皮肤损伤的修复课件

讲授人：金以超讲师纤维性修复fibroplasia

皮肤损伤的修复讲授人：金以超讲师纤维性修复皮肤损伤的修1修复repair再生Regeneration

纤维性修复不能由再生修复的损伤，通过肉芽组织增生填补缺损并转化为瘢痕组织的过程。修复再生Regeneration2肉芽组织Granulationtissue一、概念：

Granulation

tissue肉芽组织Granulationtissue一、概念：3肉芽组织的结构：

镜下：

二、肉芽组织的形态肉芽组织的结构：镜下：二、肉芽组织的形态4毛细血管多与垂直创面，在创口表面形成袢状弯曲毛细血管多与垂直创面，在创口表面形成袢状弯曲5Grossappearance：

红色颗粒样，柔软湿润，触之易出血Grossappearance：红色颗粒样，柔软湿润，触6三、肉芽组织的功能3、填补连接伤口或其他缺损

1、抗感染及保护创面

2、机化血凝块、坏死组织及其他异物

三、肉芽组织的功能3、填补连接伤口或其他缺损1、抗感染及7健康肉芽不良肉芽健康肉芽不良肉芽8四、肉芽组织的结局新生的毛细血管增生的纤维母细胞一定量的炎性细胞小动脉、小静脉闭合、消失胶原纤维、纤维细胞纤维结缔组织瘢痕组织（scartissue)吸收、消散四、肉芽组织的结局新生的毛细血管增生的纤维母细胞一定量的炎9GranulationtissueScartissueGranulationtissueScartissue10五、瘢痕组织对机体的影响利1.保持组织器官完整性2.保持组织器官坚固性五、瘢痕组织对机体的影响利1.保持组织器官完整性2.保持组织11弊1.瘢痕收缩2.瘢痕粘连弊1.瘢痕收缩2.瘢痕粘连123.瘢痕疙瘩(keloid)3.瘢痕疙瘩(keloid)134.瘢痕膨出4.瘢痕膨出14六、肉芽组织和瘢痕

组织的形成过程及机制血管生成成纤维细胞增殖和迁移细胞外基质成分的积聚和成纤维组织的重建六、肉芽组织和瘢痕

组织的形成过程及机制血管15（一）血管生成的过程从发生学和组织学的观点出发，把广义的血管新生（neovascularization）分为两种类型:endothelialprogenitorcell,EPCangioblast最近研究证明，血液中存在EPC，它参与重症缺血区域血管的形成，所以病理状态下的血管生成，既包括广义的血管形成，又有狭义的血管生成。血管形成（vasculogenesis）血管生成（angiogenesis）（一）血管生成的过程从发生学和组织学的观点出发，把广义的血管16出芽方式的血管生成及包含的步骤：Vasodilation------NOIncreased

permeability------VEGF•Proliferationofendothelialcellsjustbehindtheleadingfrontofmigratingcells•Remodelingintocapillarytubes•Migrationofendothelialcellstowardtheareaoftissue

injury出芽方式的血管生成及包含的步骤：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总结和展望Howtodealwithscar？总结和展望Howtodealwithscar？27皮肤损伤的修复课件28

讲授人：金以超讲师纤维性修复fibroplasia

皮肤损伤的修复讲授人：金以超讲师纤维性修复皮肤损伤的修29修复repair再生Regeneration

纤维性修复不能由再生修复的损伤，通过肉芽组织增生填补缺损并转化为瘢痕组织的过程。修复再生Regeneration30肉芽组织Granulationtissue一、概念：

Granulation

tissue肉芽组织Granulationtissue一、概念：31肉芽组织的结构：

镜下：

二、肉芽组织的形态肉芽组织的结构：镜下：二、肉芽组织的形态32毛细血管多与垂直创面，在创口表面形成袢状弯曲毛细血管多与垂直创面，在创口表面形成袢状弯曲33Grossappearance：

红色颗粒样，柔软湿润，触之易出血Grossappearance：红色颗粒样，柔软湿润，触34三、肉芽组织的功能3、填补连接伤口或其他缺损

1、抗感染及保护创面

2、机化血凝块、坏死组织及其他异物

三、肉芽组织的功能3、填补连接伤口或其他缺损1、抗感染及35健康肉芽不良肉芽健康肉芽不良肉芽36四、肉芽组织的结局新生的毛细血管增生的纤维母细胞一定量的炎性细胞小动脉、小静脉闭合、消失胶原纤维、纤维细胞纤维结缔组织瘢痕组织（scartissue)吸收、消散四、肉芽组织的结局新生的毛细血管增生的纤维母细胞一定量的炎37GranulationtissueScartissueGranulationtissueScartissue38五、瘢痕组织对机体的影响利1.保持组织器官完整性2.保持组织器官坚固性五、瘢痕组织对机体的影响利1.保持组织器官完整性2.保持组织39弊1.瘢痕收缩2.瘢痕粘连弊1.瘢痕收缩2.瘢痕粘连403.瘢痕疙瘩(keloid)3.瘢痕疙瘩(keloid)414.瘢痕膨出4.瘢痕膨出42六、肉芽组织和瘢痕

组织的形成过程及机制血管生成成纤维细胞增殖和迁移细胞外基质成分的积聚和成纤维组织的重建六、肉芽组织和瘢痕

组织的形成过程及机制血管43（一）血管生成的过程从发生学和组织学的观点出发，把广义的血管新生（neovascularization）分为两种类型:endothelialprogenitorcell,EPCangioblast最近研究证明，血液中存在EPC，它参与重症缺血区域血管的形成，所以病理状态下的血管生成，既包括广义的血管形成，又有狭义的血管生成。血管形成（vasculogenesis）血管生成（angiogenesis）（一）血管生成的过程从发生学和组织学的观点出发，把广义的血管44出芽方式的血管生成及包含的步骤：Vasodilation------NOIncreased

permeability------VEGF•Proliferationofendothelialcellsjustbehindtheleadingfrontofmigratingcells•Remodelingintocapillarytubes•Migrationofendothelialcellstowardtheareaoftissue

injury出芽方式的血管生成及包含的步骤：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