[libribook.com] Traumatic Scar Tissue Management 1st Edition
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[libribook.com] Traumatic Scar Tissue Management 1st Edition

hongchingyee
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size/depth, anatomic region, and local mechanical tension all factor into woundhealing process and subsequent nature of the scar (Niessen et al. 1999, Cho et al.2014).Multiple studies on hypertrophic and keloid scar formation have been conductedover several decades, leading to many therapeutic strategies to prevent orattenuate excessive scar formation. Most therapeutic approaches remainclinically unsatisfactory, however, with an agreement that there is a meagerunderstanding of the complex mechanisms underlying the processes of scarringand wound contraction and fibroproliferative disorders in general (Gauglitz et al.2011, Rabello et al. 2014).Scar pathogenesis involves cellular and extracellular matrix (ECM) componentsin both the epidermal and dermal layers that are regulated by a wide array ofinterfering factors in the inflammation, proliferation, and remodeling stages ofhealing (Huang et al. 2013).Hypertrophic scarring after deep or partial-thickness wounds is common. Areview of the literature on the prevalence of hypertrophic scarring found thatfemales, children, young adults, and people with darker, more pigmented skinare particularly at risk and, in this subpopulation, the prevalence is up to 75%(Engrav et al. 2007). Hypertrophic scars are morphologically characterized by(Linares 1996, Cho et al. 2014):• Abnormal collagen• Reduced elastin• Persistent cellularity• Alterations in proteoglycan composition and amount• Prolonged inflammatory reaction resulting in persistent hypervascularity andexcess deposition of ground matrix.FeatureHypertrophic scar(HS)Keloid scar (KS)Demographic prevalence Pigmented skin Age 10–30, rare in elderlyRegional prevalenceRisk factorsAcross areas of highstress/tension (e.g.joints)Common complicationAnterior chest,shoulders, earlobes,upper arms andcheeksBoth

following burn injury,bacterial colonizationand wound infectionEtiology/pathophysiologyIncreased, alteredphenotype, fibroblasts,which exhibit a higherexpression of TGF-β1than normal fibroblastsIncreased or prolongedTGF-β1 activityIncreased MFBs –contributing toincreasedECM/collagen synthesisand tissue contractionMFBs in HSs are lesssensitive to apoptoticsignals, which canprolong collagendeposition and result infibrosisAcidicmucopolysaccharidesAlterations in PGcomposition andamountPersistenthypervascularityPersistent &/orhypercellularityUsually develops within1–3 months followingtrauma or infectionRapid growth phase forup to 6 months, tend tospontaneously regressWill eventually enterthe final stage of woundhealingIncreased infiltrationof immune cells –supporting KSformation is driven byT cellkeratinocyte/fibroblastinteractionsPossiblyincreased/excessiveMFBsMay developanywhere from a yearup to several yearsafter minor injuriesand may even formspontaneously on themid-chest in theabsence of any knowninjuryMore sustained andaggressive than HSsDo not regressspontaneously, tend toreoccur followingexcisionFailure to enter thefinal stage of woundhealingPersistent/pathologicalwound-healing signals orimproper regulation ofwound healing cellsProlonged inflammatoryresponseOverproduction of fibroblastproteinsOverabundant collagendeposition resulting inECM, dermal and epidermalfibrosis. Failed release ofcollagenase in properamount/timing contributesto lower degradation of andexcessiveproliferation/deposition ofcollagenAberrant epidermalregulation of dermalremodeling – epidermalkeratinocytesintercommunicate withunderlying fibroblasts, thisintercommunication playsan important role inpathophysiological scarformation – keratinocytesinduce fibroblasts to secreteCT growth factor, acofactor/downstreammediator of TGF-β drivenfibrosisAberrant activation ofkeratinocytes prolongsepidermal inflammationleading to abnormalepidermal interactions,suggesting that fibroblastmediated collagenproduction is not adequatelyregulated by keratinocytes –leading to excess collagendepositionHistopathologicalcharacteristicsAbnormal/overabundantECM/collagen,primarily, larger thanusual Type III collagenwith abundant whorllikenodules containingMFBs, reduced elastinFlattened epidermisThick/hyalinized(‘*keloidal collagen’),irregularly branched,disorganized Type Iand III collagenbundles withoutnodules. Nonflattenedepidermis.Randomly orientedIncreased a-smooth muscleactin (a-SMA)More fibronectin than innormal skinRandomly orientedexcessive collagen fibersExpanded dermis

following burn injury,

bacterial colonization

and wound infection

Etiology/pathophysiology

Increased, altered

phenotype, fibroblasts,

which exhibit a higher

expression of TGF-β1

than normal fibroblasts

Increased or prolonged

TGF-β1 activity

Increased MFBs –

contributing to

increased

ECM/collagen synthesis

and tissue contraction

MFBs in HSs are less

sensitive to apoptotic

signals, which can

prolong collagen

deposition and result in

fibrosis

Acidic

mucopolysaccharides

Alterations in PG

composition and

amount

Persistent

hypervascularity

Persistent &/or

hypercellularity

Usually develops within

1–3 months following

trauma or infection

Rapid growth phase for

up to 6 months, tend to

spontaneously regress

Will eventually enter

the final stage of wound

healing

Increased infiltration

of immune cells –

supporting KS

formation is driven by

T cellkeratinocyte/fibroblast

interactions

Possibly

increased/excessive

MFBs

May develop

anywhere from a year

up to several years

after minor injuries

and may even form

spontaneously on the

mid-chest in the

absence of any known

injury

More sustained and

aggressive than HSs

Do not regress

spontaneously, tend to

reoccur following

excision

Failure to enter the

final stage of wound

healing

Persistent/pathological

wound-healing signals or

improper regulation of

wound healing cells

Prolonged inflammatory

response

Overproduction of fibroblast

proteins

Overabundant collagen

deposition resulting in

ECM, dermal and epidermal

fibrosis. Failed release of

collagenase in proper

amount/timing contributes

to lower degradation of and

excessive

proliferation/deposition of

collagen

Aberrant epidermal

regulation of dermal

remodeling – epidermal

keratinocytes

intercommunicate with

underlying fibroblasts, this

intercommunication plays

an important role in

pathophysiological scar

formation – keratinocytes

induce fibroblasts to secrete

CT growth factor, a

cofactor/downstream

mediator of TGF-β driven

fibrosis

Aberrant activation of

keratinocytes prolongs

epidermal inflammation

leading to abnormal

epidermal interactions,

suggesting that fibroblast

mediated collagen

production is not adequately

regulated by keratinocytes –

leading to excess collagen

deposition

Histopathological

characteristics

Abnormal/overabundant

ECM/collagen,

primarily, larger than

usual Type III collagen

with abundant whorllike

nodules containing

MFBs, reduced elastin

Flattened epidermis

Thick/hyalinized

(‘*keloidal collagen’),

irregularly branched,

disorganized Type I

and III collagen

bundles without

nodules. Nonflattened

epidermis.

Randomly oriented

Increased a-smooth muscle

actin (a-SMA)

More fibronectin than in

normal skin

Randomly oriented

excessive collagen fibers

Expanded dermis

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