Why it makes biological sense to let a scab facilitate the healing of an acute wound in otherwise healthy skin
How does a scab form?
Wound healing is a complex system of co-evolving interactions between keratinocytes, platelets, fibroblasts, endothelial and immune cells, and the extracellular matrix. Skins wounds develop a scab as an integral early step of the mammalian wound-healing program. A scab is a temporary protective crust which forms from the components of the initial rapidly formed haemostatic clot.
Immediately after injury, the body initiates haemostasis, with platelet aggregation and fibrin network formation, creating a provisional seal over the wound. This fibrin-rich clot constitutes the core of the scab and acts as the protective crust on the wound surface. The scab begins as a haemostatic clot and becomes a visible crust as it dries.
What is the function of a scab?
Crust formation is an integral part of re-epithelialising dynamics.
The temporary barrier of the scab provides a substrate for epidermal cell migration and re-epithelialisation, enabling orderly wound closure. The scab is a scaffold-like surface which supports the migration of keratinocytes and the re-epithelialization process as the wound edges advance. Epidermal cellto move across the wound bed beneath the crust, until the wound edges close.
The scab protects the wound bed from external microbe intrusion and desiccation while repair processes unfold.
Scab formation stabilizes the wound site. In the absence of a scab, the complex immune and growth factor signaling of the wound bed is altered, and re-epithelialization can be delayed.
What is the scab microbiome?
Scab crusts serve as microbial niches which influence healing trajectories. Microbial communities within the skin wound environment, including biofilms, modulate healing. These microbial communities are interacting with and supporting the healing function of a host of immunoregulatory factors within the wound bed.
A dry crust also displaces excessive biofilm development in infected wounds, contributing to microbial control.
The crust’s relationship to infection is nuanced, because crusts can harbor microbes in compromised wounds, particularly in biofilm-dominated contexts, such as chronic venous or diabetic ulcers, which may negatively influence healing trajectories and infection control. In these toxic microenvironments of chronic wounds, moist wound healing has an important role.
But desiccation-based strategies and dry crusts have been shown, in specific settings, to remove biofilm burdens, operating as antimicrobial or barrier strategies, which fits with an evolutionary perspective on the benefits of the scab.
Foetal skin doesn't scab but the lactating nipple is an entirely different and highly dynamic microenvironment
Foetal skin can heal with minimal or no scar formation, a phenomenon linked to distinct inflammatory and extracellular matrix dynamics, different to adult wound healing. This scarless healing in-utero is not typically accompanied by the same crust-forming trajectory seen in adult wounds, suggesting that crust formation is a feature of the adult repair program rather than an unavoidable universal step in wound closure.
From an evolutionary perspective, this finding suggests that scab formation is protection for the extero-utero environment (air, increased microbial exposure). Attempts to mimic foetal wound healing by eliminating scabs and keeping the wound moist increases risk, since linear interventions into complex biological systems (like the healing wound on the nipple of a breastfeeding or lactating woman) often result in unintended outcomes.
Moist wound dressings are designed to prevent excessive scab formation by maintaining the wound surface in a hydrated state, which supports epithelialization while reducing dry crust formation. This is relevant to wounds in the context of burns and chronically damaged tissues (e.g. venous ulcers, pressure ulcers, diabetic ulcers), where epithelialisation is interrupted by a toxic microenvironment.
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Selected references
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Park E, Long SA, Seth AK, Geringer M. The use of desiccation to treat Staphylococcus aureus biofilm-infected wounds. Wound Repair and Regeneration. 2016;24:394-401.
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Ho CY, Chou HY, Wang SH, Lan CY, Shyu VB, Chen CH, Tsai CH. A Comprehensive Analysis of Moist Versus Non-Moist Dressings for Split-Thickness Skin Graft Donor Sites: A Systematic Review and Meta-Analysis. Health Sci Rep. 2025 Jan 17;8(1):e70315. doi: 10.1002/hsr2.70315. PMID: 39831076; PMCID: PMC11739794.