皮膚損傷的修復(fù)課件

講授人：金以超講師纖維性修復(fù)fibroplasia

皮膚損傷的修復(fù)講授人：金以超講師纖維性修復(fù)皮膚損傷的修1修復(fù)repair再生Regeneration

纖維性修復(fù)不能由再生修復(fù)的損傷，通過肉芽組織增生填補(bǔ)缺損并轉(zhuǎn)化為瘢痕組織的過程。修復(fù)再生Regeneration2肉芽組織Granulationtissue一、概念：

Granulation

tissue肉芽組織Granulationtissue一、概念：3肉芽組織的結(jié)構(gòu)：

鏡下：

二、肉芽組織的形態(tài)肉芽組織的結(jié)構(gòu)：鏡下：二、肉芽組織的形態(tài)4毛細(xì)血管多與垂直創(chuàng)面，在創(chuàng)口表面形成袢狀彎曲毛細(xì)血管多與垂直創(chuàng)面，在創(chuàng)口表面形成袢狀彎曲5Grossappearance：

紅色顆粒樣，柔軟濕潤(rùn)，觸之易出血Grossappearance：紅色顆粒樣，柔軟濕潤(rùn)，觸6三、肉芽組織的功能3、填補(bǔ)連接傷口或其他缺損

1、抗感染及保護(hù)創(chuàng)面

2、機(jī)化血凝塊、壞死組織及其他異物

三、肉芽組織的功能3、填補(bǔ)連接傷口或其他缺損1、抗感染及7健康肉芽不良肉芽健康肉芽不良肉芽8四、肉芽組織的結(jié)局新生的毛細(xì)血管增生的纖維母細(xì)胞一定量的炎性細(xì)胞小動(dòng)脈、小靜脈閉合、消失膠原纖維、纖維細(xì)胞纖維結(jié)締組織瘢痕組織（scartissue)吸收、消散四、肉芽組織的結(jié)局新生的毛細(xì)血管增生的纖維母細(xì)胞一定量的炎9GranulationtissueScartissueGranulationtissueScartissue10五、瘢痕組織對(duì)機(jī)體的影響利1.保持組織器官完整性2.保持組織器官堅(jiān)固性五、瘢痕組織對(duì)機(jī)體的影響利1.保持組織器官完整性2.保持組織11弊1.瘢痕收縮2.瘢痕粘連弊1.瘢痕收縮2.瘢痕粘連123.瘢痕疙瘩(keloid)3.瘢痕疙瘩(keloid)134.瘢痕膨出4.瘢痕膨出14六、肉芽組織和瘢痕

組織的形成過程及機(jī)制血管生成成纖維細(xì)胞增殖和遷移細(xì)胞外基質(zhì)成分的積聚和成纖維組織的重建六、肉芽組織和瘢痕

組織的形成過程及機(jī)制血管15（一）血管生成的過程從發(fā)生學(xué)和組織學(xué)的觀點(diǎn)出發(fā)，把廣義的血管新生（neovascularization）分為兩種類型:endothelialprogenitorcell,EPCangioblast最近研究證明，血液中存在EPC，它參與重癥缺血區(qū)域血管的形成，所以病理狀態(tài)下的血管生成，既包括廣義的血管形成，又有狹義的血管生成。血管形成（vasculogenesis）血管生成（angiogenesis）（一）血管生成的過程從發(fā)生學(xué)和組織學(xué)的觀點(diǎn)出發(fā)，把廣義的血管16出芽方式的血管生成及包含的步驟：Vasodilation------NOIncreased

permeability------VEGF?Proliferationofendothelialcellsjustbehindtheleadingfrontofmigratingcells?Remodelingintocapillarytubes?Migrationofendothelialcellstowardtheareaoftissue

injury出芽方式的血管生成及包含的步驟：Vasodilation-17?Suppressionofendothelialproliferationandmigrationanddepositionofthebasementmembrane?Recruitmentofperiendothelialcells(pericytesforsmallcapillariesandsmoothmusclecellsforlargervessels)toformthematurevessel?Suppressionofendothelial18Theprocessofangiogenesisinvolvesavarietyofgrowth

factors,cell–cellinteractions,interactionswithECMproteins,andtissueenzymes.1、GrowthFactorsInvolvedinAngiogenesis

VEGF

BasicFibroblastGrowthFactor(bFGF)

AngiopoietinsVEGFstimulatesbothmigrationandproliferationofendothelialcells,initiatestheprocessofcapillarysproutinginangiogenesis.VEGF

contributestothe

formationofthevascularlumen.Theprocessofangiogenesisin19bFGF-2participatesinangiogenesismostlybystimulatingtheproliferationofendothelialcells.Italsopromotesthemigrationofmacrophagesandfibroblaststothedamagedarea,andstimulatesepithelialcellmigrationtocoverepidermalwounds.Ang1andAng2

aregrowthfactorsthatplayaroleinangiogenesisandthestructuralmaturationof

newvessels.bFGF-2participatesinangioge20

Matrixmetalloproteinases(MMPs)

degradetheECMtopermitremodelingand

extensionofthevasculartube.

2、ECMproteinsParticipatingintheprocessofvesselsproutinginangio-genesis.Providingthescaffoldforvesselgrowth.Integrins,especiallyαγβ3,

haveimportantroleinformationandstabilityofvessel.Matrixmetalloproteinases(MM21ActivationofFibroblastsandDepositionofECM

Twosteps:

(1)MigrationandproliferationoffibroblastsintothesiteofinjuryMany

growthfactors,includingPDGF,FGF-2,andTGF-β,drive

fibroblaststosynthesizeconnectivetissueproteins.Themajorsourceofthesefactorsisinflammatorycells,particularlymacrophages,whicharepresentatsitesofinjuryandingranulationtissue.ActivationofFibroblastsand22Proliferatingfibroblastsandnewvessels

Fibroblastssynthetic

DepositionofECM

Collagensynthesis

iscriticaltothedevelopmentofstrengthinahealingwoundsite.Collagensynthesisbyfibroblastsbeginsearlyinwoundhealing(days3to5)andcontinuesforseveralweeks,dependingonthesizeofthewound.Netcollagenaccumulation

dependsnotonlyonincreasedsynthesisbutalsoondiminishedcollagendegradation.(2)DepositionofECMproteinsProliferatingfibroblastsand23Ultimately,thegranulationtissueevolvesintoascarcomposedoflargelyinactive,spindle-shapedfibroblasts,densecollagen,fragmentsofelastictissue,andotherECMcomponents.Asthescarmatures,thereisprogressivevascularregression,whicheventuallytransformsthehighlyvascularizedgranulationtissueintoapale,largelyavascularscar.Ultimately,thegranulationti24GrowthFactorsInvolvedinECM

Deposition

andScarFormationTGF-βstimulatestheproductionofcollagen,fibronectin,andproteoglycans,anditinhibitscollagendegradationbybothdecreasingproteinaseactivityandincreasingtheactivityoftissueinhibitorsofproteinases.PDGFcausesmigrationandproliferationoffibroblastsandsmoothmusclecellsandmaycontributetothemigrationofmacrophages

.CytokinesmayalsofunctionasgrowthfactorsandparticipateinECMdepositionandscarformation.IL-1andIL-13actonfibroblaststostimulatecollagensynthesis,andcanenhancetheproliferationandmigrationoffibroblasts.GrowthFactorsInvolvedinECM25RemodelingofConnectiveTissue

AbalancebetweensynthesisanddegradationofECMproteins.ThedegradationofcollagensandotherECMcomponentsisaccomplishedbyafamilyofmatrixmetalloproteinases(MMPs)Tissueinhibitorsofmetalloproteinases(TIMP)RemodelingofConnectiveTissu26總結(jié)和展望Howtodealwithscar？總結(jié)和展望Howtodealwithscar？27皮膚損傷的修復(fù)課件28

講授人：金以超講師纖維性修復(fù)fibroplasia

皮膚損傷的修復(fù)講授人：金以超講師纖維性修復(fù)皮膚損傷的修29修復(fù)repair再生Regeneration

纖維性修復(fù)不能由再生修復(fù)的損傷，通過肉芽組織增生填補(bǔ)缺損并轉(zhuǎn)化為瘢痕組織的過程。修復(fù)再生Regeneration30肉芽組織Granulationtissue一、概念：

Granulation

tissue肉芽組織Granulationtissue一、概念：31肉芽組織的結(jié)構(gòu)：

鏡下：

二、肉芽組織的形態(tài)肉芽組織的結(jié)構(gòu)：鏡下：二、肉芽組織的形態(tài)32毛細(xì)血管多與垂直創(chuàng)面，在創(chuàng)口表面形成袢狀彎曲毛細(xì)血管多與垂直創(chuàng)面，在創(chuàng)口表面形成袢狀彎曲33Grossappearance：

紅色顆粒樣，柔軟濕潤(rùn)，觸之易出血Grossappearance：紅色顆粒樣，柔軟濕潤(rùn)，觸34三、肉芽組織的功能3、填補(bǔ)連接傷口或其他缺損

1、抗感染及保護(hù)創(chuàng)面

2、機(jī)化血凝塊、壞死組織及其他異物

三、肉芽組織的功能3、填補(bǔ)連接傷口或其他缺損1、抗感染及35健康肉芽不良肉芽健康肉芽不良肉芽36四、肉芽組織的結(jié)局新生的毛細(xì)血管增生的纖維母細(xì)胞一定量的炎性細(xì)胞小動(dòng)脈、小靜脈閉合、消失膠原纖維、纖維細(xì)胞纖維結(jié)締組織瘢痕組織（scartissue)吸收、消散四、肉芽組織的結(jié)局新生的毛細(xì)血管增生的纖維母細(xì)胞一定量的炎37GranulationtissueScartissueGranulationtissueScartissue38五、瘢痕組織對(duì)機(jī)體的影響利1.保持組織器官完整性2.保持組織器官堅(jiān)固性五、瘢痕組織對(duì)機(jī)體的影響利1.保持組織器官完整性2.保持組織39弊1.瘢痕收縮2.瘢痕粘連弊1.瘢痕收縮2.瘢痕粘連403.瘢痕疙瘩(keloid)3.瘢痕疙瘩(keloid)414.瘢痕膨出4.瘢痕膨出42六、肉芽組織和瘢痕

組織的形成過程及機(jī)制血管生成成纖維細(xì)胞增殖和遷移細(xì)胞外基質(zhì)成分的積聚和成纖維組織的重建六、肉芽組織和瘢痕

組織的形成過程及機(jī)制血管43（一）血管生成的過程從發(fā)生學(xué)和組織學(xué)的觀點(diǎn)出發(fā)，把廣義的血管新生（neovascularization）分為兩種類型:endothelialprogenitorcell,EPCangioblast最近研究證明，血液中存在EPC，它參與重癥缺血區(qū)域血管的形成，所以病理狀態(tài)下的血管生成，既包括廣義的血管形成，又有狹義的血管生成。血管形成（vasculogenesis）血管生成（angiogenesis）（一）血管生成的過程從發(fā)生學(xué)和組織學(xué)的觀點(diǎn)出發(fā)，把廣義的血管44出芽方式的血管生成及包含的步驟：Vasodilation------NOIncreased

permeability------VEGF?Proliferationofendothelialcellsjustbehindtheleadingfrontofmigratingcells?Remodelingintocapillarytubes?Migrationofendothelialcellstowardtheareaoftissue

injury出芽方式的血管生成及包含的步驟：Vasodilation-45?Suppressionofendothelialproliferationandmigrationanddepositionofthebasementmembrane?Recruitmentofperiendothelialcells(pericytesforsmallcapillariesandsmoothmusclecellsforlargervessels)toformthematurevessel?Suppressionofendothelial46Theprocessofangiogenesisinvolvesavarietyofgrowth

factors,cell–cellinteractions,interactionswithECMproteins,andtissueenzymes.1、GrowthFactorsInvolvedinAngiogenesis

VEGF

BasicFibroblastGrowthFactor(bFGF)

AngiopoietinsVEGFstimulatesbothmigrationandproliferationofendothelialcells,initiatestheprocessofcapillarysproutinginangiogenesis.VEGF

contributestothe

formationofthevascularlumen.Theprocessofangiogenesisin47bFGF-2participatesinangiogenesismostlybystimulatingtheproliferationofendothelialcells.Italsopromotesthemigrationofmacrophagesandfibroblaststothedamagedarea,andstimulatesepithelialcellmigrationtocoverepidermalwounds.Ang1andAng2

aregrowthfactorsthatplayaroleinangiogenesisandthestructuralmaturationof

newvessels.bFGF-2participatesinangioge48

Matrixmetalloproteinases(MMPs)

degradetheECMtopermitremodelingand

extensionofthevasculartube.

2、ECMproteinsParticipatingintheprocessofvesselsproutinginangio-genesis.Providingthescaffoldforvesselgrowth.Integrins,especiallyαγβ3,

haveimportantroleinformationandstabilityofvessel.Matrixmetalloproteinases(MM49ActivationofFibroblastsandDepositionofECM

Twosteps:

(1)MigrationandproliferationoffibroblastsintothesiteofinjuryMany

growthfactors,includingPDGF,FGF-2,andTGF-β,drive

fibroblaststosynthesizeconnectivetissueproteins.Themajorsourceofthesefactorsisinflammatorycells,particularlymacrophages,whicharepresentatsitesofinjuryandingranulationtissue.ActivationofFibroblastsand50Proliferatingfibroblastsandnewvessels

Fibroblastssynthetic

DepositionofECM

Collagensynthesis

iscriticaltothedevelopmentofstrengthinahealingwoundsite.Collagensynthesisbyfibroblastsbeginsearlyinwoundhealing(days3to5)andcontinuesforseveralweeks,dependingonthesizeofthewound.Netcollagenaccumulation

dependsnotonlyonincreasedsynthesisbutalsoondiminishedcollagendegradation.(2)DepositionofECMproteinsProliferatingfibroblastsand51Ultimately,thegranulationtissueevolvesintoascarcomposedoflargelyinactive,spindle-shapedfibroblasts,densecollagen,fragmentsofelastictissue,andotherECMcomponents.Asthescarmatures,thereisprogressivevascularregression,whicheventuallytransformsthehighlyvascularizedgranulationtissueintoapale,largelyavascularscar.Ultima