Abnormal Scarring: Dysregulated Collagen Deposition and Failed Wound Remodelling

Hypertrophic scar and Keloid are forms of abnormal wound healing in which tissue repair occurs, but normal remodelling fails. Rather than restoring flexible, functional skin, the healing process becomes excessive, prolonged, and structurally disordered.

What You Need to Know

Abnormal scarring happens when wound healing does not switch off collagen production at the right time. In normal healing, the body lays down collagen quickly to close and stabilise the wound, then gradually breaks down and reorganises that collagen so the scar becomes flatter, softer, and stronger. When this regulatory step fails, fibroblasts keep producing collagen and other extracellular matrix proteins beyond what is needed, so the scar remains raised, firm, and less flexible than surrounding skin.

A few linked processes tend to drive this collagen “overbuild”:

• inflammation that stays active for too long, keeping pro-scarring signals switched on

• fibroblasts that remain highly activated, continuing to deposit collagen rather than slowing down

• reduced collagen breakdown, so excess matrix accumulates instead of being remodelled

Hypertrophic scars and keloids sit on the same spectrum of dysregulated remodelling rather than representing completely separate healing pathways. Both involve persistent collagen deposition and altered growth factor signalling, but they behave differently in how that collagen overgrowth is contained within the original wound area or extends beyond it. The key idea is that abnormal scarring is not “better healing”, it is healing that has lost its normal brakes.

Beyond the Basics

Normal Remodelling and Collagen Balance

In normal wound healing, early collagen laid down during proliferation is gradually replaced with stronger, more organised fibres. As remodelling progresses, fibroblast activity decreases, inflammatory signalling resolves, and excess extracellular matrix is broken down, allowing the scar to soften and gain tensile strength. This balance depends on tightly regulated feedback between collagen synthesis and degradation. When the signals that downregulate fibroblast activity fail to activate, collagen continues to accumulate beyond functional need, setting the foundation for abnormal scarring.

Persistent Inflammation as a Driver of Excess Scarring

Inflammation is a key driver of fibroblast activation, but it is meant to be temporary. When wounds remain inflamed due to infection, repeated mechanical stress, delayed closure, or ongoing tissue injury, pro-fibrotic signalling persists. Cytokines and growth factors continue to stimulate collagen synthesis while simultaneously inhibiting collagen breakdown. This prolonged inflammatory environment explains why wounds that heal slowly or remain chronically irritated are at significantly higher risk of developing hypertrophic scars or keloids.

Fibroblast Overactivity and Collagen Overproduction

Fibroblasts are the primary cells responsible for collagen and extracellular matrix production during healing. In abnormal scarring, fibroblasts become excessively responsive to growth signals and fail to downregulate their activity as remodelling should begin. Collagen deposition continues unchecked, producing a dense, disorganised matrix that is mechanically stiff and poorly aligned. This excess matrix reduces tissue flexibility, alters normal skin mechanics, and contributes to pain, tightness, and functional limitation.

Hypertrophic Scars: Localised Failure of Regulation

Hypertrophic scars occur when excessive collagen production remains confined to the original wound boundaries. These scars are raised, thickened, and firm, reflecting sustained fibroblast activity within the healing area. Although collagen regulation is abnormal, some inhibitory control is retained, which is why hypertrophic scars may slowly regress over time. Risk is increased by deep dermal injury, prolonged inflammation, and mechanical tension that continues to stimulate fibroblasts within the wound margins.

Keloids: Loss of Growth Containment

Keloids represent a more profound failure of regulatory control. In this setting, collagen deposition extends beyond the original wound edges into surrounding normal tissue. Fibroblasts demonstrate heightened sensitivity to growth factors and reduced responsiveness to inhibitory signals that would normally limit repair. Once established, keloids rarely regress and may continue to expand long after wound closure, reflecting a sustained pro-fibrotic state rather than ongoing injury.

Role of Growth Factors and Signalling Pathways

Growth factors that are essential for normal healing become pathogenic when their expression is excessive or prolonged. These signals amplify fibroblast proliferation and collagen synthesis, tipping the balance toward matrix accumulation. In healthy remodelling, inhibitory pathways counteract these signals to restore equilibrium. In abnormal scarring, this counter-regulation fails, allowing collagen production to outpace degradation and resulting in persistent scar elevation and stiffness.

Mechanical Tension and Tissue Stress

Mechanical forces strongly influence fibroblast behaviour. High tension across healing wounds stimulates collagen production as the tissue attempts to reinforce itself against stress. Areas exposed to stretching, repetitive movement, or pressure therefore experience sustained pro-fibrotic signalling. This explains why abnormal scarring is more common over joints, the chest, shoulders, and sternum, where mechanical load remains high throughout healing.

Structural and Functional Consequences

Excess collagen fundamentally alters tissue mechanics. Scar tissue becomes rigid, poorly elastic, and vulnerable to discomfort, restricted movement, or recurrent breakdown. Sensory changes and pain may develop due to altered nerve integration within dense scar tissue. Abnormal scarring is therefore not simply a cosmetic outcome but a disorder of failed remodelling with meaningful functional consequences.

Clinical Connections

Abnormal scarring often becomes apparent when a wound has closed but the tissue remains raised, firm, itchy, or painful and does not soften with time. This pattern fits with ongoing fibroblast activity and persistent collagen deposition rather than infection, which is why scars can be symptomatic even when the skin surface is intact and there are no systemic features. Scars over high-tension areas, across joints, or in wounds that took longer to close are more likely to stay metabolically active and become functionally limiting, because mechanical stress continues to stimulate collagen production and reduces normal remodelling.

In practice, assessment focuses on identifying modifiable drivers that keep the scar in an “active” state and on tracking whether the scar is maturing or becoming more restrictive. Useful clinical cues include:

• increasing firmness, thickness, itch, or pain rather than gradual softening

• reduced range of motion or skin tethering when the scar crosses a joint or mobile tissue plane

• ongoing irritation from friction, pressure, or repeated minor breakdown at the scar edge

Management links directly to the underlying remodelling imbalance. Minimising tension, reducing irritation, and supporting stable healing conditions aim to limit continued collagen stimulation and allow the scar to progress toward maturation. Once excessive matrix deposition becomes established, reversal is difficult, so early attention to factors that prolong inflammation or mechanical stress matters more than product changes alone. Where function is threatened, early referral is appropriate because contracture risk increases when dense scar tissue forms across joints, skin creases, or areas that are repeatedly stretched.

Concept Check

1. Why does excessive collagen deposition indicate failed remodelling rather than failed healing?

2. How does persistent inflammation promote abnormal scarring?

3. Why do hypertrophic scars remain within wound boundaries while keloids extend beyond them?

4. How does mechanical tension influence fibroblast activity?

5. Why can abnormal scarring impair function even after wound closure?