Short
term
effects
of
non-surgical
periodontal
treatment
on
gingival
crevicular
fluid
levels
of
tissue
plasminogen
activator
(t-PA)
and
plasminogen
activator
inhibitor
2
(PAI-2)
in
patients
with
chronic
and
aggressive
periodontitis
§
Gu¨lay
Tu¨ter
a,*
,
Burcu
O¨zdemir
a,
Bu¨lent
Kurtis¸
a,
Muhittin
Serdar
b,
Ays¸egu¨l
Atak
Yu¨cel
c,
Eylem
Ayhan
aaGaziUniversity,FacultyofDentistry,DepartmentofPeriodontology,Ankara,Turkey bGu¨lhaneMilitaryMedicalAcademy,DepartmentofBiochemistry,Ankara,Turkey cGaziUniversity,FacultyofMedicine,DepartmentofImmunology,Ankara,Turkey
1.
Introduction
Plasminogen activatorsystemplays acrucial roleinmany physiological processes, including tissue remodelling, cell migration,woundhealingangiogenesis,aswellas pathologi-caleventssuchasacuteandchronicinflammatoryreactions, tumourinvasionandmetastasis.1Proenzymeplasminogenis
convertedtoactiveplasminbyplasminogenactivatorsystem which is regulated by protease activators, tissue type plasminogenactivator(t-PA)andurokinasetypeplasminogen activator (u-PA)and theirinhibitors, plasminogenactivator inhibitors1(PAI-1)and2(PAI-2).2
Plasmins actas proinflammatory agentsas theyinduce neutrophilaggregation,plateletdegranulation,synthesesand secretion of arachidonic acid derivates and stimulate the
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Articlehistory:
Accepted10August2012
Keywords:
Tissueplasminogenactivator Plasminogenactivatorinhibitor2 Periodontaldiseases
Gingivalcrevicularfluid
a
b
s
t
r
a
c
t
Objective: Thepurposeofthisstudywastoevaluatethegingivalcrevicularfluid(GCF)levels
oftissuetypeplasminogenactivator(t-PA)andplasminogenactivatorinhibitor2(PAI-2)in aggressiveperiodontitis(AgP),chronicperiodontitis(CP)andperiodontallyhealthycontrol subjects,before(BT)andafter(AT)thenon-surgicalperiodontaltreatment.
Design: Systemicallyhealthy12CPand13AgPpatientsand20controlsubjectswereincluded
inthisstudy.Plaqueindex,gingivalindex,probingdepthandclinicalattachmentlevelswere recordedandGCFsampleswerecollectedBTandAT.AssaysforGCFt-PAandPAI-2levelswere carriedoutbyanenzymelinkedimmunosorbentassay(ELISA).Thex2,WilcoxonandMann– WhitneyUtestsandSpearmancorrelationcoefficientwereusedfordataanalyses.
Results: Statisticallysignificantreductionsinclinicalindexscoreswerenotedinboth
peri-odontitisgroupsaftertreatment.NosignificantdifferencesweredetectedinGCFlevelsoft-PA andPAI-2betweenCPandAgPgroupsateitherBTorAT.Therewasastatisticallysignificant decreaseinGCFPAI-2levelsinCPaftertherapy(p<0.01).GCFt-PAlevelsinCPandAgPgroups exhibitedsignificantcorrelationswithPDandCALmeasurementsatbothBTandAT(p<0.01).
Conclusion: SignificantdecreasewasdetectedforGCFPAI-2levelsinCPandclinical
param-etersinbothCPandAgPbynon-surgicalperiodontaltreatment.
#2012ElsevierLtd.Allrightsreserved.
§
GCFt-PAandPAI-2levelsmaybeusedasmarkerstoassessperiodontaldiseaseandtreatmentefficiency.
*Correspondingauthorat:DepartmentofPeriodontology,FacultyofDentistry,GaziUniversity,BiskekCaddesi82,Sokak06510Emek, Ankara,Turkey.Tel.:+905322262425.
E-mailaddress:gulay@gazi.edu.tr(G.Tu¨ter).
Available
online
at
www.sciencedirect.com
journalhomepage:http://www.elsevier.com/locate/aob
0003–9969/$–seefrontmatter#2012ElsevierLtd.Allrightsreserved.
release of inflammatory cytokines tumour necrosis factor-alpha(TNF-a),interleukin(IL)-1-alpha(IL-1-a)and -beta (IL-1b).1,3–5They directlydegradeextracellularmatrix (ECM)or contribute to their destruction via activation of matrix metalloproteinases(MMPs)andblockingtheeffectsoftissue inhibitorsofMMPs.6Theproteolyticactivityofplasminogen activatorsareinhibitedbyPAI-1whichisprimarilyproduced byendothelialandmalignantcells,andPAI-2whichismainly produced by monocytes, macrophages, epithelial cells and fibroblasts.7,8
Periodontal diseases have long knownto have complex pathogenesisandtheyhavebeenproposedthatitisthehost responsetothelong-termbacterialchallenge.9The periodon-talconnectivetissueECMprovidestheenvironmentforallcell interactions occurring during development, pathology,and regenerationprocesses.10During periodontitis, these struc-turesand componentsaresignificantlydisruptedand peri-odontitisischaracterizedbythelossofcollagenfibresand other ECM constituents of tooth supporting periodontal tissues. A possible mechanism for the degradation of periodontalECMistheindependentand/orcooperativeaction ofbothhumanandbacterialproteinases.11
It is well known that the least invasive approach to examinedestructiveprocessofperiodontaldiseaseinvolves analysisofgingivalcrevicularfluid(GCF),aninflammatory exudatepresentinthegingivalcrevice.12Previously,t-PA, u-PA,PAI-1andPAI-2weredetectedinGCF.13Furthermore,high concentrationsoft-PAandPAI-2inGCFwereindicatedandit wassuggestedthattheywerelocallyproducedandmightbe involvedintheaggravationofgingivalinflammation.14Yin etal.statedthatt-PAandPAI-2mightplayasignificantrolein the periodontaltissue destructionandtissue remodelling, andthat t-PA andPAI-2in GCFmight be used asclinical markers to evaluate the periodontal diseases and assess treatment.15 Previouslysome studies13,15,16examined t-PA andPAI-2levelsinGCFofhealthysubjects,periodontitisand gingivitis patients and observed the alterations after the periodontaltreatment.Howeverthereisstilllackof informa-tion on GCF t-PA and PAI-2 levels of different forms of periodontitis.Webelievethatevaluationoft-PAandPAI-2 levelsinchronicandaggressiveperiodontitiswillcontribute tobetterunderstandingofperiodontaldiseasepathogenesis andperiodontaltreatment.
Theaimsofthepresentstudyweretoevaluatetheeffectof non-surgical periodontal treatment on clinical parameters andtocompareGCFlevelsoft-PAandPAI-2inchronicand aggressiveperiodontitispatients,inadditiontoinvestigatethe relationshipbetweenclinicalparametersandGCF t-PAand PAI-2levels.
2.
Materials
and
methods
2.1. Studypopulationandstudydesign
Atotalof12chronicperiodontitis(CP)(8malesand4females withameanageof448years),13aggressiveperiodontitis (AgP)(5malesand8femaleswithameanageof264years) and20clinicallyhealthycontrolgroupsubjects(C)(7males and13femaleswithameanageof293years)wereincluded
inthepresentstudy.Controlgroupsubjectshadnohistoryof periodontaldiseaseandallparticipantswererecruitedfrom individualsreferredtoGaziUniversity,FacultyofDentistry, DepartmentofPeriodontologyeitherfordentaltreatmentor onlyfordentalcheck-up,betweenMarch2008andDecember 2009.TheprotocolofthisstudywasapprovedbytheEthical Committee of the Faculty of Dentistry, Gazi University, Ankara,Turkeyandthestudywasconductedinaccordance with the Helsinki Declaration of 1975, as revised in 2000. Informedwrittenconsentwasobtainedfromallsubjectsafter the detailsoftheclinicalprocedures,including periodontal measurementsandGCFsamplingwereexplained.
Periodontal disease status was determined according to clinical and radiographic criteria. The classifications of the studygroupsweremadeaccordingtocriteriaproposedbythe 1999 International World Workshop for a Classification of Periodontal Disease and Conditions.17 Chronic periodontitis patients showing radiographic evidence of bone loss and attachmentlosswithaminimumof8teethhavingperiodontal pockets greater than 4mm were included into the study. Diagnosisofaggressiveperiodontitiswasdeterminedaccording tothefollowingcriteria:patients<35yearsofage,andcases withatleasteightteethwithprobingdepth>6mmandwith radiographic evidenceofalveolarbonelossweretakeninto consideration.Atleastthreeoftheseeightteethwithprobing depth>6mmwerenotfirstmolarsorincisors.Otherfactors suchasfamilyaggregation,rapidprogressionandthe relation-shipbetweenlocal factorsandperiodontaldestructionwere alsoconsidered.Rapidprogressionwasdeterminedaccording toclinical,radiographicandetiologicmanifestationsof aggres-siveperiodontitis.Allsubjectswereingoodgeneralhealth,were non-smokers and none had received periodontaltreatment during the past6months or receivedantibioticmedication duringthepast3months.Nosubjectswithahistoryofsystemic conditionssuchasheartdisease,diabetesandothertypesof disorders which could influence the course of periodontal diseasewereenrolled.Enrolledsubjectsdidnotusea medica-tionthatcouldaffectthemanifestationsofperiodontaldisease, suchasantibiotics,phenytoin,cyclosporine,anti-inflammatory drugs,orcalciumchannelblockers.Noneofthewomenwere pregnantinpostmenopausalorlactationperiod.
2.2. Periodontalclinicalmeasurementsandnon-surgical periodontaltherapy
Interandintra-examinercalibrationswereperformedpriorto initiationofthestudy.Inter-examinerreliabilitywas deter-mined byhavingeachexaminermake dualmeasurements alongwiththoseoftheProjectDirectoronatleast2patients, andtoremediateanymeasurementdifferences>1mmor1 score. Intra-examiner reliability was determined by taking repeatedmeasurementsfromthesamepocketatthe calibra-tion session and on about 20% of the cases (randomly determined)duringthestudy.
mid-lingual,disto-lingual)usingwithaWilliamsperiodontal probe(NordentManufacturingInc.,ElkGroveVilage,IL,USA) calibrated in millimetres. The deepest six pockets of each subjectwerechosenforclinicalrecordingsandGCFsampling. Therefore,forobtainingGCFsamples,72(12CPpatients6 sites) pockets were sampled in CP group, 78 (13 AgP patients6sites)pockets weresampled inAgP groupand 120(20participants6)pocketsweresampledinCgroupat eachofthetestappointments.
Periodontitis patients received non-surgical periodontal treatmentconsistedoforalhygieneinstruction,scalingand rootplaningwithultrasonicandhandinstruments,whichwas performed without any adjunctive therapy and completed within2weeksfromthebeginningofthestudy.After6weeks frombaselinemeasurements,clinicalmeasurementsandGCF samplingwererepeatedforperiodontitisgroups.
2.3. GCFsamplingandprocessing
GCFsampleswerecollectedusingperiopaperstrips(Oraflow Inc.,Box219,Plainview,NY,USA)whichwerecommercially available. The sample site was gently air-dried and all supragingival plaque was removed. The area was carefully isolatedtopreventsamplesfrombeingcontaminatedbysaliva. The paper strips were inserted into the crevice until mild resistancewasfeltandnotmorethan1mm.Thepaperstrips wereleftinplacefor30s.Carewastakentoavoidmechanical injuryofthegingivaltissues.Stripscontaminatedbybleedingor exudate were discarded. Stripswere placed separatelyinto codedsealedplasticmicrocentrifugetubesandcoveredwith paraffinandthenstoredat 708Cuntilprocessed.
2.4. GCFenzyme-linkedimmunosorbentassayanalysis fort-PAandPAI-2
Levels of t-PA and PAI-2 in GCF samples wereassayed by standard enzyme-linked immunosorbent assay (ELISA) kits (Imubind1ELISAKit,AmericanDiagnosticaInc.,500WestAve.,
P.O. Box 110215, Stamfordt, CT, USA), according to the manufacturer’sinstructions.Microcentrifugetubes,containing paperstripswithabsorbedGCF,wereremovedfromstorageand warmedupto48C,thenelutedusingacentrifugalmethod.20 Elutionwascarriedoutbyadding150mlofsamplebuffer(1% bovineserumalbumin1phosphatebufferedsaline1Wash buffer)tothestrips.Themicrocentrifugetubescontainingthe stripsandthebufferwerevortexedfor1minandincubatedover nightat48C.Followingmorningsamplesvortexedfor3minat roomtemperature.Afterthecentrifugationat6000rpm10min, fluidassayedbyELISAfort-PAandPAI-2.TheELISAplateswere thenassessedspectrophotometricallyatopticdensity(OD)at 450nmwithareferencefilterofODat540nm.ThelevelsofGCF t-PAandPAI-2ineachsamplewerecalculatedusingtheknown concentrationvalues ofstandards included with the kit by means of regression-correlation analysis using a computer basedstatisticsprogramMicrosta.
2.5. Statisticalanalysis
StatisticalanalyseswereperformedbytheSPSS(SPSSv.11.5 Inc.,Chicago,IL,USA)statisticalprogram.Beforethestatistical
analysisamongthegroups,One-Sample Kolmogorow–Simir-novtestwasperformed.Accordingtotheresultsofthistest, non-parametric analysiswas determined. Theresultswere shown asmedianand 25–75percentilesintheparentheses (quarters).Thex2testwasusedtodeterminewhetherthere
wasastatisticaldifferenceamongthegroupswithrespectto gender. Wilcoxon test was used for evaluation of the differences before and after the treatment. Mann–Whitney UtestwasusedforevaluationofthedifferencesbetweenCP and C and also between AgP and C before and after the treatment.ThecorrelationsbetweenclinicalindicesandGCF t-PAandPAI-2levelswereanalyzedwithSpearman correla-tion coefficient. p-Value <0.05 was considered statistically significant.
3.
Results
Amongthegroups,nostatisticallysignificantdifferenceswere foundforthegenderoftheparticipants(p=0.191),butthere wasastatisticallysignificantdifferencebetweenthemeanage ofthegroups(p<0.001).
The descriptive measurements of clinical indices are summarizedinTable1.PI,GIandPDscoresfoundsignificantly decreasedinCPandAgPAT(p<0.001).Meanwhile,CALscores also decreased after treatment but the alteration was only significant for CP group.GCF volumes decreased after non-surgical periodontal treatment, however GCF volumes were foundhigherinbothCPandAgPgroupsthanC,BTandAT.
GCFlevelsoft-PAandPAI-2areshowninFig.1.Beforethe periodontal treatment GCF levels of t-PA and PAI-2 were significantly higherin CPand AgP groups than inC group (p<0.001). Afterperiodontal therapy, remarkable decrease wasseeninGCFlevelsoft-PAanditsinhibitorPAI-2forboth groups, althoughonlysignificantreductionwasdetectedin GCFPAI-2levelsofCPgroup(p<0.01).Therewasasignificant differenceinGCFt-PAlevelsbetweenCPandC,aswellasAgP andCgroupsaftertreatment(p<0.01andp<0.001, respec-tively). Butbothgroupsstillpresentedhigherlevelsoft-PA thancontrolgroupAT.However,thedifferencesofGCFPAI-2 levels betweenbothCPandC,andAgP andCgroupswere statisticallynon-significantattheposttreatmenttimepoint (p=0.80andp=0.27,respectively).Nosignificantdifferencein GCFlevelsoft-PAandPAI-2wasdetectedbetweenCPandAgP groupsbeforeoraftertreatment(fort-PAp=0.44and0.78,and forPAI-2p=0.82andp=0.32,respectively).
A positivecorrelationwas foundbetweenGCF t-PA and PAI-2levelsbeforetreatment(Table2).Thereweresignificant and positivecorrelationsamong allclinicalparametersand bothGCFt-PAandPAI-2levelsBT.Apositivecorrelationwas alsonotedbetweent-PAlevelsandPD,aswellasCAL,after treatment.GCFvolumewasfoundpositivelycorrelatedwith alltheclinicalparametersandalsowithGCFt-PAandPAI-2 levelsbeforeandaftertreatment,exceptPIaftertreatment.
4.
Discussion
periodontaltissues.21Destructionofthe periodontaltissues duetoperiodontitishasbeenreportedtobeassociatedwith plasminogenactivator system, including t-PA and PAI-2 in GCF.13,15
InthisstudyweaimedtodetermineGCFlevelsoft-PA, PAI-2 and their relationship with clinical parameters in chronic andaggressive periodontitis patients, and also to examinetheeffectsofnon-surgicalperiodontaltreatmenton theclinicalparametersandenzymeanditsinhibitor.Toour knowledge,thisis thefirststudy evaluatingthe effectsof non-surgicalperiodontaltherapyonGCFlevelsoft-PAandits inhibitor PAI-2 in chronic and aggressive periodontitis groupsseparately.
Bıyıkog˘luet al.22comparedperiodontalconditions,GCF levelsoft-PA,PAI-2,interleukin-1b(IL-1b)andprostaglandin E2(PGE2)inrheumatoidarthritispatientsandsystemically
healthy individuals with periodontitis, gingivitis or peri-odontally healthy controls. Among systemically healthy individuals, theyreported higherGCFt-PAconcentrations and total amounts in periodontitis group than gingivitis patientsandhealthycontrols, butthe differencewasonly significant between periodontitis and healthy controls.22 Authorsfoundthehighestconcentrationandtotalamounts ofPAI-2atgingivitisgroupandlowerPAI-2concentrations andhigherPAI-2totalamountsinperiodontitisgroupthan healthycontrolswithinsystemicallyhealthysubjects,even though the differences were not statistically significant.22 WealsofoundhigherGCFPAI-2levelsinbothCPandAgP than C,but contrarily these differences were statistically significantinourstudy.Asadifferencefromtheirstudy,our participants received non-surgical periodontal treatment andthatallowedustoevaluateandcompareGCFt-PAand PAI-2levelsafterthetreatment,aswellasbeforetreatment. Moreover,inthepresentstudy,unlikethestudyofBıyıkog˘lu et al.,22 we evaluated GCF t-PA and PAI-2 levels of systemicallyhealthyindividuals.Further,Bıyıkog˘luet al.22 didnotmentionthattheirperiodontitisgroupconsistedof chronicoraggressiveperiodontitispatientsorboth,whereas Table1–ComparisonofclinicalparametersandGCFvolumes,beforeandaftertreatment,withineachgroupand comparisonofclinicalparametersandGCFvolumes,beforeandaftertreatmentamongthegroups.
Clinicalparameters Chronicperiodontitis(CP)(n=12) Aggressiveperiodontitis(AgP)(n=13) Control(C)(n=20)
BT AT p* BT AT p*
PI 1.50(0.31–2.26)y
0.28(0.07–0.64) 0.003 0.85(0.77–1.28) 0.30(0.01–0.82) 0.006 0.15(0.07–0.3)
GI 1.37(1.0–1.84) 0.37(0.14–1.10) 0.003 1.45(1.05–1.89) 0.39(0.22–1.39) 0.003 0.08(0.02–0.22)
PD(mm) 3.88(3.51–4.64) 3.09(2.87–3.39) 0.003 4.25(3.45–4.57) 3.55(2.97–3.90) 0.030 1.36(1.20–1.44)
CAL(mm) 4.8(3.99–5.64) 4.00(3.26–4.56) 0.004 4.25(3.87–4.84) 3.75(3.03–4.20) 0.080 1.07(0.84–1.18)
GCFvolume(ml) 3.02(2.57–3.53) 2.1(1.86–3.41) 0.130 3.35(2.45–3.97) 2.65(2.3–4.12) 0.360 0.92(0.76–1.24)
Clinicalparameters CP–C pz
CP–C pz
AgP–C pz
AgP–C pz
CP–AgP pz
CP–AgP pz
BT AT BT AT BT AT
PI <0.001 0.200 0.001 0.470 0.250 0.890
GI <0.001 0.020 <0.001 0.001 0.560 0.530
PD(mm) <0.001 <0.001 <0.001 <0.001 0.660 0.030
CAL(mm) <0.001 <0.001 <0.001 <0.001 0.250 0.430
GCFvolume(ml) <0.001 <0.001 <0.001 <0.001 0.660 0.230
* Changebetweenbeforeandaftertreatmentwithinagroup.
y
Thedataareexpressedasmedianvaluesandthenumbersintheparenthesesarethe25thand75thpercentilesoftherawdata.
z
Comparisonbetweengroups(Mann–WhitneyUtest).
Table2–ThecorrelationsbetweenGCFvolume,GCFt-PA andPAI-2levelsandclinicalparameters,before/after treatment(Spearmancorrelationcoefficients).
Parameters PAI-2(ng) t-PA(ng) GCFvolume(ml)
BT/AT BT/AT BT/AT
t-PA(ng) 0.569**/– 0.797**/0.512**
PAI-2(ng) 0.569**/– 0.765**/0.355*
PI 0.406**/– 0.415**/– 0.470**/–
GI 0.570**/– 0.524**/– 0.673**/0.325
PD(mm) 0.542**/– 0.679**/0.579** 0.712**/0.515**
CAL(mm) 0.561**/– 0.705**/0.591** 0.739**/0.597**
*Correlationissignificantatthe0.05level(2-tailed).
** Correlationissignificantatthe0.01level(2-tailed).
in our study GCF enzyme and its inhibitor levels were evaluatedseparatelyforchronicandaggressive periodonti-tisgroupsaswellasperiodontallyhealthy controlsbefore andaftertreatment.Apartfromdifferencesofthetwostudy design,concordantwiththeresultsofBıyıkog˘luetal.,22we foundsignificantly highert-PAlevels inboth,chronicand aggressiveperiodontitisgroupsthanhealthycontrols,before treatment(Fig.1).
Kardes¸ler et al.23 evaluated if type 2 diabetes mellitus increaseGCFlevels ofIL-1b,PGE2, t-PAandPAI-2, onthree
groups which consisted of a group with type 2 diabetes mellitusand periodontaldisease, agroup withperiodontal diseasebutsystemicallyhealthyandagroupwhose systemi-cally and periodontally healthy. Differently from Kardes¸ler et al.,23 our studygroup consisted of systemically healthy subjects, andperiodontitis patientshad subdivisions asCP andAgP.Authorsfoundhighert-PAandPAI-2totalamount and t-PA concentration increase in GCF of periodontitis patientscomparedto healthysubjects, within systemically healthypatients; however, unlikeour results, those differ-ences were statistically insignificant.23 Moreover, they reported lower PAI-2 concentrations in periodontitis group thancontrols.Asanotherdissimilaritytheirpatientsdidnot getanytreatmenteither.Yinetal.15measuredthe concentra-tion oft-PA and PAI-2 in GCF fromhealthy, gingivitis and periodontitissitesinordertoevaluatewhetherthelevelof t-PA and PAI-2 can differentiate thesedisease states ofthe periodontium.AuthorsreportedsignificantlyincreasedGCF t-PA and PAI-2 amounts in periodontitis sites compared to gingivitisandhealthysites.15InagreementwithYinetal.,15in thepresentstudywefoundsignificantlyincreasedGCFt-PA andPAI-2amountsinbothperiodontitisgroupscomparedto controlsubjects.
Kinnby et al.13 evaluated GCFt-PA and PAI-2levels in gingivitispatientsandreportedthat bothlevels decreased after non-surgical periodontal therapy. In line with their resultswefounddecreasedGCFt-PAandPAI-2levelswith therapy, whereas those reductions were not statistically significantforGCFt-PAlevelsinourstudy.13Incontrastwith theirstudy,insteadofgingivitiswe evaluatedchronicand aggressive periodontitispatients inour study. Yinet al.15 reportedreductionsinbothGCFt-PAandPAI-2 concentra-tions after 2 weeks periodontal treatment; however they found statistically significant difference only in PAI-2 concentrations.Consistentwiththeliterature,aswestated beforeinthe present study,all GCFt-PAandPAI-2levels decreased with therapy in both periodontitis groups, but onlyinchronicperiodontitisgroupreductionsofPAI-2levels werestatisticallysignificant.Veryrecently,Kardesleretal.16 evaluatedeffectsofinitialperiodontaltreatmentonGCF IL-6,t-PA,PAI-2andalbuminlevelsintype2diabeticpatients andsystemicallyhealthysubjectswithperiodontitis. Differ-ent from our study, their study groups did not include systemicallyandperiodontallyhealthycontrolsbut includ-ed a diabetes mellitus group with periodontitis.16 They reported decreased levels of GCF t-PA and PAI-2 total amounts and concentrations in chronic periodontitis, 1 and3monthsafterinitialperiodontaltreatment, however, diverging from previous reports and our present results, onlyt-PAtotalamountreductionswerereportedstatistically
significantatbothobservationtimescomparedtobaseline. Ontheotherhand,similarwithfindingsofKardesleretal.16 we detected statistically significant correlations between GCFt-PAandPAI-2levelsinourstudywhichunderlinedthe importanceofPAI-2attheregulationoft-PA.Inaccordance withapreviousreport,15ourresultssuggestedthatGCF PAI-2 regulates t-PA and tissue proteolysis in periodontal destruction.This regulatoryeffectmayexplainthe reason ofdecreasedGCFenzymeinhibitorlevelsbesidesdecreased GCFenzymelevelsafternon-surgicalperiodontaltreatment inourstudy.
Thepresentdatashowedthetotalamountoft-PAand PAI-2 in GCF were significantly correlated with all clinical parameters, and alsoa significant correlation between the leveloft-PAandPAI-2inGCFbeforetreatment(Table2).After the non-surgicalperiodontal treatment, only the GCF t-PA levelwasfoundtobesignificantlycorrelatedwithPDandCAL. Thepresent datashowedthatincreasedt-PAincrease was directly associated with tissue destruction and this was reflectedtotheclinicalparametersasreductionofbothPD andCALaftertreatmentconcordantwiththereductionof t-PA.Inthisstudy,weevaluatedGCFt-PAandPAI-2levelsand their alterations in chronic and aggressiveperiodontitis as well as in periodontal health. In conclusion, the present resultsofourstudysuggestthatt-PAanditsinhibitorPAI-2 play an important part in destruction of tooth supporting structures during the periodontal disease. Non-surgical periodontal treatment without any adjunctive therapy appeared to decrease GCF t-PA and PAI-2 levels. However therewasonlyasignificantreductioninthelevelsofPAI-2for chronicperiodontitisgroupsaftertherapy.Accordingtothe results, for both periodontitis groups, there was a trend towards t-PA reduction aftertreatment, but its levels still remained higher than healthy periodontal status (control group).Withinthelimitsofthisstudy,ourdatasuggestthat GCFt-PAandPAI-2levelsmaybeusedasmarkerstoassess periodontal disease and treatment efficiency. Further con-trolled clinical studies with larger scale can help better understandingofassociationsbetweenplasminogenactivator system, inflammatorymediatorsand destructiveprocess of periodontaldiseases.
Funding
This study was financially supported by Gazi University ResearchGrant(03/2006-19).
Competing
interests
Nonedeclared.
Ethical
approval
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