牙周病与免疫VIP免费

五、牙周病与免疫Theoralcavityharborsmorethan700bacterialspecies,coexistingwithprobablymillionsofviralgenomiccopies.口腔定居的细菌有700多种与数百万病毒基因组复制物共存（ATsuoAmano,2010,Periodontology2000）Oralbacteria口腔中的细菌：--Freetosaliva在唾液中--Attachmentinbiofilm附着在生物膜BetweencloselyrelatedSalivaasacarrier,isconducivetohorizontalandverticaltransmissionofbacteriaInUnitedStates,75percentofadultpopulationssufferfromperiodontaldisease.美国占75%成年人群体不同程度患有牙周病1/3childrenof6~11yearsold,and2/3ofadolescentpopulationhavesomedegreeofperiodontalproblems.1/3的6~11岁儿童，2/3青春期人群也有某种程度的牙周问题Over200kindsofbacterialformdentalplaque,adheretothesurfaceoftheteethandgums,andcauseperiodontalinfections.牙周感染细菌达200余种PeriodontitisⅠGingivitisbleeding，DeepgingivalPocket<3mmⅡPeriodontitisbleeding，swelling，initialboneloss,DeepperiodontalPocket=5mmⅢmajorstagebleeding，swelling，majorboneloss，DeepperiodontalPocket＞6mmPeriodontalPocket:auniquemicro-environment牙周袋是独特的微环境escapethephysicalseparationforce逃逸物理分离力hardtissuesurface不剥脱更新的硬组织表面junctionalepithelialization,basicallynotdifferentiation有结合上皮，基本上不分化non-keratinizingepithelium无角化facultativeanaerobic→anaerobic兼性厌氧→厌氧nutrition,humidity,pH,Eh营养、湿度、pH、Eh龈下细菌附着和聚集模式图RootsurfacePellicleP.gP.gP.gP.gP.gSubgingivalbiofilmformation龈下生物膜形成Initialcolonization早期定居者：actinomyces,streptococcisucceededcolonization微生物交替后：periodontalpathogens致病微生物定植Pg，AA,forsythia,T.denticoleFusobacteriumnucleatum1996confirmedthreebacteriaforperiodontalpathogens:Actinobacillusactinomycetemcomitans(AA)Tannerellaforsythia(TF)Porphyromonasgingivalis(Pg)1996,牙周致病菌AA，TF，PgRecentviewschange,pathogeniccapacityofAAandotherculturableornon-culturablebacteriashouldbeconfirmed.近期：AA待证实50%oralmicrobialcannotbecultivatedandcanbeidentifiedthroughextramethods:口腔中有50%微生物不能培养，可通过下述方法鉴定：quantitativeRT-PCR定量PCRphylogenetic16s-rRNAgeneclonelibraryanalysis用基因组或16srRNA探针checkerboardhybridization棋盘杂交high-throughputfingerprinttechnology高通量指纹技术pyrophosphatesequencing454技术（焦磷酸盐测序）metagenometechnology宏基因组技术Generalview:PeriodontitisiscausedbyendogenousG-periodontalbacteria.目前普遍认为：牙周炎是由内源性G-牙周细菌所致Redcomplex:Porphyromonasgingivalis牙龈卟啉菌Tannerellaforsythia弗赛菌Treponemadenticola齿密螺旋体Potentialvirulencefactors潜在毒力因子Neutralizationforlocalhostdefensemechanisms中和局部宿主防御机制Destructionofperiodontaltissue破坏牙周组织P.Gingivalis牙龈卟啉菌G-厌氧、杆状、繖附着、与红色菌群共同构成生物膜adheretohostcells（integrins）通过整合素附着Secretoryproteinase分泌蛋白溶解酶、破坏牙龈附着Afterinvasion,associationwiththechangeofintracellularsignalingpathways入侵后改变信号通路分泌脂多糖，是细菌内毒素的主要成分畸形血管生成Tannerellaforsythia弗赛菌厌氧G-菌，cytophaga-BacteroidetesfamilyNewpathogensthrough16srRNAdetection16srRNA检测分泌富含亮氨酸的重复蛋白（leucine-rich-repeatprotein,BSPA）,使细菌容易附着，是重要的毒力因子启动单核细胞释放炎症细胞因子，成骨细胞释放趋化因子，导致炎症和骨吸收G-口腔螺旋体家族，绝对厌氧，纤细、螺旋、能动、可弯曲Virulencefactors毒力因子——内毒素Accumulationingingivalpocket,usinga...