病理學(xué)課件 病理緒論-14

ChapterOne

IntroductiontoPathologySectionA:DifinitionofPathologySectionB:DevelopmentofPathologySectionC:ObjectivesofResearchSectionD:LearningofPathologyWilliamOslerAsisourpathology,soisourmedicine.病理為醫(yī)之本SectionA:DEFINITIONOFPATHOLOGYWithouttheconceptofsurgicaltreatment,oneisnotagoodphysician.Withouttheknowledgeofpathology,oneisnodoctor.Withouttheconceptofclinicaltreatment,oneisnotagoodpathologist.DefinitionofpathologyPathologyistostudydiseasesbyscientificmethods.Diseasemaybedefinedasanabnormalalterationofstructureorfunctioninanypartofthebody.Pathology:4aspectsofdiseaseETIOLOGY:Causeofdisease.PATHOGENESIS:Mechanismsofdevelopmentofdisease.MORPHOLOGY:Thestructuralalterationsinducedincellandtissues.FUNCTIONALCONSEQUENCES:Functionalconsequencesofthemorphologicchanges,asobservedclinically(clinico-pathologicalcorrelation,CPC).1.EtiologyKnowledgeofetiologyremainsthebackbone:DiseasediagnosesUnderstandingthenatureofdiseasesTreatmentofdiseases.1.EtiologyWhilemuchstillneedstobeuncoveredtolinkabnormalgenesandtheexpressionofdisease,gonearethetimewhenthemechanismsofmostdiseaseswereunknown?orobscure?ormysterious?Oneetiologicagent—onediseaseSeveraletiologicagents—onediseaseOneetiologicagent—severaldiseasesBASICRULESOFETIOLOGYCausesofcellinjuryanddiseaseOxygendeprivation(hypoxia,ischemia)NutritionalimbalancesPhysicalagentsChemicalagentsanddrugsInfectiousagentsImmunologicreactionsGeneticderangementsHYPOXIAIschemia(lossofbloodsupply)Inadequateoxygenation(cardiorespiratoryfailure)Decreaseofoxygen-carryingcapacityoftheblood(anemiaorCOpoisoning)HYPOXICINJURYLossofoxidativephosphorylationandATPgenerationbymitochondria.ResultinginaerobicglycolysisbydecreasedATP(withincreaseinAMP)Depletedglycogen.ReducedintracellularpH:Lacticacidandinorganicphosphate.MitochondrialdamageClumpingofnuclearchromatin.FourbiochemicalthemesOxygen-derivedfreeradicals.Lossofcalciumhomeostasisandincreasedintracellularcalcium.ATPdepletion.Defectsinmembranepermeability.PHYSICALAGENTSTraumaHeatColdRadiation(UV)ElectricshockCHEMICALAGENTSANDDRUGSEndogenousproducts:ureaExogenousagents:Therapeuticdrugs:hormonesNon-therapeuticagents:leadoralcoholMECHANISMSOFCHEMICALINJURYDirectly:MercuryofmercuricchloridebindstoSHgroupsofcellmembraneproteins,causingincreasedpermeabilityandinhibitionofATPase-dependenttransport.Indirectly:

Byconversiontoreactivetoxicmetaboliteswhichinturncausecellinjuryeitherbydirectcovalentbindingtomembraneproteinandlipid,ormorecommonlybytheformationoffreeradicals.MECHANISMSOFCHEMICALINJURY

MechanismofCCl4injuryCCl4inSERoflivercell(P-450)–CCl3.–lipidperoxidationandautocatalyticreactions–swellingandbreakdownofER,dissociationofribosome,anddecreasedhepaticproteinsynthesis(lossoflipidacceptorprotein–fattychangeoflivercell)–progressivecellularswelling,plasmamembranedamage,andcelldeath.FREERADICALINITIATIONAbsorptionofenergy(UVlightandx-rays)OxidativemetabolicreactionsEnzymaticconversionofexogenouschemicalsordrugs(CCl4>CCl3.)Oxygen-derivedradicalsSuperoxideCellinjurycausedbyfreeradicalsPeroxidationoflipids.Crosslinkingproteinsbytheformationofdisulfidebonds.InductionofDNAdamagethathasbeenimplicatedbothincellkillingandmalignanttransformation.INFECTIOUSAGENTSPrionVirusesRickettsiaeBacteriaFungiParasites肺---CMVGeneticdisorders:670per100050%ofspontaneousabortusesduringearlymonthsofgestation(chromosomalabnormalities)Chromosomalabnormalities:Trisomy21Single-genedisorders(APC)DisorderswithmultifactorialinheritanceGeneticderangementsAdenomatous

polyposiscoliAPCloci,5q21Adenomatous

polyposisincolons(inteens).100%malignanttransformation(40ys).NormalAPCproteininthecytoplasm.Severalpartners,including-catenin.Causingdegradationof-cateninmaintaininglowlevelof-catenininthecytoplasm.AbnormalAPC:-catenin

enteringthenucleusactivatingtranscriptionofgrowth-promotinggenes.PolymeraseChainReaction

DetectionofAPCDNAinFeces家族性高膽固醇血癥靶基因低密度脂蛋白受體基因技術(shù)方法單鏈構(gòu)象多態(tài)性分析溫度梯度凝膠電泳測序應(yīng)用范圍雜合子患者

(人群中1/500)

純合子患者

(人群中1/1，000，000)

A606T(hmz)infamilyANormalcontrol2.PATHOGENESISThecoreofthescienceofpathology—thestudythepathogenesisofthedisease.PATHOGENESISPathogenesisThesequenceeventsintheresponseofthecellsortissuestotheetiologicagent,fromtheinitialstimulustotheultimateexpressionofthedisease.PathogenesisImmunologic,cytogeneticandmolecularanalysesoftissuesandcellsareincreasinglybecomingguidestorenderdiagnoses,toassessprognosis,andtosuggesttherapy.ABCD117CD34GIST：發(fā)病機制受體偶聯(lián)的酪氨酸激酶基因功能獲得性突變（gainoffunctionmutation）是主要的致癌事件1,2－KIT：80％-85%1－PDGFRA：7％2－野生型（無法檢測到的突變）：10-15%1

突變導(dǎo)致激活的酪氨酸激酶受體持續(xù)的異常表達(dá)(KIT或PDGFRA)3伊馬替尼（格列衛(wèi)）治療PDGFRA，血小板源性生長因子受體；PDGFRA，血小板源性生長因子受體基因1.CorlessCLetal.JClin

Oncol.2004;22:3813-3825.2.HeinrichMCetal.Science.2003;299:708-710.3.TrentJCetal.Curr

Opin

Oncol.2006;18:386-395.3.MORPHOLOGY大葉性肺炎Morphologicchange

CharacteristicforthediseaseDiagnosticfortheetiologicproceessFunctionalderangementsClinicalsignificanceMORPHOLOGYMorphologyremainsattheheartofdiagnosticpathology.

DevelopmentofPathologySectionBOrganpathologyCellpathologyMolecularpathologyCellPathologyRudolfWirchow(1821-1902),AGermanpathologistThefounderofmoderncellpathologySectionCOBJECTIVESANDMETHODSOFRESEARCH

AutopsyBiopsyCytologyExperimentalstudies

Invitro:

TissuecultureOrgancultureCellculture

Invivo:

ExperimentalanimalsNudemiceAutopsy(尸檢)：(A5800)主述：F/46工人?；颊咭蚝粑щy1天，神志不清12小時，急診入院?，F(xiàn)病史：患者自覺呼吸困難，全身不適，意識模糊，幾小時后神志不清，入三院診治。查體實驗室檢查：血壓低，心率快，體溫進(jìn)行性升高。雙肺中小水泡音。肛試子白血球15-20個/HPF，RBC2-3個/HPF，潛血（+）。末梢血WBC2-3萬/mm3。診斷：考慮為痢疾、感染性休克。2002年7月11日下午心臟驟停，搶救無效死亡。檢查腸系膜血管脾靜脈血栓AVPancreas診斷腸系膜靜脈、脾靜脈、門靜脈血栓性靜脈炎伴阻塞性血栓形成，小腸出血性壞死，急性腹膜炎感染中毒性休克死亡Biopsy-活體組織檢查1）Macroscopicobservation2）MicroscopicobservationFormalin-fixedparaffin-embedded

Freshtissue:FrozensectionFrozensectionBreastmass:Benignlesion:localresectionInfiltratingductalcarcinoma:mastectomy+removalofregionalLN病理學(xué)檢查申請單臨床醫(yī)師向病理醫(yī)師發(fā)出的會診邀請單疾病診治過程中的有效醫(yī)學(xué)文書各項信息必須真實，應(yīng)由主管臨床醫(yī)師親自逐項認(rèn)真填寫并簽名臨床醫(yī)師向病理醫(yī)師傳遞關(guān)于患者的主要臨床信息:癥狀、體征、各種輔助檢查結(jié)果和手術(shù)所見、診斷意向和對病理學(xué)檢查提出的某些特殊要求TheimportanceofclinicaldataAge：SLLrareinpatientslessthan20ysMFHmainlyinagedpeopleLocation：LiposarcomaindeepertissueplainAngioblastoma同一戰(zhàn)壕的戰(zhàn)友診斷意向：腹部腫快？發(fā)燒待查？結(jié)腸腫物？重要化驗結(jié)果：

PSA、AFPCytology-細(xì)胞學(xué)ExperimentalstudyRESEARCHMETHODSMacroscopicobservationMicroscopicobservation(HE)EMImmunohistochemistryHybridizationPCRFlowcytometryMicroarray1.ElectronicmicroscopyCelljunctionCytoskeletonNeuroendocrinegranulesMelanosomesMitochondria

HER2（紅色）/CEP17（綠色）無擴增有擴增2.Hybridization:FISH,CISHALKBREAKAPARTPROBES,FISH彌漫性間變性大細(xì)胞性淋巴瘤,t（2;5）(NPM－ALK)In-situHybridizationEBERinNasopharyngealcarcinoma3.ImmunohistochemistryDiagnsticMarkersPrognosticmarkersPredictivemarkers(Targetchemotherapy)Follicularlymphoma

T(14;18)(q32;q21)t(14,18)(q32,q21)抗凋亡的bcl2基因持續(xù)表達(dá)2021Predictivemarkers

(Targetchemotherapy)

Breastcarcinoma：HerceptinGIST(gastrointestinalstromaltumor)：

Gleevec(格列衛(wèi))Bcelllymphomas:CD20amtibodies（美羅華）1+2+3+Immunohistochemistry

Treatment:HER-2/neuinbreastcarcinomaO+4.PCRPolymeraseChainReaction

ChromosomalTranslocation靶基因：

SYT-SSX1，t(x;18)(p11.23;q11)

SYT-SSX2，t(x;18)(p11.21;q11)

技術(shù)方法:RT-PCR

應(yīng)用范圍：

90%以上的滑膜肉瘤，特別是不常見部位的、發(fā)生于老年的滑膜肉瘤滑膜肉瘤病歷1病歷2M75bp100bp107bp通

III通

III5.MicroarrayscDNAMicroarrayDiffuselargecelllymphomaNEJM2002;346:1937-476.FLOWCYTOMETRYGeneticHallmarkofCompleteMoleDiploidDNAcompositionPaternal/androgenicgenome46XpXp23XSpermEmptyEggCOMPLETEMOLEPaternalChromosomeOnly(Androgenetic)PARTIALMOLE23XSperm23XSperm23XEgg69XpXpXmPaternalandMaternalChromosome(Triploid)FLOWCYTOMETRYFORPLOIDYLEARNINGOFPATHOLOGYSectionDGeneralpathologyisconcernedwiththebasicreactionsofcellsandtissuestoabnormalstimulithatunderliealldiseases.Systemicpathologyexaminesthespecificresponsesofspecializedorgansandtissuestomoreorlesswelldefinedstimuli.MajorpointsDefinitionCausesPathogenesisLesionsEffectsChineseproverbIhear,Iforget;Isee,Iremember;Ido,Iunderstand.ChapterTwo

CellandTissueInjury

CELLINJURYANDNECROSISGeneralmechanisms:Maintenanceoftheintegrityofcellmembranes.AerobicrespirationandproductionofATP.Synthesisofenzymesandstructureproteins.Preservationoftheintegrityofthegeneticapparatus.CELLSREACTTOADVERSEINFLUENCESADAPTINGSUSTAININGREVERSIBLEINJURYSUFFERINGIRREVERSIBLEINJURYANDDYINGSectionA:CellularAdaptation

SectionB:Degeneration

(reversibleinjury)

SectionC:CellDeath

SectionD:CellularAging

SectionA

Cellularadaptation:AtrophyHypertrophyHyperplasia

MetaplasiaCELLULARADAPTATIONExcessivephysiologicstresses.Somepathologicstimuli.Anew,butalteredstatepreservingtheviabilityofthecell.ATROPHYDecreaseinmassofthecellHYPERTROPHY

IncreaseinmassofthecellAtrophyPhysiologicalPathological

Fig2-5PATHOLICALATROPHY

Decreasedworkload(廢用性).Lossofinnervation(神經(jīng)性).Diminishedbloodsupply(貧血性).Pressure(壓迫性).Inadequatenutrition(營養(yǎng)不良性).Lossofendocrinestimulation(內(nèi)分泌性).Aging(老年性).MorphologyofatrophyBrownatrophyReductioninthenumberofcellorganelles.Increaseinthenumberofautophagicvacuoles.Lipofuscingranules(Brownatrophy)AtrophyEffects:ReversibleDecreaseinfunctionalcapacityHYPERTROPHYPhysiologicalPathological

Fig2-6HYPERTROPHYIncreasedfunctionaldemand.Specifichormonalstimulation.HYPERTROPHYPathologic:工作性代償性替代性內(nèi)分泌性HYPERPLASIAThemythofPrometheus.

Fig2-1HYPERPLASIA

Physiologichyperplasia:HormonalhyperplasiaCompensatoryhyperplasiaPathologichyperplasia:Excessivehormonalstimulation.EffectsoflocallyproducedGFsontargetcells.PARTIALHEPATECTOMYPrimingProliferationGroeth

lnhibitionGROWTHFACTORSANDCYTOKINESHGFTGF-EGFTNF-IL-6OthersADJUVANTSNorepinephrineInsulinGlucagonThyroidhormoneGROWTHINHIBITORSTGF-

OthersGrowthfactorsAdjuvanisMatrixdegradationProliferated

endometriumComplexhyperplasiaMetaplasiaOneadultcelltypeisreplacedbyanother.Geneticreprogrammingofstemcells.Epithelialandmesenchymal

metaplasia.Squamous

metaplasia

BronchialepitheliaEpitheliainbileductCervicalepitheliaIntestinalmetaplasiaofgastricepitheliaBonemetaplasia.慢性萎縮性胃炎，AB/PAS

染色：胃腺上皮--腸上皮化生chronicgastritis胃粘膜腸化Degeneration：Definition1.ACUTECELLULARSWELLINGSectionBEtiologyIschemicInfectiousToxic

心肌空泡變CELLULARSWELLINGEM:線粒體腫脹內(nèi)質(zhì)網(wǎng)擴張核糖體脫失糖原顆粒減少CELLULARSWELLINGEffects:Reversible,mildDecreaseinfunctionalcapacity

IntracellularaccumulationAnormalcellularconstituentaccumulatedinexcess,(e.g.Water,lipid,protein,carbohydrates,pigment)Anabnormalsubstance:exogenousendogenousIntracellularaccumulationAnormalendogenoussubstance,buttherateofmetabolismisinadequatetoremoveGeneticoracquireddefectsinmetabolism,packaging,transportorsecretion--storagedisease.Anabnormalexogenoussubstanceisdepositedduetothecellunabletodegradeortransportittoothersites2.FATTYCHANGEEtiologyIschemicInfectiousToxic

Starvation,corticosteroidtherapyHepatitistypeCAlcoholExcessiveentryoffreefattyacidsintotheliver(starvation,corticosteroidtherapy).Enhancedfattyacidsynthesis.Decreasedfattyacidoxidation.

Dncreased

esterificationoffattyacid---triglycerides(alcohol).Decreasedapoproteinsynthesis(CCl4).Impairedlipoproteinsecretionfromtheliver(alcohol).FATTYCHANGEMorphologyoffattychangeSudanIII,OilredO,OsmicacidLiverHeartKidney脂肪肝嚴(yán)重的肝細(xì)胞脂肪變性，并出現(xiàn)一系列臨床異?！螀^(qū)脹滿、痛、厭油食轉(zhuǎn)氨酶高等心肌脂肪變LipidsSteatosis(fattychanges)

clearvacuolesinliver,heartCholesterolandcholesterolestersAtherosclerosis

XanthomasInflammationandnecrosis

CholesterolosisIntracellularhyalinechangesHyalinedegenerationofarteriolesHyalinedegenerationofconnectivetissue3.Hyalinechanges(degeneration)

Absorptionofproteincausinghyalinedropletsinproximalepithelialcellsinthekidney.

Russelbodiesinplasmacells.Viralinclusionsinthecytoplasmorthenucleus.Massesofalteredintermediatefilaments(Mallorybodies).IntracellularhyalinechangesProteinreabsorptiondropletsintherenaltubularepithelium.膠元纖維玻璃樣變Aheterogeneousgroupofpathogenicfibrillarproteinsaccumulatingintissuesandorgans.ExcesssynthesisResistancetocatabolism4.AMYLOIDOSISChemicalnatureofamyloidfibrilsTwomajorforms:AL(amyloidlightchainprotein)AA(amyloid-associatedprotein):

DerivedfromserumAA(12kd)synthesizedinliverandelevatedininflammatorystates.Minorformsofamyloidfibrils:Transthyretin(TTR):Amutantformofaserumproteininfamilialamyloid

polyneuropathy.AvariantofTTRinaging.Beta-2-microglobulin(thecomponentofclassIMHCmolecules)inlong-term

hemidialysis.

primary(B-celldyscrasia,AL)Secondaryorreactive(AA):Collagendiseases,bronchiectasis,chronic

osteomyelitis.

Hemodialysis-related:Beta-2-microglobulindeposition.Hereditary(AA)ClinicalformsofamyloidosisSystemicamyloidosis:

Nodular(tumor-formingdeposits,B-celldyscrasia,AL)Endocrineamyloidosis(procalcitonin)

Amyloidosisofaging:Heart,lung,pancreas,spleen,brain.LocalizedamyloidosisAmyloidosisoftheliverischaracterizedbyhomogeneouseosinophilicmaterialinthesinusoids5.GlycogenExcessiveintracellulardepositsofglycogenareseeninpatientswithanabnormalityineitherglucoseorglycogenmetabolismClearvacuolesinthecytoplasmDMGlycogenstoragedisease肝糖元，卡紅

Exogenous:

CarbonTattooingEndogenous:

LipofuscinMelanin

Hemosiderin

Bilirubin6.Pigmentation文身之皮膚痣，黑色素肺GPC，含鐵血黃素，F(xiàn)e肝血色病Idiopathichemochromatosis

膽汁與膽色素DystrophiccalcificationMetastaticcalcification7.Pathologiccalcification

Necrotictissues

AtheromaDamagedheartvalves

DystrophiccalcificationFig2-13冠狀動脈鈣化

IncreasedsecretionofparathyroidhormoneDestructionofbonetissueVitaminD-relateddisorders:

SarcoidosisRenalfailureMetastaticcalcificationHypercalcimiaMetastaticcalcificationAffectingInterstitialtissueofgastricmucosaKidneysLungsPulmonaryveinsSystemicarteries肺轉(zhuǎn)移性鈣化肺轉(zhuǎn)移性鈣化SectionCCELLDEATH一、NECROSISDefinitionCausesLesionTypesFatesNECROSISThesumofthemorphologicchangesthatfollowcelldeathinlivingtissueandorgan:Denaturationofproteins.Enzymaticdigestionoforganellesandcytosol.Swelling,denaturationandcoagulationofproteinsBreakdownofcellularorganellesCellrupture

Commontypeofnecrosisafterexogenousstimuli.Enzymaticdigestionbylysosomalenzymesofthedeadcellsthemselves.AUTOLYSISHETEROLYSISDigestionbylysosomalenzymesofimmigrantleukocytes.ThreepatternofnuclearchangesKaryolysis(DNaseactivity)Pyknosis(DNAcondensation)Karyorrhexis(fragmentationofpyknoticnucleus)MorphologicappearanceofnecrosisIncreasedeosinophilia:LossofRNAinthecytoplasmIncreasedbindingofeosintodenatured

cytoplasmic

proteinMoreglassyhomogeneousappearanceLossofglycogenparticlesVacuolatedandmoth-eatencytoplasmCalcificationofnecroticcellsTYPESOFCELLDEATH

necrosis

Coagulationnecrosis

Caseousnecrosis

Gangrene

Liquefactionnecrosis(fatnecrosis)

FibrinoidnecrosisApoptosis1.CoagulationnecrosisDenaturesofbothstructuralandenzymaticproteinsbyinjuryorthesubsequentincreasingintracellularacidosis.HerpessimplexhepatitiswithscatteredfociofcoagulativenecrosisCaseousnecrosisAsubtypeofcoagulationnecrosisWhiteandcheesyTuberculosisCompletelyobliteratedtissuearchitectureTB，干酪樣壞死GangreneAsubtypeofcoagulationnecrosisDrygangreneWetgangreneGasgangrene2.LiquefactivenecrosisBacterialorfungalinfectionsCentralnervoussystemAmebiasis肺膿腫腸阿米巴，液化性壞死腸阿米巴，液化性壞死腦軟化FatnecrosisTraumaticActivatedpancreaticlipasesAcutepancreatitis:fatnecrosisandinflammatorycellsindamagedpancreaticparenchyma3.FibrinoidnecrosisThecombinationofcelldeathanddepositionoffibrin-likematerialFibrinImmunoglobulinOtherplasmaproteinsFibrinoidnecrosis

DeeplyeosinophilicCollagendiseasesNecroticvasculitisMalignanthypertension纖維素樣壞死AbsorptionDischarge:ErosionUlcerSinusFistulaCavitationOrganizationEncapsulationCalcificationFatesofnecrosis二、APOPTOSIS(Programmedcelldeath)

Programmeddestructionofcellsduringembryogenesis.Hormonedependentinvolutionoftissuesintheadult.Celldeletioninproliferatingcellpopula-

tions(intestinalcryptepithelium),tumors,andlymphoidorgans.

Pathologicatrophyinparenchymal

organsafterductobstruction.CelldeathbycytotoxicTcells.Cellinjuryincertainviraldiseases.Celldeathproducedbyavarietyofinjuriousstimuligiveninlowdoses(dthermalinjury).MORPHOLOGICALFEATURESOFAPOPTOSISCellshrinkageChromatincondensationandfragmentation.Formationofcytoplasmicblebsandapoptoticbodies.Phagocytosisofapoptoticbodiesbyadjacenthealthycellsormacrophages.Lackofinflammation.

Necrosis

ApoptosisStimuliHypoxiaPhysicalToxinsPathologicalHistology

CellswellingSinglecellCoagulationNChromatinDisruptionofcondensationorganellesApoptoticbodiesDNA

RandomInternucleosomalbreakdown

Diffuse

Necrosis

ApoptosisMechanismATPdepletionGeneactivationMembraneEndonucleaseinjuryFreeradicalsTissue

InflammationNoinflammation

reaction

PhagocytosisofapoptoticbodiesFig1-18Biochemicalfeaturesofapoptosis1.PROTEINCLEAVAGE:

Caspases(cysteineprotease)Nuclearscaffold

Cytoskeletalprotein2.PROTEINCROSS-LINKING:

Transglutaminase

Cytoplasmicproteinshrunkenshalls

apoptoticbodiesBiochemicalfeaturesofapoptosis3.DNAbreakdown:50-300kbpiecesCa2+,Mg2+dependentendonucleasesDNAoligonucleosomesDNAladders(alsoseeninnecrosis)4.PHAGOCYTICRECOGNITION

Receptorsonmacrophagesforthesurfacecomponents(phosphatidylserine,thrombospondin)onapoptoticbodies.Fig1-19Apoptosis-associatedgenesbcl-2,c-myc,p53Fig1-20SectionD:CellularAging

AnumberofcellfunctiondeclineOxidativephosphorylationisreducedAdecreasedcapacityforuptakeofnutrientsandforrepairofDNAdamageAccumulationoflipofuscinAgeneticallydeterminedclockEffectsofcontinuousexposuretoexogeneousinfluenceSectionA:RegenerationSectionB:FibrousRepairSectionC:WoundhealingSectionD:FractureRepairChapterThree:RepairLabilecellsStablecellsPermanentcellsRegenerationcapacitySectionA:

Regeneration1.Completelyregeneration2.FibrousrepairLabilecells

Normallydividedactivelytoreplacecellsthatarebeingcontinuouslostfromthebody.

Thechancesofrestorationbyregenerationareexcellent.

Includingepithelialstemcellsinbasallayer,hematopoieticstemcellinbonemarrow.TheregenerativecapacitytypesofcellsStablecells

Alonglifespanandarecharacterizedbyalowrateofdivision,retainthecapacitytoenterthemitoticcellcycleiftheneedarises.Chancesofregenerationremain.Includingparenchymalcellofsolidglandularorgan(liver,pancreas)andmesenchymalcells.TheregenerativecapacitytypesofcellsPermanentcells

Nocapacityformitoticdivisioninpostnatallife.

Neurons,striatedandcar