Pathophysiology of Scarring
This chapter focuses on the basic pathophysiological mechanisms associated with scarring. Anatomy and physiology of the skin, as well as our current understanding of how scar tissue forms, and how the process of scarring can be modulated are described.
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Wound Healing and Scarring
When cutaneous integrity is disrupted, wound healing and the formation of scars are essential in providing a protective barrier against infection and fluid loss [1]. Wound healing is a complex process triggered by an initial insult, which progresses in a systematic manner and is categorised into three specific phases: inflammatory, proliferative and remodelling [2]. The duration of this cascade of events varies between individuals and can take many months to complete [2]. Within minutes of the initial insult, clot formation at the wound site initiates the inflammatory phase [2] by attracting inflammatory cells, in particular neutrophils, which migrate to the area of trauma [3]. Neutrophil-specific enzymes, including collagenases, are hypothesised to contribute to scar formation by resulting in areas of excessive tissue loss, thereby leaving large defects which are ultimately replaced during the remodelling phase by scar tissue [4]. Chemotactic agents also result in migration of monocytes to the region of injury which are transformed into macrophages on reaching the wound site and not only act in an inflammatory manner but also play a vital role in the proliferative phase by stimulating angiogenesis and reepithelialisation [5]. The proliferative phase ensues over the next few days to weeks and consists of a chain of events resulting in repair of both the dermal and epidermal layers [3]. This stage involves a range of processes including angiogenesis, granulation tissue formation, deposition of collagen, re-epithelialization and retraction of the wound which ultimately results in scar formation [6]. In the process of angiogenesis, a rich network of capillaries created from surrounding healthy blood vessels N. Sargazi · D. Bodansky Mersey Regional Burns and Plastic Surgery Unit, St Helens and Knowsley Teaching Hospitals NHS Trust, Prescot, Merseyside, UK K. Shokrollahi (*) Burns and Plastic Surgery Unit, Whiston Hospital, Liverpool, UK
are formed throughout the wound [6]. These are initially fragile and relatively permeable, resulting in a degree of tissue oedema [6]. Next, collagen deposition occurs as a result of secretion of extracellular matrix proteins by fibroblasts following their migration and proliferation in the wound [6].The resulting vascularised, pink fibrous tissue is termed granulation tissue and acts to replace the clot previously formed at the site of trauma [6]. Once adequate quantities of matrix are laid down, fibroblasts differentiate into myofibroblasts and initiate wound contraction [6]. Re-epithelialisation occurs early in this process, with keratinocytes migrating from wound edges to cover the granulation tissue and proliferating across the denuded area of skin [5], thereby differentiating into a new layer of epidermis [3]. In its final stage, the wound enters the maturation phase during which the granulation tissue undergoes remodelling by its constituent cells, thereby allowing organisation of the scar [3]. Scar formation is the normal physiological response to cu
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