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Mohamed Magdy Badr: How Do Acute Wounds Turn Into Chronic Wounds?
Mohamed Magdy Badr, MD, WCSP/LinkedIn
Nov 21, 2025, 14:23

Mohamed Magdy Badr: How Do Acute Wounds Turn Into Chronic Wounds?

Mohamed Magdy Badr, Wound Care Consultant at Armed Force Rehabilitation Center, posted on LinkedIn:

”How Do Acute Wounds Turn Into Chronic Wounds?

A Molecular-Level Look Into the Biology of Non-Healing

Not all wounds heal the same. Some progress smoothly through hemostasis, inflammation, proliferation, and remodeling. Others become stuck, turning into chronic, non-healing wounds that persist for months.
But the real story starts at the molecular level.

1. Prolonged, Dysregulated Inflammation

  • In normal healing, inflammation lasts 48–72 hours.
  • In chronic wounds, inflammatory cells remain activated for weeks.
  • Excess neutrophils release destructive enzymes
  • Continuous production of pro-inflammatory cytokines (IL-1, IL-6, TNF-α)
  • Increased ROS → cellular damage

This creates a toxic, self-perpetuating loop.

 

2. Elevated Proteases (MMPs) and Reduced Inhibitors (TIMPs)

Chronic wounds show:

  • High MMPs → degrade extracellular matrix, growth factors, and new tissue
  • Low TIMPs → no balance

Result: the wound bed becomes chemically hostile, unable to form granulation tissue.

 

3. Biofilm: The Silent Saboteur

  • Up to 80% of chronic wounds contain biofilms.
  • Biofilm communities:
  • Suppress immune response
  • Block antibiotics
  • Maintain low-grade inflammation
  • Delay epithelial migration

This keeps the wound locked in an inflammatory state.

 

4. Impaired Perfusion and Cellular Hypoxia

Reduced oxygen affects every molecular step:

  • ↓ ATP → weaker fibroblast function
  • ↓ collagen synthesis
  • ↑ susceptibility to infection
  • ↑ inflammatory mediators

Hypoxia changes the entire gene expression profile of the wound.

 

5. Cellular Senescence

  • Fibroblasts, keratinocytes, and endothelial cells become senescent:
  • Lose ability to divide
  • Stop responding to growth factors
  • Release more inflammatory cytokines (SASP phenotype)
  • The wound essentially loses its “healing machinery.”

 

6. Growth Factor Depletion

Chronic wounds have:

  • Lower levels of PDGF, VEGF, TGF-β
  • Poor receptor response
  • Rapid degradation by proteases

Without these signals, angiogenesis, epithelialization, and matrix formation cannot progress.

The Result? A Wound Stuck in the Inflammatory Phase

Instead of moving to proliferation, the wound becomes trapped in a molecular cycle of:

  • Persistent inflammation
  • Biofilm activity
  • Cellular senescence
  • Enzymatic imbalance
  • Poor perfusion

This is how an acute wound transforms into a chronic one.

Final Message

Understanding the molecular biology of chronic wounds isn’t academic — it is essential for designing better treatments, selecting smarter dressings, breaking biofilms, and improving patient outcomes.”

Mohamed Magdy Badr

Stay informed with Hemostasis Today.

(inflammation Biology Cellular Damage Endothelial Cells Health Hematology Hemostasis Hemostasis Today Medicine Mohamed Magdy Badr Proliferation thrombosis Wound Wound Healing
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