an 710032, China.
Department of Operative Dentistry and Endodontics, School of Stomatology, The Fourth Military Medical University & State Key Laboratory of Military Stomatology & National Clinical Research Center for Oral Diseases & Shaanxi Key Laboratory of Stomatology, Xi'an 710032, China.
Zhonghua Kou Qiang Yi Xue Za Zhi. 2020 May 9;55(5):337-342. doi: 10.3760/cma.j.cn112144-20191203-00434.
To study the bacterial microleakage at the interface between dental implant and abutment in rats. Under aseptic conditions, suspension of 0.25 μl of (Pg) (10(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(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. The 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. experiments found that Pg had penetrated from the implant within a week by observation and culture. In animal study, the presence of 10(2)-10(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/mm(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/mm(2)] (0.05). 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.
研究大鼠牙种植体与基台界面的细菌微渗漏情况。在无菌条件下，将0.25 μl牙龈卟啉单胞菌（Pg）（10⁹ CFU/ml）悬液加入定制种植体中。连接基台后，将悬液置于含1 ml脑心浸液（BHI）培养基的微量离心管（Ep管）中培养。7天和14天后，取Ep管中的液体进行接种，观察细菌生长情况。选取6只雄性SD大鼠，植入12枚种植体，分为实验组（4枚种植体）、阴性对照组（4枚种植体）和空白对照组（4枚种植体）。6只大鼠双侧上颌各植入2枚种植体。在第二次手术时，向实验组种植体内加入0.25 μl Pg（10⁹ CFU/ml）悬液，向对照组加入0.25 μl培养液，空白对照组不添加任何物质。采用实时定量聚合酶链反应（qPCR）评估各组Pg和总细菌数量。通过组织形态计量学评估种植体周围黏膜的炎性细胞浸润情况。该模型直接证实了种植体-基台界面（IAI）存在细菌微渗漏，动物模型通过实验组微间隙附近炎性细胞浸润间接证实了微渗漏的存在。通过观察和培养发现，Pg在一周内已从种植体中穿出。在动物研究中，实验组检测到10² - 10⁴个Pg，阴性对照组和空白对照组未检测到。同时，在光镜下，实验组微间隙周围结缔组织中有炎性细胞聚集，且炎性细胞密度从微间隙向结缔组织冠方和根方逐渐降低，而空白对照组和阴性对照组结缔组织中仅有散在炎性细胞。实验组在微间隙冠方0.25 - 0.50 mm、0 - 0.25 mm区域以及微间隙根方0 - 0.25 mm、0.25 - 0.50 mm区域的炎性细胞密度分别为976（655）、1673（1245）、2267（819）和895（162）个细胞/mm²，显著高于相应位置的空白对照组[分别为201（180）、321（351）、309（236）和218（272）个细胞/mm²]（P < 0.05）。大鼠牙种植体中的Pg可通过种植体-基台界面微渗漏进入，引起种植体周围软组织炎症，且炎症具有一定的分布特征。
