PROSTHODONTICS - American College of Prosthodontists

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division)inwhichchromosomesdivideandareseparatedandcytokinesis(celldivision)inwhichthecell’scytoplasmdividestocreatetwodaughtercells.InterphaseisatermusedtorefertoG1,SandG2phasescollectively.Inessence,thetimebetweencelldivisions(Mphases)isinterphase.GIphase,thefirstpartofinterphase,isthatpartofthecellcyclewhencellularfunctionsunrelatedtocelldivisionareactive.SphaseisconsideredtobeginwhenDNAsynthesisstartsandisconsideredtoendwhenDNAsynthesisiscomplete.Innormalcelldivision,attheendofSphase,thecell’sDNAcontenthasdoubled.UponcompletionofSphase,thecellentersG2phaseduringwhichmicrotubulesproductioniselevatedtopreparethecellforMphasewherecelldivisiontakesplace. Figure1Tosummarize,thereiscellgrowth(G1phase)followedbyDNAreplication(Sphase),thenpreparationforcelldivision(G2phase),andfinallycelldivision(Mphase).Acellthathasbecomesignificantlydysfunctionalmayactivate“self‐destruct”cellprogramsresultingincelldeathasaresultofapoptosis.Incontrast,cellsthatarerelativelyfunctionalbutquiescent[non‐proliferative]aresometimesreferredtoasbeinginG0phase.However,acellinG1mayemergeatalatertimeandonceagainproliferate.Inaddition,cellsthatarefullydifferentiatedmayfunctionnormallyforanextendedperiodoftimewithouttheabilitytobeginreplicationagain.Regulationofcellcycleprogressioninvolveshundredsofproteins,suchascyclinsandcyclindependentkinases(CDKs),andreliesonmanykeyprotein‐proteininteractionsaswellas 162010 CDEL Re-recognition of the Specialty Report 200 of 279
tightregulationoftranscriptionalevents.Aspreviouslymentioned,inanefforttoensurefidelityofthecellcycle,error‐preventionmechanismsarepresentTheSixHallmarksofaCancerCell1.Self‐sufficiencyingrowthsignalsInnormalcircumstances,foracelltoundergocelldivision,mitogenicstimuliintheformofproliferation‐inducingproteinsinteractwithcellsurfacereceptorstomanipulatekeyintracellularpathwaystobegincelldivision.Indeed,cellsrelyontheseextra‐cellularsignalstoproliferate.Indentistry,tissue‐guidedregenerationintheformofboneaugmentationisincreasinglymakinguseofproteinssuchasplatelet‐derivedgrowthfactors,insulin‐likegrowthfactorsandfibroblastgrowthfactorstoenhancecellularproliferationandhenceimprovetheaugmentationoutcome.Inaddition,theuseofplateletrichplasmaisbasedupontheassumptionthatthispreparationisespeciallyrichingrowthfactors.Cancercells,incontrasttonormalcells,acquiretheabilitytoproliferatewithlessdependenceonnormalextracellularsignals.Threemechanismscanbeemployed:increasedmitogenicsignalproductionbyadjacentcells(whichimpliestheabilitytocontrolnearbycells)orbythemselves;modifyingthenumberand/ortypeofcellsurfacereceptorsthatareresponsivetomitogenicsignals;andpresenceofintracellularoncogenesthatpermitbypassoftheneedforextracellularsignalingtoinducemitosis.2.Insensitivitytoanti‐growthsignalsJustasthereareextracellularsignalsthatinduceproliferation,thereareextracellularsignalsthatpreventproliferation.Theseanti‐proliferationsignalscanbeeithersolubleproteinsthatengagespecificcellsurfacereceptorsortheycanbecell‐cellinteractionsorcell‐extracellularmatrixinteractions.TheneteffectofallofthesemechanismsistopreventcellproliferationeitherbyinducingpassagetoG0(quiescence)orelsebycausingdifferentiationtothepointwhereacelllosesitsabilitytoproliferate.Therefore,acellintendingtoproliferateuntowardlyneedstoovercomeeitherorbothoftheseanti‐growthmechanisms.EmergencefromG1isakeyregulatorystepandpro‐proliferationandanti‐proliferationsignalsaffectthisemergencetoasignificantdegree.SomeofthemolecularmechanismsinvolvedinmaintainingtheG1statepertaintothefunctionoftheretinoblastomaproteinanditsassociatesthatactanti‐proliferatively.Disruptionorinactivationofretinoblastomaproteinpathwayfunctions“releasesthebrake”,asitwere,andproliferationcanoccur.Inaddition,whereasspecificoncogenescaninduceproliferationbybypassingtheneedforextracellulargrowthsignals,otheroncogenescanimpedeprogressionofacelltothedifferentiated,andhencenon‐proliferative,state.Inparticular,thec‐myconcogeneappearscapableofreleasingtherestraintsoncellproliferationduetoinductionofterminalcelldifferentiation.3.EvadingapoptosisApoptosis,programmedcelldeath,isavitalmechanismtoensurethatcells“pasttheirprime”areremovedfromthesceneleavingthehealthiest,andconsequentlythemostusefulcellstocarryoutfunctionsvitaltissues,organsandtheentirebody.Histopathologicalevidenceindicatesthatlowerratesofapoptosisareseenincancertumoursthaninneighboringunaffectedtissues. 172010 CDEL Re-recognition of the Specialty Report 201 of 279
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COUNCIL ON DENTAL EDUCATION AND LIC
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A. General InformationThe American
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The American College of Prosthodont
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Changes in Scope of PracticeThe Ame
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ReferencesThe American College of P
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ENVISIONED FUTURE~ 10-30 YEAR HORIZ
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Prosthodontists will provide prosth
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GOALS AND OBJECTIVES~ 3-5 YEAR PLAN
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E4. Create effective linkages to fu
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Journal of ProsthodonticsImplant, E
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December 2005, Supplement, Volume 1
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28 Cllas$caizon of Complete Edentul
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Page 159 and 160: COUNCIL ON DENTAL EDUCATION AND LIC
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Page 185 and 186: ORALCANCERSCREENING,EXAMINATIONANDB
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Page 199: THEPROCESSOFONCOGENESISIntroduction
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Page 245 and 246: Accreditation Standards forAdvanced
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Page 249 and 250: Mission Statement of theCommission
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PrefaceMaintaining and improving th
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Definitions of Terms Used in Prosth
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Educationally Qualified: An individ
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Intent: Major changes have a direct
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STANDARD 2 - PROGRAM DIRECTOR AND T
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STANDARD 3 - FACILITIES AND RESOURC
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STANDARD 4 - CURRICULUM AND PROGRAM
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Intent: Students will have in depth
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4-18 Students/Residents must be exp
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STANDARD 5 - ADVANCED EDUCATION STU
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STANDARD 6 - RESEARCHAdvanced speci
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