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A COMPILATION
ON
INFLAMMATION AND HEALING
SESSION 2016-2017
Department of Rog Nidan
Dayanand Ayurvedic College, Jalandhar
INDEX
1. INFLAMMATION
A) DEFINITION
B) CAUSES
C) SIGNS OFINFLAMMATION
D) TYPES OF INFLAMMATION
E) ACUTE INFLAMMATION
F) REGULATION INFLAMMATION
G) CHEMICAL MEDIATORS OF INFLAMMATION
H) CHRONICINFLAMMATION
2. HEALING
A) DEFINITION
B) REGENERATION
C) REPAIR
D) WOUND HEALING
INFLAMMATION
Inflammation isdefinedasthe local response of livingmammaliantissuestoinjurydue to anyagent.It
isa bodydefense reactioninordertoeliminate orlimitthe spreadof injuriousagentaswell asto
remove the consequentnecrosedcellandtissues.
CAUSES
The agentscausinginflammationmaybe asunder:
1.Physical agentslike heat,cold, radiation,mechanical trauma.
2.Chemical agentslike organicandinorganicpoisons.
3.Infective agentslike bacteria,viruses,andtheirtoxins.
4.Immunological agents like cell-mediatedandantigen-antibodyreactions.
Thus inflammationisdistinctfrominfection –the formeristhe protective response bythe bodywhile
the latteris invasionintothe bodybyharmful microbesandtheirresultantill effectsbytoxin.
Inflammationinvolves twoprocesses:
a) inflammatory response
b) healing
SIGNS OF INFLAMMATION
The famous5 cardinal signs of inflammationas:
1. Redness
2. Swelling
3. Heat
4. Pain
5. Loss of function
Inflammation and Healing
TYPES OF INFLAMMATION
Dependinguponthe defensecapacityof the hostand durationof response inflammationcanbe
classifiedinto AcuteandChronic
1. Acute inflammationisa shortdurationand representsthe earlybodyreactionandisusually
followedbyrepair.The mainfeaturesof acute inflammationare
a) accumulationof fluidandplasmaatthe affectedsite.
b) intravascularactivationof the platelets
c) polymorphonuclearneutrophilsasinflammatorycells.
2. Chronic inflammationisof longerdurationandoccurs eitherafterthe causative agentof acute
inflammationpersistsforalongtime or the stimulusissuchthat it induceschronicinflammation
fromthe beginning.The characteristicfeature of chronicinflammationispresence of chronic
inflammatorycellssuchaslymphocytesplasmacellsandmacrophages.
ACUTE INFLAMMATION
The changesis acute inflammationcanbe conveniently describedunderthe following2headings:
1. Vascular events
2. Cellularevents
Vascular events
Alterationinthe microvasculature isthe earliestresponse totissue injury.These alterationsinclude :
a) Haemodynamicchanges
b) Changesinvascularpermeability
A) Haemodynamicchanges – the earliestfeatures of inflammatoryresponse resultfromchanges
inthe vascularflowandcalibre of small bloodvesselsinthe injuredtissues.The sequence of
these changesisas under:
1. Irrespective of the type of injuryimmediate vascularresponse isof transientvasoconstrictionof
arterioles.Withmildformof injurythe bloodflow maybe re-establishedin3-5secswhile with
more severe injuryvasoconstrictionlastforabout5 mins.
2. Nextfollows persistentprogressive vasodilatation whichinvolvesmainlythe arterioles .
Vasodilatationresultsinincreasedbloodvolume inmicrovascularbedof the areawhichis
responsible forrednessandwarmthatthe site of acute inflammation.
3. Progressive vasodilatationinturnmayelevate local hydrostaticpressure resultingin
transudationof fluidintoextracellularspace .Thisisresponsibleforswellingatlocal site.
4. Slowingor stasisof microcirculation occurs . Slowingisattributedtoincreasedpermeabilityof
microvasculature the resultsinincreasedconcentrationof redcells.
5. Stasisor slowingisfollowedby leucocytic marginationor peripheral orientationof leucocytes
alongthe vascularendotheliumafterthisthese move andmigrate throughgaps between
endothelial cells into the extravascularspace.Thisprocessiscalledasemigration.
The reactionelicited isknownas tripleresponse or red lineresponse consistingof following :
1. Red line appearswithinafewsecondsfollowingstrokingandresultsfromlocal vasodilatationof
capillariesandvenules.
2. Flareis the bright reddishappearance orflushsurroundingthe redline andresultsin
vasodilatationof adjacent arterioles.
3. Wheal isthe swellingoredemaof the surroundingskinoccuringdue totransudationof fluidinto
the extravascularspace .
B) Altered vascularpermeability-
PATHOGENESIS- inandaround inflamedtissue compartmentwhichcomesfrombloodplasmabyits
escape throughthe endothelial wall of peripheral vascularbed.Inthe initial stage the escape of
fluidisdue tovasodilatationandconsequentelevationinhydrostaticpressure.Thisistransudate in
nature.The presence of edemadue toincreasedvascular permeability of microvascularbed
MECHANISM OF INCREASED VASCULAR PERMEABILITY-
1) CONTRACTION OF ENDOTHELIAL CELLS-Thisismost commonmechanismof increasedleakiness
that affectsvenulesexclusivelywhilecapillariesandarterioles remainunaffected.The
endothelial cellsdeveloptemporarygapsbetweenthemdue totheircontractionresultingin
vascularleakiness.Itismediatedbyhistamine
2) RETRACTION OF ENDOTHELIAL CELLS- inthismechanismthere isstructural re-organisationof
the cytoskeletonof endothelial cellsthatcausesreversible retractionatthe intercellular
junctions.Thischange tooaffectsthe venulesandismediatedbycytokinessuchas interleukin -
1.
3) DIRECT INJURYTO ENDOTHELIAL CELLS- Directinjuryto the endothelial causescell necrosisand
appearance of physical gapsat the sitesof detachedendothelialcells.Processof thrombosis is
intiatedatthe site of endothelial cells.
4) ENDOTHELIAL INJURYMEDIATED BY LEUCOCYTES –Adherence of leucocytestothe
endotheliumatthe site of inflammationmayresultinactivationof leucocytes.The activated
leucocytesrelease proteolyticenzymesandtoxicoxygenspecieswhichmaycause increased
vascularleakinessandendothelialinjury.
5) NEOVASCULARISATION- Inadditionthe newly formedcapillariesunderthe influenceof
vascularendothelial growthfactorduringthe processof repairandin tumorsare excessively
leaky.
CELLULAR EVENTS
The cellularphase of inflammationconsistsof 2processes:
1. Exudationof leucocytes
2. Phagocytosis
1. Exudationof leucocytes- the escape of leucocytesfromthe lumenof microvasculature tothe
interstitialtissue isthe mostimportantfeatureof inflammatoryresponse .the acute inflammation
includesfirstlineof bodydefense followedbymonocytes andmacrophages.The changes leadingto
migrationof leucocytesare:
a) Changesin the formed elements ofblood- inthe earlystage of inflammation the rate of flow of
bloodisincreaseddue tovasodilatation.Butsubsequentlythere isslowingof bloodstream.due to
slowingandstasisthe central streamof cellswidensandperipheral plasmazone becomesnarrower
because of lossof plasmaby exudation.Thisphenomenonisknownas margination.
b) Rollingandadhesion- Peripherallymarginationandpavementedneutrophilsslowlyrolloverthe
endothelial cellsliningthe vessel walls.Thisisfollowedbytransientbondbetweenthe leucocytesand
endothelial cellsbecoming firmer.Itincludes3phases:
1)selectins
2)integrins
3)immunoglobulinssuperfamilyadhesionmolecules
c)Emigration –afterstickingof neutrophilstoendotheliumthe formermove alongthe endothelial cells
isfoundwhere the neutrophilsthrowoutcytoplasmicpseudopods.Subsequentlythe neutrophilslodged
betweenthe endothelial cellsandbasementmembrane crossthe basementmembrane bydamagingit
locallywithsecretedcollagenasesandescape intothe extravascularspace thisisknownas emigration.
d) Chemotaxis-The chemotacticfactor( cytokines,plateletfactoretc) mediatedtransmigrationof
leucocytesaftercrossingseveral barriers( endothelium,basementmembrane ,etc) toreach the
interstitial tissuesiscalledchemotaxis
2. Phagocytosis-phagocytosisisdefinedasthe processof engulfmentof solidparticulatematerialbythe
cells(cell-eating).The cellsperformingthisfunctionare called phagocytes.There are mainlytwotypesof
phagocyticcells:
a) Polymorphonuclearneutrophils(PMNs) whichappearearlyinacute inflammatoryresponse also
calledas microphages.
b) Circulatingmonocytesandfixedtissue mononuclearphagocytescalled macrophages .
The processof phagocytosisissimilarforbothpolymorphsandmacrophagesandinvolvesthe following
4 steps:
1.Recognitionandattachment stage(opsonisation)
2. Engulfment stage
3. Secretionstage
4. Digestionordegradationstage
CHEMICAL MEDIATORS OF INFLAMMATION
Chemical factorsor permeabilityfactorsare of increasedvascularpermeability,these are large and
increasingnumberof endogenouscompoundswhichcanenhance vascularpermeability.However,
currentlymanychemical mediatorshave beenidentifiedwhichpartake inotherprocessesof acute
inflammationaswell eg:vasodilatation,chemotaxis,fever,painetc.
The substancesactingas chemical mediatorsof inflammationmaybe releasedfromthe cells,the
plasma,or damagedtissue itself.Theyare broadlyclassifiedinto2groups:
1)Mediatorsreleasedby cells
2)Mediatorsoriginating from plasma
REGULATION OF INFLAMMATION
The onsetof inflammatoryresponsesoutlinesabove may have potentiallydamaginginfluence onthe
hosttissuesasevidentinhypersensitivity conditions.Such self damagingeffectsare keptincheckby
the host mechanismssoasto resolve inflammation.Mechanisms are:
a)Acute phase reactants-these are releasedinplasmainresponse totissue traumaandinfection.These
are mainlysynthesisedinliverandtosome extentinmacrophages.
b)Corticosteroids– glucocorticoidsactas anti inflammatory agents.
c)Free cytokine receptors- cytokinesinserumcorrelateswithdiseaseactivity.
d)SuppressorT cells- prohibitionof suppressortcellsisseenwhichinhibitsthe functionof TandB cells.
e)Anti-inflammatory chemical mediators-ithasananti- inflammatoryaction
MORPHOLOGY OF ACUTEINFLAMMATION
1. PSEUDOMEMBRANOUSINFLAMMATION-Itisinflammatoryresponse of mucoussurface to
toxinsof diphtheriaorirritantgases.asa resultof denudationof epithelium,plasmaexudeson
the surface where it coagulatesandtogetherwithnecrosedepithelium.
2. ULCER- ulcersare local defectsvonthe surface of an organ producedinflammation.Common
sitesforulcerationare the stomach,intestinal ulcersintyphoidfever,ulcersof legs.inthe
acute stage there isinfiltrationbypolymorphswithvasodilatationwhilelongstandingulcers
developinfiltrationbylymphocytesandmacrophages.
3. SUPPURATION(ABSCESSFORMATION)-Whenacute bacterial infectionisaccompaniesby
intense neutrophilicinfiltrate inthe inflamedtissue,itresultsintissue necrosis.A cavityis
formedwhichiscalledabscessandcontainsa pusand processof abscessformationiscalled
suppuration.
4. CELLULITIS- it isa diffuse inflammationof softtissue resultingfromspreadingeffectsof
substanceslike hyaluronidase releasedbysome bacteria.
5. BACTERIAL INFECTIONOF BLOOD-Thisincludes:a) bacteraemia
b) Septicaemiameans presence of rapidlymultiplyinghighlypathogenicbacteriainthe blood
c) Pyaemia
SYSTEMIC EFFECTS OF ACUTE INFLAMMATION
1.FEVER- occurs due to bacteraemia.It is thoughtbe mediatedthroughrelease of factorslike
prostaglandins,interleukinsandtumornecrosisfactorinresponse toinfection.
2.LEUCOCYTOSIS- Commonlyaccompaniesthe acute inflammatoryreactions.Typhoidfeverisan
acute inflammationhoweverinducesleucopeniawithrelative lymphocytosis.
3.LYMPHANGITIS- It isone of the importantmanifestationsof localisedinflammatoryinjury.The
lyphaticsandlymphnodesthatdrainthe inflamedtissuesshow reactiveinflammatorychangesin
the form of lymphangitis.
4.SHOCK- It may occur insevere cases.Massive releaseof cytokine amediatorof inflammation in
response tosevere tissueinjuryresultsinprofuse systemicvasodilatation,increasedvascular
permeabilityandintravascularvolume loss.The neteffectof these changesishypotensionand
shock.
FATEOF ACUTE INFLAMMATION
The acute inflammation processcanculminate inone of the 4 outcomes:
1.RESOLUTION-It meanscomplete returntonormal tissue followingacute inflammation.Thisoccur
whentissue changesare slightandcellular changesare reversible.
2.HEALING-Thistakesplace whentissue destructioninacute inflammationisextensive sothatthere
isno tissue regenerationbutthere isactuallyhealingbyfibrosis.
3.SUPPURATION-Whenthe pyogenicbacteriacausing acute inflammationresultinsevere tissue
necrosisthe processproressestosuppuration.Intiallythere isintenseneutrophillicinfiltration.
4.CHRONIC INFLAMMATION-The acute inflammationmayprogresstochronic inflammation in
whichthe processesof inflammationandhealingproceedsidebyside.
CHRONIC INFLAMMATION
DEFINITION AND CAUSES: Chronicinflammationisdefinedasprolongedprocessinwhichtissue
destructionandinflammationoccurat same time.
Causes:1.Chronicinflammationfollowingacute inflammation –whenthe tissue destructionisextensive
or the bacteriasurvive andpersistinsmall numbersatthe site of acute inflammation.
2. Recurrentattacks of acute inflammation- whenrepeatedboutsof acute inflammationculminatein
chronicityof the processe.g.recurrenturinarytract infection.
3. Chronicinflammationstartingde novo- whenthe infectionwithorganismof low pathogenicityis
chronicfrom the beginning.E.g.infectionwith Myobacteriumtuberculosis
GENERAL FEATURES OF CHRONIC INFLAMMATION
1.MONONUCLEAR CELL INFILTRATION-chronicinflammatorylesionsare infiltratedbymononuclear
inflammatorycellslikephagocytesandlymphoidcells.The bloodmonocytesonreachingthe
extravascularspace transformintotissue macrophages.besidesthe role of macrophagesin
phagocytosistheymaygetactivatedinresponse tostimuli suchascytokines.
2. TISSUE DESTRUCTION OR NECROSIS-Tissue destructionandnecrosisare central feature of most
formsof chronicinflammatorylesions.Thisisbrought byactivatedmacrophageswhichreleaseavariety
of biologicallyactivesubstances.E.g.protease,lipase .etc.
3. PROLIFERATIVE CHANGES –Asa resultof necrosisproliferationof small bloodvesselsandfibroblastis
stimulatedresultinginformation of inflammatorygranulationtissue.Eventuallyhealingbyfibrosisand
collagenlayingtakesplace.
SYSTEMIC EFFECTS OF CHRONIC INFLAMMATION
1.FEVER-Invariablythere ismildfeveroftenwithloss of weightandweakness.
2.ANAEMIA-Chronicinflammationisaccompaniedbyanaemiaof varyingdegree.
3.LEUCOCYTOSIS
4.ESR- Itis elevated
5.AMYLOIDOSIS-Longertermcasesof chronic suppurative inflammationmaydevelop secondary
systemic amyloidosis.
TYPES OF CHRONIC INFLAMMATION
1.NON-SPECIFIC-Whenthe irritantsubstance producesanon-specificchronic inflammatory reaction
withformationof granulationtissueandhealingbyfibrosis,like chroniculcer.
2.SPECIFIC-Wheninjuriousagentcausesacharacteristichistologictissue response like,tuberculosis.
Inflammation and Healing
HEALING
Injuryto tissue mayresultincell deathandtissue destruction. Healingonthe otherhandisthe body
response toinjuryinanattemptto restore normal structure and function.The processof healing
involves2processes:
1. Regeneration-whenhealingtakesplace byproliferationof parenchymal cellsandusuallyresults
incomplete restorationof the original tissue .
2. Repair – whenthe healingtakesplace byproliferationof connective tissue elementsresultingin
fibrosisandscarring .
REGENERATION
Some parenchymal cellsare shortlivedwhile othershave long lifespan.Inordertomaintainproper
structure of tissuesthese cellsare underthe constantregulatorycontrol of theircell cycle.Theseinclude
growthfactor such as :epidermal growthfactor,fibroblastgrowthfactor,plateletgrowthfactor.All the
cellsdivide atdifferentpace ,dependingupontheircapacitytodivide sotheyare dividedinto3groups:
1. Labile cells:the cellscontinue tomultiplythroughoutlifeundernormal physiologicalcondition.
2. Stable cell:these cellsdecreaseorlose their abilitytoproliferateafteradolescencebutretain
the capacity to multiplyinresponse tostimulithroughoutthe adultlife.
3. Permanentcells :these cellslose theirabilitytoproliferate aroundthe time of birth.
So regeneration of anytype of parenchymal cellsinvolve the following2processes:
1. Proliferationof original cellsfromthe marginof injurywithmigrationsoastocover the gap.
2. Proliferationof migratedcellswithsubsequentdifferentiationandmaturationsoasto
reconstitute the originaltissue.
REPAIR
Repairisthe replacementof injuredtissue byfibroustissue.Twoprocessesare involvedinrepair:
1. Granulationtissue formation;and
2. Contractionof wounds
Repairresponse takesplace byparticipationof mesenchymal cells,endothelial cells,macrophages,
platelets,andthe parenchymal cellsof the injuredorgan.
(A) Granulationtissue formation- The termgranulationtissue derivesitsname fromslightly
granularand pinkappearance of the tissue .Each granule correspondshistologicallyto
proliferationof newbloodvesselswhichare slightlyliftedonsurface bythincoveringof
fibroblastandyoungcollagen.The 3 followingphases:
1. Phase of inflammation: followingtrauma,bloodclotsat the site of injury. There isacute
inflammatoryresponse withexudationof plasma,neutrophilsandsome monocyteswithin24
hours.
2. Phase of clearance : combinationof proteolyticenzymesliberatedfromneutrophils,autolytic
enzymesfromdeadtissue cellsandphagocyticactivityof macrophagesclearoff the necrotic
tissue ,debrisandred bloodcells.
3. Phase of ingrowth of granulation tissue : the phase consistsof 2 mainprocesses: a)
Angiogenesis:formationof newbloodvesselsatthe site of injurytakesplace byproliferationof
endothelial cellsfromthe marginsof severedbloodvessels.Initially,the proliferatedendothelial
cells are solidbudsbutwithinfew hoursdeveloplumenandstartcarrying blood.Soonthese
bloodvesselsdifferentiate intomusculararteriolesthinwalled .The processof angiogenesis is
stimulatedbyproteolyticdestructionof basementmembrane .
b) fibrogenesis:the newlyformedbloodvessels are presentinamorphousgroundsubstance .The new
fibroblastoriginatefromfibrocytesaswell asby mitoticdivisionof fibroblasts.Some of thesefibroblasts
have combinationof morphologicandfunctional characteristicsof smoothmuscle cells.Collagenfibrils
begintoappearby about 6th
day. More and more collagenfibresare formedandnew bloodvessels
decrease.Thisresultsinformationof inactive lookingscarknownascicatrisation.
(B) Contraction Of Wound– the woundstartscontractingafter2-3 days andthe processbythe
14th
day. Duringthisperiodthe woundisreducedbyapproximately80% of itsoriginal size.Contracted
woundresultsinrapidhealingsince lessersurface of injuredtissue hastobe replaced.Inorderto
explainthe mechanismof woundcontractionanumberof factorshave beenproposed:
1. Dehydrationasresultof removal of fluidbydryingof wound.
2. Contractionof collagen
3. Discoveryof myofibroblastsappearinginactive granulationtissue.These cellshave features
intermediate betweenfibroblastsandsmoothmuscle cells.Theirmigrationintowoundareaand
active contractiondecrease theirsize.
Inflammation and Healing
WOUND HEALING
Healingof skinwoundsprovidesaclassical exampleof combinationof regenerationandrepair.Thiscan
be accompaniedbyone of the twofollowingways:
1. Healingby first intention(primary union)
2. Healingby second intention( secondary union)
Healing by first intention
Thisis definedashealingof woundwhichhasfollowingfeatures:
a) Cleananduninfected
b) Surgicallyincised
c) Withoutmuchlossof cellsandtissue
d) Edgesof woundandapproximatedbysurgical sutures.
The eventsinprimaryunionare :
- - Initial haemorrhage – immediatelyafterinjurythe space betweenthe approximatedsurface of
incisedwoundfilledwithbloodwhichthenclotsandsealsthe woundagainstdehydrationand
infection. Acute inflammatoryresponse - thisoccurs within24 hrs of appearance of
polymorphsfromthe marginsof incision.By3rd
day , polymorphsare replacedbymacrophages.
Epithelial changes– the basal cellsof epidermisformboththe cut marginsstart proliferatingand
migratingtowardsincisionalspace inthe formof epithelial spurs.The migratedepithelial cellsseparate
the underlyingviable dermisfromthe overlyingnecroticmaterial andclotformingscabwhichcastsoff .
By 5th
daymultilayerednewepidermisinformedwhichisdifferentiatedintosuperficial anddeeper
layers.
- Organisation - bythe 3rd
dayfibroblastalsoinvade the woundarea.Bythe 5th
day new collagen
fibrilsstartformingwhichdominatetill healingiscompleted.In4 weeksthe scartissue with
scanty cellularandvascularelements afew inflammatorycellsandepithelialisedsurface is
formed.
- Surface tracks – each suture track isa separate woundandincitesthe same phenomenaasin
healingof primarywoundi.e.fillingthe space withhaemorrhage someinflammatoryreactions
.when suturesare removedaround7th
day much of epithelialisedsuture trackisavulsed
Healing by second intention
Thisis definedashealingof woundhavingthe followingcharacteristics:
1. Openwithlarge tissue defectattimesinfected
2. Havingextensive lossof cellsandtissues
3. The woundis notapproximatedbysurgical suturesbutisleftopen.
The basic eventsinsecondaryunionbutdifferinhavinglargertissue defectwhichhastobe bridged.
Hence healingtakesplace fromthe base upwardsaswell as from the marginsinwards.Thishealingis
slow, ugly,scar as comparedrapidhealingandneatscar of primaryunion.
- Initial haemorrhage – as a resultof injurythe woundspace isfilledwithbloodandfibrinclot
whichdries.
- Inflammatory phase – there isinitial acute inflammatoryresponse followedbyappearance of
macrophageswhichclearoff the debrisasin primaryunion.
- Epithelial changes – epidermal cellsfrombothmarginsof woundsproliferateandmigrate into
woundinformof epithelial spurrstill theymeetincentre andre-epithelialise the gap
completely.Howeverepithelial cellsdonotcovercompletely .
- Granulationtissue – the mainbulkof secondaryhealingisbygranulation.Granulationtissue is
formedbyproliferationof fibroblastsand neovascularisationsfromadjoiningviable element.
The newlyformedgranulationtissue isdeepred,granularand veryfragile .Withtime the scar
maturationbecomespale andwhite due toincrease incollagenanddecrease invascularity.
- Woundcontraction – contractionof woundisan importantfeature of secondaryhealingnot
seeninprimaryhealing.Due to actionin myofibroblastspresentingranulationtissuethe
woundcontracts to one-thirdtoone-fourthof itsoriginal size.
- Presence ofinfection – bacterial contaminationof anopenwounddelaysthe processof healing
due to release of bacterial toxinsthatprovoke necrosis,suppurationandthrombosis.
Inflammation and Healing
Inflammation and Healing
Complications of wound healing
Duringthe course of healing,followingcomplications mayoccur:
1. Infectionof wounddue toentryof bacteriadelaysthe healing.
2. Implantationcystformationmayoccur due to persistance of epithelial cellsinwoundafter
healing.
3. Pigmentation – healedwoundmayattimeshave rustlike colourdue to staining with
haemosiderin.Some colouredparticulate material leftinthe woundmaypersist.
4. Deficient scar formation – thismay occur due to inadequate formationof granulationtissue.
5. Incisional hernia – a weal scar, especiallyafterlaparotomy maybe site of burstingopenof
woundor an incisional wound.
6. Hypertrophied scarsand keloidformation – at time the scar formedisexcessive ,uglyand
painful.Excessive formationof collageninhealingmayresultinformationof keloids.
7. Excessive contraction
8. Neoplasia
Factors Influencing Healing
Two typesof factorsinfluence the woundhealing:
A. Local factors : 1. infection – most importantfactorwhichdelayshealing.
2. Poorblood supply to woundslowshealing
3. Foreign bodies includingsuturesinterferehealingandcause intense inflammatoryreaction.
4. Movement delayswoundhealing
5. Exposure to ionising radiation delaysgranulationtissue formation.
6. Exposure to ultravioletlight facilitates healing
B. Systemicfactors : 1. age – woundhealingisrapidinyoungand somewhatslowedinaged
2. Nutrition – deficiencyof constituentslike proteins,vit.C.andzincdelayswoundhealing 3.Systemic
infection delayswoundhealing.
4. Administration of glucocorticoids hasanti-inflammatoryeffect.
5. Uncontrolled diabetics are more prone to developinfection .
Inflammation and Healing

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Inflammation and Healing

  • 1. A COMPILATION ON INFLAMMATION AND HEALING SESSION 2016-2017 Department of Rog Nidan Dayanand Ayurvedic College, Jalandhar
  • 2. INDEX 1. INFLAMMATION A) DEFINITION B) CAUSES C) SIGNS OFINFLAMMATION D) TYPES OF INFLAMMATION E) ACUTE INFLAMMATION F) REGULATION INFLAMMATION G) CHEMICAL MEDIATORS OF INFLAMMATION H) CHRONICINFLAMMATION 2. HEALING A) DEFINITION B) REGENERATION C) REPAIR D) WOUND HEALING
  • 3. INFLAMMATION Inflammation isdefinedasthe local response of livingmammaliantissuestoinjurydue to anyagent.It isa bodydefense reactioninordertoeliminate orlimitthe spreadof injuriousagentaswell asto remove the consequentnecrosedcellandtissues. CAUSES The agentscausinginflammationmaybe asunder: 1.Physical agentslike heat,cold, radiation,mechanical trauma. 2.Chemical agentslike organicandinorganicpoisons. 3.Infective agentslike bacteria,viruses,andtheirtoxins. 4.Immunological agents like cell-mediatedandantigen-antibodyreactions. Thus inflammationisdistinctfrominfection –the formeristhe protective response bythe bodywhile the latteris invasionintothe bodybyharmful microbesandtheirresultantill effectsbytoxin. Inflammationinvolves twoprocesses: a) inflammatory response b) healing SIGNS OF INFLAMMATION The famous5 cardinal signs of inflammationas: 1. Redness 2. Swelling 3. Heat 4. Pain 5. Loss of function
  • 5. TYPES OF INFLAMMATION Dependinguponthe defensecapacityof the hostand durationof response inflammationcanbe classifiedinto AcuteandChronic 1. Acute inflammationisa shortdurationand representsthe earlybodyreactionandisusually followedbyrepair.The mainfeaturesof acute inflammationare a) accumulationof fluidandplasmaatthe affectedsite. b) intravascularactivationof the platelets c) polymorphonuclearneutrophilsasinflammatorycells. 2. Chronic inflammationisof longerdurationandoccurs eitherafterthe causative agentof acute inflammationpersistsforalongtime or the stimulusissuchthat it induceschronicinflammation fromthe beginning.The characteristicfeature of chronicinflammationispresence of chronic inflammatorycellssuchaslymphocytesplasmacellsandmacrophages.
  • 6. ACUTE INFLAMMATION The changesis acute inflammationcanbe conveniently describedunderthe following2headings: 1. Vascular events 2. Cellularevents Vascular events Alterationinthe microvasculature isthe earliestresponse totissue injury.These alterationsinclude : a) Haemodynamicchanges b) Changesinvascularpermeability A) Haemodynamicchanges – the earliestfeatures of inflammatoryresponse resultfromchanges inthe vascularflowandcalibre of small bloodvesselsinthe injuredtissues.The sequence of these changesisas under: 1. Irrespective of the type of injuryimmediate vascularresponse isof transientvasoconstrictionof arterioles.Withmildformof injurythe bloodflow maybe re-establishedin3-5secswhile with more severe injuryvasoconstrictionlastforabout5 mins. 2. Nextfollows persistentprogressive vasodilatation whichinvolvesmainlythe arterioles . Vasodilatationresultsinincreasedbloodvolume inmicrovascularbedof the areawhichis responsible forrednessandwarmthatthe site of acute inflammation. 3. Progressive vasodilatationinturnmayelevate local hydrostaticpressure resultingin transudationof fluidintoextracellularspace .Thisisresponsibleforswellingatlocal site. 4. Slowingor stasisof microcirculation occurs . Slowingisattributedtoincreasedpermeabilityof microvasculature the resultsinincreasedconcentrationof redcells. 5. Stasisor slowingisfollowedby leucocytic marginationor peripheral orientationof leucocytes alongthe vascularendotheliumafterthisthese move andmigrate throughgaps between endothelial cells into the extravascularspace.Thisprocessiscalledasemigration.
  • 7. The reactionelicited isknownas tripleresponse or red lineresponse consistingof following : 1. Red line appearswithinafewsecondsfollowingstrokingandresultsfromlocal vasodilatationof capillariesandvenules. 2. Flareis the bright reddishappearance orflushsurroundingthe redline andresultsin vasodilatationof adjacent arterioles. 3. Wheal isthe swellingoredemaof the surroundingskinoccuringdue totransudationof fluidinto the extravascularspace . B) Altered vascularpermeability- PATHOGENESIS- inandaround inflamedtissue compartmentwhichcomesfrombloodplasmabyits escape throughthe endothelial wall of peripheral vascularbed.Inthe initial stage the escape of fluidisdue tovasodilatationandconsequentelevationinhydrostaticpressure.Thisistransudate in nature.The presence of edemadue toincreasedvascular permeability of microvascularbed
  • 8. MECHANISM OF INCREASED VASCULAR PERMEABILITY- 1) CONTRACTION OF ENDOTHELIAL CELLS-Thisismost commonmechanismof increasedleakiness that affectsvenulesexclusivelywhilecapillariesandarterioles remainunaffected.The endothelial cellsdeveloptemporarygapsbetweenthemdue totheircontractionresultingin vascularleakiness.Itismediatedbyhistamine 2) RETRACTION OF ENDOTHELIAL CELLS- inthismechanismthere isstructural re-organisationof the cytoskeletonof endothelial cellsthatcausesreversible retractionatthe intercellular junctions.Thischange tooaffectsthe venulesandismediatedbycytokinessuchas interleukin - 1. 3) DIRECT INJURYTO ENDOTHELIAL CELLS- Directinjuryto the endothelial causescell necrosisand appearance of physical gapsat the sitesof detachedendothelialcells.Processof thrombosis is intiatedatthe site of endothelial cells. 4) ENDOTHELIAL INJURYMEDIATED BY LEUCOCYTES –Adherence of leucocytestothe endotheliumatthe site of inflammationmayresultinactivationof leucocytes.The activated leucocytesrelease proteolyticenzymesandtoxicoxygenspecieswhichmaycause increased vascularleakinessandendothelialinjury. 5) NEOVASCULARISATION- Inadditionthe newly formedcapillariesunderthe influenceof vascularendothelial growthfactorduringthe processof repairandin tumorsare excessively leaky. CELLULAR EVENTS The cellularphase of inflammationconsistsof 2processes: 1. Exudationof leucocytes 2. Phagocytosis 1. Exudationof leucocytes- the escape of leucocytesfromthe lumenof microvasculature tothe interstitialtissue isthe mostimportantfeatureof inflammatoryresponse .the acute inflammation includesfirstlineof bodydefense followedbymonocytes andmacrophages.The changes leadingto migrationof leucocytesare: a) Changesin the formed elements ofblood- inthe earlystage of inflammation the rate of flow of bloodisincreaseddue tovasodilatation.Butsubsequentlythere isslowingof bloodstream.due to slowingandstasisthe central streamof cellswidensandperipheral plasmazone becomesnarrower because of lossof plasmaby exudation.Thisphenomenonisknownas margination.
  • 9. b) Rollingandadhesion- Peripherallymarginationandpavementedneutrophilsslowlyrolloverthe endothelial cellsliningthe vessel walls.Thisisfollowedbytransientbondbetweenthe leucocytesand endothelial cellsbecoming firmer.Itincludes3phases: 1)selectins 2)integrins 3)immunoglobulinssuperfamilyadhesionmolecules c)Emigration –afterstickingof neutrophilstoendotheliumthe formermove alongthe endothelial cells isfoundwhere the neutrophilsthrowoutcytoplasmicpseudopods.Subsequentlythe neutrophilslodged betweenthe endothelial cellsandbasementmembrane crossthe basementmembrane bydamagingit locallywithsecretedcollagenasesandescape intothe extravascularspace thisisknownas emigration. d) Chemotaxis-The chemotacticfactor( cytokines,plateletfactoretc) mediatedtransmigrationof leucocytesaftercrossingseveral barriers( endothelium,basementmembrane ,etc) toreach the interstitial tissuesiscalledchemotaxis 2. Phagocytosis-phagocytosisisdefinedasthe processof engulfmentof solidparticulatematerialbythe cells(cell-eating).The cellsperformingthisfunctionare called phagocytes.There are mainlytwotypesof phagocyticcells: a) Polymorphonuclearneutrophils(PMNs) whichappearearlyinacute inflammatoryresponse also calledas microphages. b) Circulatingmonocytesandfixedtissue mononuclearphagocytescalled macrophages . The processof phagocytosisissimilarforbothpolymorphsandmacrophagesandinvolvesthe following 4 steps: 1.Recognitionandattachment stage(opsonisation) 2. Engulfment stage 3. Secretionstage 4. Digestionordegradationstage
  • 10. CHEMICAL MEDIATORS OF INFLAMMATION Chemical factorsor permeabilityfactorsare of increasedvascularpermeability,these are large and increasingnumberof endogenouscompoundswhichcanenhance vascularpermeability.However, currentlymanychemical mediatorshave beenidentifiedwhichpartake inotherprocessesof acute inflammationaswell eg:vasodilatation,chemotaxis,fever,painetc. The substancesactingas chemical mediatorsof inflammationmaybe releasedfromthe cells,the plasma,or damagedtissue itself.Theyare broadlyclassifiedinto2groups: 1)Mediatorsreleasedby cells 2)Mediatorsoriginating from plasma REGULATION OF INFLAMMATION The onsetof inflammatoryresponsesoutlinesabove may have potentiallydamaginginfluence onthe hosttissuesasevidentinhypersensitivity conditions.Such self damagingeffectsare keptincheckby the host mechanismssoasto resolve inflammation.Mechanisms are: a)Acute phase reactants-these are releasedinplasmainresponse totissue traumaandinfection.These are mainlysynthesisedinliverandtosome extentinmacrophages. b)Corticosteroids– glucocorticoidsactas anti inflammatory agents. c)Free cytokine receptors- cytokinesinserumcorrelateswithdiseaseactivity. d)SuppressorT cells- prohibitionof suppressortcellsisseenwhichinhibitsthe functionof TandB cells. e)Anti-inflammatory chemical mediators-ithasananti- inflammatoryaction
  • 11. MORPHOLOGY OF ACUTEINFLAMMATION 1. PSEUDOMEMBRANOUSINFLAMMATION-Itisinflammatoryresponse of mucoussurface to toxinsof diphtheriaorirritantgases.asa resultof denudationof epithelium,plasmaexudeson the surface where it coagulatesandtogetherwithnecrosedepithelium. 2. ULCER- ulcersare local defectsvonthe surface of an organ producedinflammation.Common sitesforulcerationare the stomach,intestinal ulcersintyphoidfever,ulcersof legs.inthe acute stage there isinfiltrationbypolymorphswithvasodilatationwhilelongstandingulcers developinfiltrationbylymphocytesandmacrophages. 3. SUPPURATION(ABSCESSFORMATION)-Whenacute bacterial infectionisaccompaniesby intense neutrophilicinfiltrate inthe inflamedtissue,itresultsintissue necrosis.A cavityis formedwhichiscalledabscessandcontainsa pusand processof abscessformationiscalled suppuration. 4. CELLULITIS- it isa diffuse inflammationof softtissue resultingfromspreadingeffectsof substanceslike hyaluronidase releasedbysome bacteria. 5. BACTERIAL INFECTIONOF BLOOD-Thisincludes:a) bacteraemia b) Septicaemiameans presence of rapidlymultiplyinghighlypathogenicbacteriainthe blood c) Pyaemia SYSTEMIC EFFECTS OF ACUTE INFLAMMATION 1.FEVER- occurs due to bacteraemia.It is thoughtbe mediatedthroughrelease of factorslike prostaglandins,interleukinsandtumornecrosisfactorinresponse toinfection. 2.LEUCOCYTOSIS- Commonlyaccompaniesthe acute inflammatoryreactions.Typhoidfeverisan acute inflammationhoweverinducesleucopeniawithrelative lymphocytosis. 3.LYMPHANGITIS- It isone of the importantmanifestationsof localisedinflammatoryinjury.The lyphaticsandlymphnodesthatdrainthe inflamedtissuesshow reactiveinflammatorychangesin the form of lymphangitis. 4.SHOCK- It may occur insevere cases.Massive releaseof cytokine amediatorof inflammation in response tosevere tissueinjuryresultsinprofuse systemicvasodilatation,increasedvascular permeabilityandintravascularvolume loss.The neteffectof these changesishypotensionand shock.
  • 12. FATEOF ACUTE INFLAMMATION The acute inflammation processcanculminate inone of the 4 outcomes: 1.RESOLUTION-It meanscomplete returntonormal tissue followingacute inflammation.Thisoccur whentissue changesare slightandcellular changesare reversible. 2.HEALING-Thistakesplace whentissue destructioninacute inflammationisextensive sothatthere isno tissue regenerationbutthere isactuallyhealingbyfibrosis. 3.SUPPURATION-Whenthe pyogenicbacteriacausing acute inflammationresultinsevere tissue necrosisthe processproressestosuppuration.Intiallythere isintenseneutrophillicinfiltration. 4.CHRONIC INFLAMMATION-The acute inflammationmayprogresstochronic inflammation in whichthe processesof inflammationandhealingproceedsidebyside.
  • 13. CHRONIC INFLAMMATION DEFINITION AND CAUSES: Chronicinflammationisdefinedasprolongedprocessinwhichtissue destructionandinflammationoccurat same time. Causes:1.Chronicinflammationfollowingacute inflammation –whenthe tissue destructionisextensive or the bacteriasurvive andpersistinsmall numbersatthe site of acute inflammation. 2. Recurrentattacks of acute inflammation- whenrepeatedboutsof acute inflammationculminatein chronicityof the processe.g.recurrenturinarytract infection. 3. Chronicinflammationstartingde novo- whenthe infectionwithorganismof low pathogenicityis chronicfrom the beginning.E.g.infectionwith Myobacteriumtuberculosis
  • 14. GENERAL FEATURES OF CHRONIC INFLAMMATION 1.MONONUCLEAR CELL INFILTRATION-chronicinflammatorylesionsare infiltratedbymononuclear inflammatorycellslikephagocytesandlymphoidcells.The bloodmonocytesonreachingthe extravascularspace transformintotissue macrophages.besidesthe role of macrophagesin phagocytosistheymaygetactivatedinresponse tostimuli suchascytokines. 2. TISSUE DESTRUCTION OR NECROSIS-Tissue destructionandnecrosisare central feature of most formsof chronicinflammatorylesions.Thisisbrought byactivatedmacrophageswhichreleaseavariety of biologicallyactivesubstances.E.g.protease,lipase .etc. 3. PROLIFERATIVE CHANGES –Asa resultof necrosisproliferationof small bloodvesselsandfibroblastis stimulatedresultinginformation of inflammatorygranulationtissue.Eventuallyhealingbyfibrosisand collagenlayingtakesplace. SYSTEMIC EFFECTS OF CHRONIC INFLAMMATION 1.FEVER-Invariablythere ismildfeveroftenwithloss of weightandweakness. 2.ANAEMIA-Chronicinflammationisaccompaniedbyanaemiaof varyingdegree. 3.LEUCOCYTOSIS 4.ESR- Itis elevated 5.AMYLOIDOSIS-Longertermcasesof chronic suppurative inflammationmaydevelop secondary systemic amyloidosis. TYPES OF CHRONIC INFLAMMATION 1.NON-SPECIFIC-Whenthe irritantsubstance producesanon-specificchronic inflammatory reaction withformationof granulationtissueandhealingbyfibrosis,like chroniculcer. 2.SPECIFIC-Wheninjuriousagentcausesacharacteristichistologictissue response like,tuberculosis.
  • 16. HEALING Injuryto tissue mayresultincell deathandtissue destruction. Healingonthe otherhandisthe body response toinjuryinanattemptto restore normal structure and function.The processof healing involves2processes: 1. Regeneration-whenhealingtakesplace byproliferationof parenchymal cellsandusuallyresults incomplete restorationof the original tissue . 2. Repair – whenthe healingtakesplace byproliferationof connective tissue elementsresultingin fibrosisandscarring .
  • 17. REGENERATION Some parenchymal cellsare shortlivedwhile othershave long lifespan.Inordertomaintainproper structure of tissuesthese cellsare underthe constantregulatorycontrol of theircell cycle.Theseinclude growthfactor such as :epidermal growthfactor,fibroblastgrowthfactor,plateletgrowthfactor.All the cellsdivide atdifferentpace ,dependingupontheircapacitytodivide sotheyare dividedinto3groups: 1. Labile cells:the cellscontinue tomultiplythroughoutlifeundernormal physiologicalcondition. 2. Stable cell:these cellsdecreaseorlose their abilitytoproliferateafteradolescencebutretain the capacity to multiplyinresponse tostimulithroughoutthe adultlife. 3. Permanentcells :these cellslose theirabilitytoproliferate aroundthe time of birth. So regeneration of anytype of parenchymal cellsinvolve the following2processes: 1. Proliferationof original cellsfromthe marginof injurywithmigrationsoastocover the gap. 2. Proliferationof migratedcellswithsubsequentdifferentiationandmaturationsoasto reconstitute the originaltissue. REPAIR Repairisthe replacementof injuredtissue byfibroustissue.Twoprocessesare involvedinrepair: 1. Granulationtissue formation;and 2. Contractionof wounds Repairresponse takesplace byparticipationof mesenchymal cells,endothelial cells,macrophages, platelets,andthe parenchymal cellsof the injuredorgan. (A) Granulationtissue formation- The termgranulationtissue derivesitsname fromslightly granularand pinkappearance of the tissue .Each granule correspondshistologicallyto proliferationof newbloodvesselswhichare slightlyliftedonsurface bythincoveringof fibroblastandyoungcollagen.The 3 followingphases:
  • 18. 1. Phase of inflammation: followingtrauma,bloodclotsat the site of injury. There isacute inflammatoryresponse withexudationof plasma,neutrophilsandsome monocyteswithin24 hours. 2. Phase of clearance : combinationof proteolyticenzymesliberatedfromneutrophils,autolytic enzymesfromdeadtissue cellsandphagocyticactivityof macrophagesclearoff the necrotic tissue ,debrisandred bloodcells. 3. Phase of ingrowth of granulation tissue : the phase consistsof 2 mainprocesses: a) Angiogenesis:formationof newbloodvesselsatthe site of injurytakesplace byproliferationof endothelial cellsfromthe marginsof severedbloodvessels.Initially,the proliferatedendothelial cells are solidbudsbutwithinfew hoursdeveloplumenandstartcarrying blood.Soonthese bloodvesselsdifferentiate intomusculararteriolesthinwalled .The processof angiogenesis is stimulatedbyproteolyticdestructionof basementmembrane . b) fibrogenesis:the newlyformedbloodvessels are presentinamorphousgroundsubstance .The new fibroblastoriginatefromfibrocytesaswell asby mitoticdivisionof fibroblasts.Some of thesefibroblasts have combinationof morphologicandfunctional characteristicsof smoothmuscle cells.Collagenfibrils begintoappearby about 6th day. More and more collagenfibresare formedandnew bloodvessels decrease.Thisresultsinformationof inactive lookingscarknownascicatrisation. (B) Contraction Of Wound– the woundstartscontractingafter2-3 days andthe processbythe 14th day. Duringthisperiodthe woundisreducedbyapproximately80% of itsoriginal size.Contracted woundresultsinrapidhealingsince lessersurface of injuredtissue hastobe replaced.Inorderto explainthe mechanismof woundcontractionanumberof factorshave beenproposed: 1. Dehydrationasresultof removal of fluidbydryingof wound. 2. Contractionof collagen 3. Discoveryof myofibroblastsappearinginactive granulationtissue.These cellshave features intermediate betweenfibroblastsandsmoothmuscle cells.Theirmigrationintowoundareaand active contractiondecrease theirsize.
  • 20. WOUND HEALING Healingof skinwoundsprovidesaclassical exampleof combinationof regenerationandrepair.Thiscan be accompaniedbyone of the twofollowingways: 1. Healingby first intention(primary union) 2. Healingby second intention( secondary union) Healing by first intention Thisis definedashealingof woundwhichhasfollowingfeatures: a) Cleananduninfected b) Surgicallyincised c) Withoutmuchlossof cellsandtissue d) Edgesof woundandapproximatedbysurgical sutures. The eventsinprimaryunionare : - - Initial haemorrhage – immediatelyafterinjurythe space betweenthe approximatedsurface of incisedwoundfilledwithbloodwhichthenclotsandsealsthe woundagainstdehydrationand infection. Acute inflammatoryresponse - thisoccurs within24 hrs of appearance of polymorphsfromthe marginsof incision.By3rd day , polymorphsare replacedbymacrophages. Epithelial changes– the basal cellsof epidermisformboththe cut marginsstart proliferatingand migratingtowardsincisionalspace inthe formof epithelial spurs.The migratedepithelial cellsseparate the underlyingviable dermisfromthe overlyingnecroticmaterial andclotformingscabwhichcastsoff . By 5th daymultilayerednewepidermisinformedwhichisdifferentiatedintosuperficial anddeeper layers. - Organisation - bythe 3rd dayfibroblastalsoinvade the woundarea.Bythe 5th day new collagen fibrilsstartformingwhichdominatetill healingiscompleted.In4 weeksthe scartissue with scanty cellularandvascularelements afew inflammatorycellsandepithelialisedsurface is formed. - Surface tracks – each suture track isa separate woundandincitesthe same phenomenaasin healingof primarywoundi.e.fillingthe space withhaemorrhage someinflammatoryreactions .when suturesare removedaround7th day much of epithelialisedsuture trackisavulsed
  • 21. Healing by second intention Thisis definedashealingof woundhavingthe followingcharacteristics: 1. Openwithlarge tissue defectattimesinfected 2. Havingextensive lossof cellsandtissues 3. The woundis notapproximatedbysurgical suturesbutisleftopen. The basic eventsinsecondaryunionbutdifferinhavinglargertissue defectwhichhastobe bridged. Hence healingtakesplace fromthe base upwardsaswell as from the marginsinwards.Thishealingis slow, ugly,scar as comparedrapidhealingandneatscar of primaryunion. - Initial haemorrhage – as a resultof injurythe woundspace isfilledwithbloodandfibrinclot whichdries. - Inflammatory phase – there isinitial acute inflammatoryresponse followedbyappearance of macrophageswhichclearoff the debrisasin primaryunion. - Epithelial changes – epidermal cellsfrombothmarginsof woundsproliferateandmigrate into woundinformof epithelial spurrstill theymeetincentre andre-epithelialise the gap completely.Howeverepithelial cellsdonotcovercompletely . - Granulationtissue – the mainbulkof secondaryhealingisbygranulation.Granulationtissue is formedbyproliferationof fibroblastsand neovascularisationsfromadjoiningviable element. The newlyformedgranulationtissue isdeepred,granularand veryfragile .Withtime the scar maturationbecomespale andwhite due toincrease incollagenanddecrease invascularity. - Woundcontraction – contractionof woundisan importantfeature of secondaryhealingnot seeninprimaryhealing.Due to actionin myofibroblastspresentingranulationtissuethe woundcontracts to one-thirdtoone-fourthof itsoriginal size. - Presence ofinfection – bacterial contaminationof anopenwounddelaysthe processof healing due to release of bacterial toxinsthatprovoke necrosis,suppurationandthrombosis.
  • 24. Complications of wound healing Duringthe course of healing,followingcomplications mayoccur: 1. Infectionof wounddue toentryof bacteriadelaysthe healing. 2. Implantationcystformationmayoccur due to persistance of epithelial cellsinwoundafter healing. 3. Pigmentation – healedwoundmayattimeshave rustlike colourdue to staining with haemosiderin.Some colouredparticulate material leftinthe woundmaypersist. 4. Deficient scar formation – thismay occur due to inadequate formationof granulationtissue. 5. Incisional hernia – a weal scar, especiallyafterlaparotomy maybe site of burstingopenof woundor an incisional wound. 6. Hypertrophied scarsand keloidformation – at time the scar formedisexcessive ,uglyand painful.Excessive formationof collageninhealingmayresultinformationof keloids. 7. Excessive contraction 8. Neoplasia Factors Influencing Healing Two typesof factorsinfluence the woundhealing: A. Local factors : 1. infection – most importantfactorwhichdelayshealing. 2. Poorblood supply to woundslowshealing 3. Foreign bodies includingsuturesinterferehealingandcause intense inflammatoryreaction. 4. Movement delayswoundhealing 5. Exposure to ionising radiation delaysgranulationtissue formation. 6. Exposure to ultravioletlight facilitates healing B. Systemicfactors : 1. age – woundhealingisrapidinyoungand somewhatslowedinaged 2. Nutrition – deficiencyof constituentslike proteins,vit.C.andzincdelayswoundhealing 3.Systemic infection delayswoundhealing. 4. Administration of glucocorticoids hasanti-inflammatoryeffect. 5. Uncontrolled diabetics are more prone to developinfection .