Excessive Scarring

Slide 1 · Excessive Scarring

Hypertrophic scars • Keloids • Proud flesh • Contractures

Tissue repair and its pathologic deviations

Dr Abu Suraih Sakhri

MBBS, MD (Pathology)

www.abusuraihsakhri.com

Slide 2 · Scope: Excessive scarring and abnormal repair

Excess matrix deposition may produce raised scars that alter skin contour.

Excess granulation tissue may obstruct epithelial resurfacing.

Excess wound contraction may deform tissue and limit joint movement.

Excess collagen

Raised scars

Excess granulation

Proud flesh

Excess contraction

Contracture

Slide 3 · Normal repair must be understood first

Tissue repair replaces or restores structures after injury.

Regeneration restores cells when the supporting framework remains suitable.

Scarring deposits connective tissue when full restoration is not possible.

Mild injury

Intact scaffold

Regeneration

Proliferation

Tissue restored

Restitution

More severe injury → connective-tissue scar

Slide 4 · Why some wounds heal with a scar

Deeper injury can damage the connective-tissue framework.

Loss of a supporting scaffold makes complete restitution difficult.

Collagen-rich connective tissue provides mechanical continuity, not full regeneration.

Epidermis

Dermis

Schematic

Slide 5 · Repair and regeneration are different outcomes

Regeneration restores components of the original tissue.

Scar formation patches defects with collagen-rich connective tissue.

A wound may use both processes in varying proportions.

Mild injury

Intact scaffold

Regeneration

Proliferation

Tissue restored

Restitution

Order shown conceptually; Stages overlap

Slide 6 · Three major phases of cutaneous healing

Inflammation clears injured material and initiates the repair response.

Granulation tissue brings cells, vessels and extracellular matrix into the defect.

Extracellular-matrix remodeling changes the early repair tissue into a scar.

Inflammation

Initiation

Granulation

Tissue rebuilding

ECM remodeling

Maturation

Order shown conceptually; Stages overlap

Slide 7 · A clot initiates structural repair

A platelet-rich hemostatic plug forms within minutes of injury.

It controls bleeding and provides an initial provisional scaffold.

Subsequent inflammatory and reparative cells enter the injured region.

Clot

Initiation

Leukocytes

Tissue rebuilding

Repair tissue

Maturation

Order shown conceptually; Stages overlap

Slide 8 · Inflammatory cells prepare the wound

Neutrophils appear early at wound margins.

Monocytes and macrophages subsequently become important.

Removal of the offending cause precedes stable tissue reconstruction.

Inflammatory cells

Repair coordination

Recruits cells

Growth signals

Matrix deposition

Slide 9 · Macrophages coordinate repair

Macrophages help eliminate injurious material.

They produce mediators that recruit and activate repair-associated cells.

Alternatively activated macrophages contribute to the shift toward connective-tissue deposition.

Macrophage

Repair coordination

Recruits cells

Growth signals

Matrix deposition

Slide 10 · Granulation tissue is an active repair compartment

New capillaries, fibroblasts and loose matrix characterize granulation tissue.

Edema and inflammatory cells can still be present.

It is distinct from the later dense, relatively avascular scar.

Early repair

New capillaries + fibroblasts

Late repair

Dense collagen, fewer vessels

The compartments differ in vascularity and matrix density

Slide 11 · Angiogenesis supplies the healing wound

New capillaries sprout from existing vessels.

Endothelial migration and proliferation precede maturation.

Pericyte recruitment and basement-membrane deposition stabilize vessels.

Early repair

New capillaries + fibroblasts

Late repair

Dense collagen, fewer vessels

Angiogenesis supplies a temporary vascular bed

Slide 12 · Granulation tissue evolves into a mature scar

Early granulation tissue is vascular and cellular.

Progressive collagen deposition strengthens the healing site.

With maturation, many vessels regress and dense connective tissue predominates.

Vascular granulation

Initiation

Collagen deposition

Tissue rebuilding

Pale mature scar

Maturation

Order shown conceptually; Stages overlap

Slide 13 · Primary intention limits the tissue defect

Well-apposed clean incisions leave a small gap.

Inflammation and granulation-tissue formation are comparatively limited.

A neat linear scar generally results.

Apposed wound edges

Limited granulation

Surface continuity

Narrow linear scar

Slide 14 · Secondary intention involves a larger deficit

Large or irregular wounds need more tissue replacement.

Inflammation and granulation tissue are more extensive.

Wound contraction and irregular scarring become more prominent.

Wide tissue gap

Extensive granulation

Contraction + scar

Longer, irregular healing

Slide 15 · Primary versus secondary intention

Wound dimensions govern how much tissue must be replaced.

Secondary healing generally entails more contraction.

These are healing patterns, not diagnoses of hypertrophic scarring.

Apposed wound edges

Limited granulation

Surface continuity

Narrow linear scar

Slide 16 · Events evolve over days to weeks

Initially, a clot and inflammatory cells dominate.

Granulation tissue and collagen deposition emerge over the following days.

Later remodeling turns the repair tissue into a mature scar.

Clot / inflammation

Initially

Granulation / ECM

Following days

Mature scar

Later phases

Order shown conceptually; Stages overlap

Slide 17 · Fibroblasts create the fibrous component

Fibroblasts migrate and proliferate within the repair site.

They synthesize collagen and other extracellular-matrix proteins.

Their continued synthetic activity is central to scar formation.

Fibroblast

ECM-producing cell

Migration

Proliferation

Matrix synthesis

Slide 18 · TGF-β is a principal fibrogenic signal

TGF-β enhances fibroblast migration and proliferation.

It promotes collagen and fibronectin synthesis.

It also limits extracellular-matrix degradation by inhibiting metalloproteinases.

TGF-β

Profibrotic signal

Fibroblast activation

Collagen + fibronectin

Reduced ECM breakdown

Slide 19 · Several signals cooperate in fibroblast recruitment

PDGF and FGF-2 contribute to migration and proliferation during repair.

Activated inflammatory cells provide a local source of growth factors.

The integrated repair response depends on cell–matrix interactions.

Local mediators

Repair coordination

Recruits cells

Growth signals

Matrix deposition

Slide 20 · Collagen deposition builds wound strength

Collagen accumulation contributes substantially to tensile stability.

Fibroblasts become more synthetically active as healing progresses.

Dense scar tissue is mechanically useful but is not normal skin architecture.

ECM synthesis

Fibroblasts + collagen

ECM degradation

MMP activity

Net deposition = synthesis minus degradation

Slide 21 · Myofibroblasts link matrix production and contraction

Some fibroblasts acquire smooth-muscle-like actin features.

These differentiated cells are called myofibroblasts.

They contribute to contraction of the scar during healing.

Fibroblast

Actin-associated differentiation

Myofibroblast

Contractile repair cell

Contraction draws tissue toward the defect

Slide 22 · Normal wound contraction is adaptive

Contraction reduces the size of an open wound.

Myofibroblast-driven forces act within the repair tissue.

The same mechanism can become harmful when excessive.

Fibroblast

Actin-associated differentiation

Myofibroblast

Contractile repair cell

Contraction draws tissue toward the defect

Slide 23 · Matrix degradation is necessary for remodeling

Scar maturation is not solely an accumulation process.

Matrix metalloproteinases (MMPs) degrade components of extracellular matrix.

Remodeling depends on regulated deposition and removal.

ECM synthesis

Fibroblasts + collagen

ECM degradation

MMP activity

Net deposition = synthesis minus degradation

Slide 24 · MMPs remodel collagen and matrix

MMPs include enzymes that degrade collagen and other matrix proteins.

They are generated as inactive precursors requiring activation.

Their activity is localized and tightly controlled during repair.

ECM synthesis

Fibroblasts + collagen

ECM degradation

MMP activity

Net deposition = synthesis minus degradation

Slide 25 · TIMPs restrain matrix breakdown

Tissue inhibitors of metalloproteinases (TIMPs) inhibit active MMPs.

They protect deposited matrix from uncontrolled degradation.

Net scar remodeling reflects interplay between synthesis and removal.

ECM synthesis

Fibroblasts + collagen

ECM degradation

MMP activity

Net deposition = synthesis minus degradation

Slide 26 · Excessive scarring reflects abnormal repair output

Too much deposited collagen can elevate the scar above skin level.

Overabundant granulation tissue can prevent epithelial closure.

An excessive contractile response creates deforming contractures.

Excess collagen

Raised scars

Excess granulation

Proud flesh

Excess contraction

Contracture

Slide 27 · Classify the clinically relevant deviations

Hypertrophic scar: Raised collagen-rich scar with a tendency to regress.

Keloid: Scar growth outside the original wound boundary without regression.

Proud flesh and contracture reflect other exaggerated components of healing.

Excess collagen

Raised scars

Excess granulation

Proud flesh

Excess contraction

Contracture

Slide 28 · Hypertrophic scar: A collagen-rich raised lesion

The scar projects above the surrounding skin surface.

Excess collagen underlies the abnormal contour.

The process occurs in the setting of cutaneous wound repair.

Epidermis

Dermis

Schematic

Slide 29 · Hypertrophic scars follow deeper skin injury

Thermal injury is a typical antecedent.

Traumatic injury involving the deep dermis is also characteristic.

The depth and extent of dermal damage help explain increased repair demand.

Epidermis

Dermis

Schematic

Slide 30 · Hypertrophic scars can enlarge early

These scars as often growing rapidly.

The early reparative lesion may be especially cellular and contractile.

Growth rate alone does not distinguish a hypertrophic scar from a keloid.

Time →

Qualitative schematic; No quantitative curve is implied

Slide 31 · Myofibroblasts are prominent in hypertrophic scars

Hypertrophic scars often contain abundant myofibroblasts.

Their presence links the lesion to the contractile repair response.

The cell population helps explain why scar contraction can accompany collagen deposition.

Fibroblast

Actin-associated differentiation

Myofibroblast

Contractile repair cell

Contraction draws tissue toward the defect

Slide 32 · Regression is a key hypertrophic-scar behavior

Hypertrophic scars tend to regress over several months.

Their natural history contrasts with the non-regressing keloid.

Time course should be considered alongside anatomic boundaries.

Time →

Qualitative schematic; No quantitative curve is implied

Slide 33 · Morphologic interpretation: Hypertrophic scars

The key source-described finding is excessive collagen forming a raised scar.

The lesion remains linked to the site of prior dermal injury.

A single static image cannot establish whether subsequent regression occurs.

Epidermis

Dermis

Schematic

Slide 34 · Keloid: Extension beyond the initial wound

A keloid continues past the boundaries of the original injury.

The growth is scar tissue rather than ordinary epithelial spread.

An accurate wound history makes the boundary criterion interpretable.

Epidermis

Dermis

Schematic

Slide 35 · Keloids persist rather than regress

Keloids as scars that do not regress.

Persistence separates them from the usual hypertrophic-scar trajectory.

A raised scar is not automatically a keloid without these features.

Time →

Qualitative schematic; No quantitative curve is implied

Slide 36 · Keloid formation shows individual predisposition

An apparent individual predisposition.

Predisposition is a clinical observation, not a quantified inherited risk in this source.

Do not infer a specific gene or inheritance pattern from the assigned text.

Observed susceptibility

Clinical interpretation

Not a gene test

Clinical interpretation

Clinical history

Clinical interpretation

Slide 37 · Clinical appearance varies with skin tone

Keloids may be erythematous on lighter skin tones.

They may be hyperpigmented on darker skin tones.

Color alone is insufficient: Extension and persistence define the lesion.

Erythematous

Clinical interpretation

Hyperpigmented

Clinical interpretation

Boundary matters

Clinical interpretation

Slide 38 · Keloid histology: Abundant dermal connective tissue

The textbook figure emphasizes thick connective tissue deposited in the dermis.

Histology supports an excessive collagen-deposition process.

Boundary and natural-history information remain clinical rather than purely microscopic.

Epidermis

Dermis

Schematic

Slide 39 · Anatomic interpretation of excess dermal collagen

Epidermis lies above the collagen-containing dermis.

An excessive dermal collagen mass changes surface elevation.

The schematic represents architecture, not an authentic H&E section.

Epidermis

Dermis

Schematic

Slide 40 · Hypertrophic scars versus keloids

Both are excessive scarring responses with raised collagen-rich tissue.

Keloid extension beyond original wound boundaries is decisive.

Regression over months favors the hypertrophic-scar pathway.

Hypertrophic scar

Keloid

Usually within wound

Extends beyond wound

Tends to regress

Does not regress

Raised collagen scar

Raised collagen scar

Slide 41 · Boundary is a spatial diagnostic concept

Record the extent of the original injury if available.

Compare the eventual scar perimeter with that original outline.

Outward extension is the textbook distinction for keloid.

Dashed idea: Initial wound region vs subsequent scar outline

Slide 42 · Evolution over time adds diagnostic information

An enlarging early scar may be hypertrophic or keloidal.

A tendency to regress supports hypertrophic scar.

Persistent growth beyond the injury supports keloid.

Keloid

Hypertrophic scar

Time →

Qualitative schematic; No quantitative curve is implied

Slide 43 · Color and elevation are not enough

Erythema and hyperpigmentation describe appearance, not biological category.

Elevation can occur in either collagen-rich scar type.

The joint assessment of boundary and trajectory is more discriminating.

Dashed idea: Initial wound region vs subsequent scar outline

Slide 44 · Exuberant granulation tissue is a different problem

This lesion consists of excessive granulation tissue, not simply dense mature scar.

The tissue protrudes above the adjacent skin level.

The traditional clinical term is proud flesh.

Epidermis

Dermis

Schematic

Slide 45 · Proud flesh blocks epithelial resurfacing

Elevated granulation tissue obstructs re-epithelialization.

Epithelial cells cannot restore an uninterrupted surface across the raised defect.

Thus excessive repair tissue can paradoxically delay closure.

Epidermis

Dermis

Slide 46 · Distinguish granulation tissue from mature scar

Granulation tissue is capillary-rich and relatively loose.

A mature scar is denser and substantially less vascular.

Proud flesh is primarily overproduction of the former compartment.

Early repair

New capillaries + fibroblasts

Late repair

Dense collagen, fewer vessels

The compartments differ in vascularity and matrix density

Slide 47 · Proud flesh: Intervention targets the obstruction

Cautery or surgical excision of excess granulation tissue.

The intended result is removal of the tissue blocking epithelial continuity.

These approaches are source-described principles, not a comprehensive treatment guideline.

Epidermis

Dermis

Slide 48 · Epithelial repair and connective-tissue repair must align

Surface closure requires epithelial continuity.

Underlying granulation tissue supports regeneration when properly organized.

Excess granulation illustrates how one overactive repair component disrupts another.

Epidermis

Dermis

Slide 49 · Wound contraction is normally useful

Reducing wound dimensions helps close tissue deficits.

Secondary-intention wounds show more contraction than small incisions.

Normal contraction must be distinguished from deforming contracture.

Fibroblast

Actin-associated differentiation

Myofibroblast

Contractile repair cell

Contraction draws tissue toward the defect

Slide 50 · Contracture is excessive contraction

An exaggerated decrease in wound dimensions distorts adjacent tissue.

The deformity can persist after the surface is closed.

Contracture is a functional and geometric complication of repair.

Fibroblast

Actin-associated differentiation

Myofibroblast

Contractile repair cell

Contraction draws tissue toward the defect

Slide 51 · Certain sites are especially susceptible

Palms are cited as contracture-prone sites.

Soles are also vulnerable.

The anterior thorax is another recognized location.

Palms

Grip / flexion surfaces

Soles

Weight-bearing surface

Anterior thorax

Anterior chest region

Slide 52 · Severe burns can lead to disabling contractures

Burn injury may extend through deep dermal structures.

Healing with marked contraction can alter joint movement.

The important outcome is impaired function, not just scar appearance.

Fibroblast

Actin-associated differentiation

Myofibroblast

Contractile repair cell

Contraction draws tissue toward the defect

Slide 53 · Contracture distorts the surrounding tissue

Contraction exerts forces on tissue bordering the wound.

In a mobile region, deformation may restrict a normal range of motion.

The schematic displays a mechanical concept, not patient anatomy.

Fibroblast

Actin-associated differentiation

Myofibroblast

Contractile repair cell

Contraction draws tissue toward the defect

Slide 54 · Hypertrophic scar and contracture may coexist

Myofibroblasts contribute to normal scar contraction.

Hypertrophic scars often contain many myofibroblasts.

A contracture is classified by deformation and functional effect, not simply by scar height.

Fibroblast

Actin-associated differentiation

Myofibroblast

Contractile repair cell

Contraction draws tissue toward the defect

Slide 55 · Rare fibroblastic proliferation can follow injury

Some incisional scars or traumatic wounds are followed by exuberant connective-tissue-cell proliferation.

These proliferations may recur after excision.

This discussion leads to desmoid-type aggressive fibromatosis.

Reactive process

Excess scar response

Neoplastic process

Desmoid / fibromatosis

Slide 56 · Desmoid is not simply another keloid

Aggressive fibromatosis (desmoid) is classified as a benign connective-tissue neoplasm.

Its nature differs from a collagen-rich reactive scar.

The source refers detailed tumor classification to a separate chapter.

Scar

Desmoid

Reactive scar

Benign connective-tissue neoplasm

Excess repair product

Fibroblastic proliferation

Wound-healing deviation

Desmoid / aggressive fibromatosis

Slide 57 · An integrated map of abnormal wound repair

Excess collagen produces raised fibrous scars.

Excess granulation tissue interrupts epithelial closure.

Excess contraction deforms tissues; Fibroblastic neoplasia is a separate consideration.

Excess collagen

Raised scars

Excess granulation

Proud flesh

Excess contraction

Contracture

Slide 58 · Apply the boundary–trajectory distinction

Ask whether the lesion extends beyond the former wound.

Ask whether it regresses over subsequent months.

Do not use skin color alone to decide between hypertrophic scar and keloid.

Dashed idea: Initial wound region vs subsequent scar outline

Slide 59 · Case: Raised scar after deep dermal injury

A hypothetical thermal injury heals with an elevated collagen-rich scar.

The lesion stays within the injured region and later becomes less prominent.

Interpretation: This trajectory is most consistent with a hypertrophic scar.

Epidermis

Dermis

Schematic

Slide 60 · Case: Persistent scar growth past a wound

A hypothetical healed incision develops a raised scar beyond the original edges.

The lesion remains prominent rather than regressing.

Interpretation: The defining behavior supports a keloid.

Epidermis

Dermis

Schematic

Slide 61 · Case: Healing surface blocked by raised tissue

A hypothetical wound develops a protruding mass of granulation tissue.

Surface epithelial continuity remains incomplete across that prominence.

Interpretation: Exuberant granulation tissue (proud flesh).

Epidermis

Dermis

Schematic

Slide 62 · Case: Impaired movement after major burn

A hypothetical severe burn is followed by tightening across a joint.

The healed area deforms surrounding tissues and limits movement.

Interpretation: Deforming wound contracture.

Fibroblast

Actin-associated differentiation

Myofibroblast

Contractile repair cell

Contraction draws tissue toward the defect

Slide 63 · Four abnormalities, four dominant features

Hypertrophic scar: Raised lesion and usual regression over months.

Keloid: Beyond wound margins and persistent.

Proud flesh: Raised granulation blocks epithelium; Contracture: Distortion from excessive contraction.

Excess collagen

Raised scars

Excess granulation

Proud flesh

Excess contraction

Contracture

Slide 64 · Questions to check understanding

Which finding most strongly separates keloids from hypertrophic scars?

Why can excessive granulation tissue delay complete epithelial closure?

Which cell type links collagen-rich repair to contraction?

Core concept

Repair is normally regulated in space and time

Slide 65 · Core teaching references

Robbins, Cotran & Kumar: Pathologic Basis of Disease, 11th ed. (2026).

Chapter 3: Tissue Repair; Repair by Scarring; Healing of Skin Wounds; Excessive Scarring.

The figures here are original editable schematics, not reproductions of the textbook images.

Core concept

Repair is normally regulated in space and time