Chemical Burn Injury Mechanisms and Wound Healing Dynamics

Chemical burns arise when caustic agents—acids or alkalis—penetrate the skin and subcutaneous tissues, inducing immediate protein coagulation or liquefactive necrosis. This primary insult provokes a rapid inflammatory cascade marked by release of interleukins, tumour necrosis factor-α and reactive oxygen species. Cellular membranes and extracellular matrix components are disrupted, triggering transcriptional programmes of cell death and repair. Healing proceeds through overlapping phases: an inflammatory phase of vascular dilation and leukocyte recruitment; a proliferative phase in which keratinocytes re-epithelialise the wound, endothelial cells form new capillaries and fibroblasts deposit granulation matrix; and a remodelling phase featuring myofibroblast-driven contraction, matrix maturation and scar formation. Chemical burns often penetrate more deeply than thermal injuries, leading to prolonged inflammation, imbalanced cytokine expression and a heightened risk of hypertrophic scarring. Advances in molecular understanding—especially of transforming growth factor-β, matrix metalloproteinases and matricellular signals—have begun to inform targeted interventions that accelerate decontamination, modulate inflammation, enhance neovascularisation and limit fibrosis.

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Chemical Burn Injury Mechanisms and Wound Healing Dynamics publication trend

The graph below shows the total number of articles in chemical burn injury mechanisms and wound healing dynamics across all publications each year (not limited to Nature Index journals).

Technical terms

Coagulation necrosis: Tissue death marked by protein denaturation that preserves cell outlines, characteristic of acid burns.

Liquefaction necrosis: Enzymatic breakdown of tissue structure, typical of alkali injuries.

Re-epithelialisation: Keratinocyte migration and proliferation across the wound bed to re-establish the epidermal barrier.

Granulation tissue: Highly vascular connective tissue formed by fibroblasts and endothelial cells during the proliferative phase.

Myofibroblast: Contractile fibroblast subtype expressing α-smooth muscle actin, essential for wound contraction and extracellular matrix remodelling.

Matrix metalloproteinases: Family of zinc-dependent enzymes that degrade extracellular matrix proteins to facilitate tissue remodelling.

References

1. Current progress in understanding the molecular pathogenesis of burn scar contracture. Burns & Trauma (2017).
2. Effects of IL-1β and TNF-α on the Expression of P311 in Vascular Endothelial Cells and Wound Healing in Mice. Frontiers in Physiology (2020).
3. P311 Facilitates the Angiogenesis and Wound Healing Function of MSCs by Increasing VEGF Production. Frontiers in Immunology (2022).
4. Reconstruction of Bilateral Upper and Lower Eyelid Ectropion Caused by a Liquid Unblocker Chemical Burn. Cureus (2023).