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Wound Healing Biochemistry – Phases & Molecules

Wound healing biochemistry describes the molecular and cellular processes that occur after tissue injury. It covers inflammation, cell proliferation, and tissue remodeling.

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Wound healing biochemistry describes the molecular and cellular processes that occur after tissue injury. It covers inflammation, cell proliferation, and tissue remodeling.

What Is Wound Healing Biochemistry?

Wound healing biochemistry is a branch of biochemistry and medicine that examines the molecular, cellular, and chemical events that take place after tissue injury. It provides the scientific foundation for understanding how and why wounds heal – and why this process can sometimes fail. Wound healing is a highly complex, coordinated interplay of cell types, signaling molecules, growth factors, and structural proteins.

The Four Phases of Wound Healing

The biochemical sequence of wound healing is classically divided into four temporally overlapping phases:

1. Hemostasis

Immediately after injury, hemostasis is initiated. Damaged blood vessels constrict (vasoconstriction), and platelets adhere to the injured vessel wall. Activation of the coagulation cascade – a series of clotting factors – converts fibrinogen into insoluble fibrin, which together with platelets forms a stable blood clot (thrombus). This temporarily seals the wound and provides a provisional barrier against infection.

2. Inflammatory Phase

In the first hours to days following injury, the inflammatory phase dominates. Biochemically, this phase is characterized by the release of inflammatory mediators such as histamine, prostaglandins, interleukins (e.g., IL-1, IL-6), and tumor necrosis factor-alpha (TNF-α). These molecules cause vasodilation and increase vascular permeability, allowing immune cells – particularly neutrophils and later macrophages – to migrate into the wound site. Neutrophils combat pathogens through phagocytosis and release of reactive oxygen species. Macrophages clear cellular debris and secrete key growth factors such as Transforming Growth Factor beta (TGF-β) and Platelet-Derived Growth Factor (PDGF), which initiate the next healing phase.

3. Proliferative Phase (Tissue Formation)

The proliferative phase begins after a few days and can last several weeks. Biochemically, it is dominated by cell proliferation and tissue reconstruction:

Angiogenesis: New blood vessels grow into the wound area, stimulated by Vascular Endothelial Growth Factor (VEGF), supplying the forming tissue with oxygen and nutrients.
Fibroblast activity: Fibroblasts migrate into the wound and produce large amounts of collagen (primarily type III), providing structural support. This provisional collagen forms the so-called granulation tissue.
Re-epithelialization: Keratinocytes migrate from the wound edges to cover the wound surface with a new epithelial layer, stimulated by Epidermal Growth Factor (EGF) and Keratinocyte Growth Factor (KGF).

4. Remodeling Phase

The final phase of wound healing can last months to years. During this phase, the initially deposited type III collagen is progressively replaced by the stronger type I collagen. Enzymes of the Matrix Metalloproteinase (MMP) family degrade old matrix material, while their inhibitors (TIMPs – Tissue Inhibitors of Metalloproteinases) regulate this turnover. The result is an increasingly strong scar that nevertheless achieves only approximately 70–80% of the original tissue strength.

Key Biochemical Players

Growth factors: TGF-β, PDGF, VEGF, EGF, FGF (Fibroblast Growth Factor)
Cytokines: IL-1, IL-6, IL-10, TNF-α
Structural proteins: Collagen, fibronectin, hyaluronic acid, elastin
Enzymes: Matrix metalloproteinases (MMPs), collagenases, elastases
Cells: Platelets, neutrophils, macrophages, fibroblasts, keratinocytes, endothelial cells

Disturbances of Wound Healing Biochemistry

Various factors can impair the biochemical progression of wound healing and lead to chronic wounds or excessive scar formation:

Diabetes mellitus: Elevated blood glucose levels impair macrophage and fibroblast function and disrupt angiogenesis.
Malnutrition: Deficiency of vitamin C (required for collagen synthesis), zinc (essential for enzyme systems), or proteins delays healing.
Infection: Bacterial burden can prolong the inflammatory phase and inhibit proliferation.
Keloid and hypertrophic scarring: Excessive collagen production by dysregulated fibroblasts leads to raised, abnormal scars.
Corticosteroids and immunosuppressants: These medications suppress the inflammatory response and thereby slow down healing.

Clinical Relevance

Understanding wound healing biochemistry is fundamental to the development of modern wound care. Growth factor-based therapies, moist wound dressings, negative pressure wound therapy, and bioactive wound materials all leverage biochemical principles to optimize healing. Current research is exploring approaches such as Platelet-Rich Plasma (PRP) and recombinant growth factors to more effectively treat chronic wounds.

References

Gurtner G.C. et al. - Wound repair and regeneration. Nature, 2008; 453(7193): 314-321. PubMed PMID: 18480812.
Singer A.J., Clark R.A.F. - Cutaneous wound healing. New England Journal of Medicine, 1999; 341(10): 738-746.
World Health Organization (WHO) - Chronic wounds and wound care management. WHO Technical Report, Geneva.

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