The Studies On Pathogenicity Of Different FimA Genotype Porphyromonas Gingivalis

Porphyromonas gingivalis (P.gingivalis) is considered to be one of the mostimportant infectious agent causing chronic periodontitis. Several studies havedemostrated heterogenic virulence propertied among strains of P.gingivalis, theexpression of heterogenic virulence properties is dependent on its clonal diversity.Therefore the search for virulent strains of P.gingivalis and its pathogenesis will bemeaningful directions to prevent and treat periodontitis. Fimbriae are the majoradhension structure of P.gingivalis which possess massive biological activities. ThefimA gene encoding fimbriae has wide clonal variations, it has been classified intosix groups(Ⅰ～Ⅴto Ib) on the basis of nucleotide sequences of opening reading frame.Epidemical studies show that P.gingivalis strains withⅡfimA andⅣfimA wereclosely associated with the initiation and progression of periodontitis in Japaneseand chineses.while strains withⅠfimA were associated with health periodontalstatus,which indicated that specific fimA genotypes were associated with theinitiation and progression of periodontitis,therefore fimA gene may be the key factor different fimA genotype Porphyromonas gingivalis were On the beginning. In thisstudy,we compare the differences of MMP-8, MMP-9 which produced by differentfimA genotype P.gingivalis stimulate PMNs by ELISA from the protein level.Methods The studies maily adopt the isopycnic sedimentation Separation toseparate the PMN from human peripheral blood;which interact with the suspensionof different fimA genotype P.gingivalis,then collect the clear supematant after 5min,30min,1h,2h of reaction; eventually, we detect the contents of MMP-8,MMP-9 insupematant using ELISA.Results1.The ability of MMP-8,MMP-9 produced by standard strainsP.gingivalis ATCC33277 (ⅠfimA),W83 (ⅣfimA) and clinical isolatesⅡfimA,ⅢfimA,ⅣfimA P.gingivalis sitimulates PMN is significantly stronger than thecontrol group; Indicating that the tissue destructive enzyme produced by differentfimA genotype P.gingivalis stimulate PMNs may be one aspect of pathogenicity inperiodontal diseases.2.The velocity and quantity of MMP-8 produced by standard strain P.gingivalisW83 (ⅣfimA) and clinical isolateⅡfimA P.gingivalis stimulate PMN is more thanother bacteria, and the weakest bacterium is clinical isolateⅢfimAP.gingivalis.Indicating that the pathogenicity of P.gingivalis W83 (ⅣfimA) andclinical isolateⅡfimA P.gingivalis on production of MMP-8 is stronger than others.3. The quantity of MMP-9 produced by standard strain P.gingivalisATCC33277 (ⅠfimA), W83 (ⅣfimA) and clinical isolateⅡfimA P.gingivalisstimulate PMN is more than clinical isolateⅢfimA,ⅣfimA P.gingivalis.Indicatingthat the pathogenicity of clinical isolateⅡfimA P.gingivalis on production ofMMP-9 is stronger than other clinical isolates.However there is no significantdifferences during standard strain P.gingivalis ATCC33277 (ⅠfimA),W83 (ⅣfimA) and clinical isolateⅡfimA P.gingivalis.Maybe the pathogenicity ofstandard strains and clinical isolates is different;we need the correspondingcomparisons between them.Conclusion The tissue destructive enzyme MMP-8,MMP-9 produced bydifferent fimA genotype P.gingivalis stimulate PMNs may be one aspect ofpathogenicity in periodontal diseases. The pathogenicity of clinical isolateⅡfimAP.gingivalis on production of MMP-8,MMP-9 is stronger than other clinicalisolates. Based on these findings,we meed the corresponding comparisons betweenthe standard strains P.gingivalis and clinical isolates.