Abstract
Wound healing is an essential process to restore tissue integrity after trauma. Large skin wounds such as burns often heal with hypertrophic scarring and contractures, resulting in disfigurements and reduced joint mobility. Such adverse healing outcomes are less common in the oral mucosa, which generally heals faster compared to skin. Several studies have identified differences between oral and skin wound healing. Most of these studies however focus only on a single stage of wound healing or a single cell type. The aim of this review is to provide an extensive overview of wound healing in skin versus oral mucosa during all stages of wound healing and including all cell types and molecules involved in the process and also taking into account environmental specific factors such as exposure to saliva and the microbiome. Next to intrinsic properties of resident cells and differential expression of cytokines and growth factors, multiple external factors have been identified that contribute to oral wound healing. It can be concluded that faster wound closure, the presence of saliva, a more rapid immune response, and increased extracellular matrix remodeling all contribute to the superior wound healing and reduced scar formation in oral mucosa, compared to skin.
Highlights
Wound healing is a tightly regulated process aiming to restore tissues upon damage.Irrespective of the type of wounded tissue, the process of wound healing follows four partially overlapping phases: hemostasis, inflammation, proliferation, and remodeling.Each stage involves unique cell types and molecules
Viruses and fungi have been shown to contribute to adverse wound healing, little information is available to compare skin with oral wound healing, and we focus on bacteria in the host–microbiome interaction during wound healing
Macrophages contribute to proinflammatory cytokine secretion (+) and release growth factors (o) to stimulate tissue kines (-) to dampen the immune response (F,G). (4) Remodeling phase: weeks to months after wounding,fibroblasts (G), and M2 macrophages (E) that still reside in the wound bed remodel the extracellular matrix via the secretion of matrix proteins, matrix metalloproteinases (MMPs; *), and tissue inhibitors of metalloproteases (TIMPs; *)
Summary
Wound healing is a tightly regulated process aiming to restore tissues upon damage. Irrespective of the type of wounded tissue, the process of wound healing follows four partially overlapping phases: hemostasis, inflammation, proliferation, and remodeling. Hypertrophic scar formation is associated with increased angiogenesis and a suppressed and delayed inflammatory reIn general, wounds in the oral mucosa heal relatively fast and with little scarring, despite sponse [4,5]. Similar to skin, during oral wound healing and underlying (autoimmune) diseases such as such cicatricial complications during oral wound healing and underlying (autoimmune) diseases as pemphigoid, pemphigus vulgaris, or diabetes cause delayed wound healing and scarring cicatricial pemphigoid, pemphigus vulgaris, or diabetes cause delayed wound healing inand thescarring oral mucosa. External factors such asfactors alcoholsuch and as cigarette have been in the[10,11].
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