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Inflammation plays an active role during the wound healing process. There is a direct association between the extent of injury as well as inflammation and the amount of subsequent cutaneous scarring. Evidence to date demonstrates that high levels of inflammation are associated with excessive dermal scarring and formation of abnormal pathological scars such as keloids and hypertrophic scars. In view of the multiple important cell types being involved in the inflammatory process and their influence on the extent of scar formation, many scar therapies should aim to target these cells in order to control inflammation and by association help improve scar outcome. However, most current treatment strategies for the management of a newly formed skin scar often adopt a watch-and-wait approach prior to commencing targeted anti-inflammatory therapy. Moreover, most of these therapies have been evaluated in the remodelling phase of wound healing and the evaluation of anti-inflammatory treatments at earlier stages of healing have not been fully explored and remain limited. Taken together, in order to minimise the risk of developing a poor scar outcome, it is clear that adopting an early intervention prior to skin injury would be optimal, however, the concept of pre-emptively priming the skin prior to injury has not yet been thoroughly evaluated. Therefore, the aim of this review was to evaluate the available literature regarding scar therapies that aim to target inflammation which are commenced prior to when a scar is formed or immediately after injury, with a particular focus on the role of pre-emptive priming of skin prior to injury in order to control inflammation for the prevention of poor scarring outcome. [ABSTRACT FROM AUTHOR]

Inflammation plays an active role during the wound healing process. There is a direct association between the extent of injury as well as inflammation and the amount of subsequent cutaneous scarring. Evidence to date demonstrates that high levels of inflammation are associated with excessive dermal scarring and formation of abnormal pathological scars such as keloids and hypertrophic scars. In view of the multiple important cell types being involved in the inflammatory process and their influence on the extent of scar formation, many scar therapies should aim to target these cells in order to control inflammation and by association help improve scar outcome. However, most current treatment strategies for the management of a newly formed skin scar often adopt a watch-and-wait approach prior to commencing targeted anti-inflammatory therapy. Moreover, most of these therapies have been evaluated in the remodelling phase of wound healing and the evaluation of anti-inflammatory treatments at earlier stages of healing have not been fully explored and remain limited. Taken together, in order to minimise the risk of developing a poor scar outcome, it is clear that adopting an early intervention prior to skin injury would be optimal, however, the concept of pre-emptively priming the skin prior to injury has not yet been thoroughly evaluated. Therefore, the aim of this review was to evaluate the available literature regarding scar therapies that aim to target inflammation which are commenced prior to when a scar is formed or immediately after injury, with a particular focus on the role of pre-emptive priming of skin prior to injury in order to control inflammation for the prevention of poor scarring outcome.

Mast cells (MCs) are an important immune cell type in the skin and play an active role during wound healing. MCs produce mediators that can enhance acute inflammation, stimulate re-epithelialisation as well as angiogenesis, and promote skin scarring. There is also a link between MCs and abnormal pathological cutaneous scarring, with increased numbers of MCs found in hypertrophic scars and keloid disease. However, there has been conflicting data regarding the specific role of MCs in scar formation in both animal and human studies. Whilst animal studies have proved to be valuable in studying the MC phenomenon in wound healing, the appropriate translation of these findings to cutaneous wound healing and scar formation in human subjects remains crucial to elucidate the role of these cells and target treatment effectively. Therefore, this perspective paper will focus on evaluation of the current evidence for the role of MCs in skin scarring in both animals and humans in order to identify common themes and future areas for translational research.

Mast cells (MCs) are an important immune cell type in the skin and play an active role during wound healing. MCs produce mediators that can enhance acute inflammation, stimulate re-epithelialisation as well as angiogenesis, and promote skin scarring. There is also a link between MCs and abnormal pathological cutaneous scarring, with increased numbers of MCs found in hypertrophic scars and keloid disease. However, there has been conflicting data regarding the specific role of MCs in scar formation in both animal and human studies. Whilst animal studies have proved to be valuable in studying the MC phenomenon in wound healing, the appropriate translation of these findings to cutaneous wound healing and scar formation in human subjects remains crucial to elucidate the role of these cells and target treatment effectively. Therefore, this perspective paper will focus on evaluation of the current evidence for the role of MCs in skin scarring in both animals and humans in order to identify common themes and future areas for translational research. [ABSTRACT FROM AUTHOR]

Keloids are considered as benign fibroproliferative skin tumors growing beyond the site of the original dermal injury. Although traditionally viewed as a form of skin scarring, keloids display many cancer-like characteristics such as progressive uncontrolled growth, lack of spontaneous regression and extremely high rates of recurrence. Phenotypically, keloids are consistent with non-malignant dermal tumors that are due to the excessive overproduction of collagen which never metastasize. Within the remit of keloid pathobiology, there is increasing evidence for the various interplay of neoplastic-promoting and suppressing factors, which may explain its aggressive clinical behavior. Amongst the most compelling parallels between keloids and cancer are their shared cellular bioenergetics, epigenetic methylation profiles and epithelial-to-mesenchymal transition amongst other disease biological (genotypic and phenotypic) behaviors. This review explores the quasi-neoplastic or cancer-like properties of keloids and highlights areas for future study.

Keloids are considered as benign fibroproliferative skin tumors growing beyond the site of the original dermal injury. Although traditionally viewed as a form of skin scarring, keloids display many cancer-like characteristics such as progressive uncontrolled growth, lack of spontaneous regression and extremely high rates of recurrence. Phenotypically, keloids are consistent with non-malignant dermal tumors that are due to the excessive overproduction of collagen which never metastasize. Within the remit of keloid pathobiology, there is increasing evidence for the various interplay of neoplastic-promoting and suppressing factors, which may explain its aggressive clinical behavior. Amongst the most compelling parallels between keloids and cancer are their shared cellular bioenergetics, epigenetic methylation profiles and epithelial-to-mesenchymal transition amongst other disease biological (genotypic and phenotypic) behaviors. This review explores the quasi-neoplastic or cancer-like properties of keloids and highlights areas for future study. [ABSTRACT FROM AUTHOR]

Abnormal scarring and its accompanying esthetic, functional, and psychological sequelae still pose significant challe nges. To date, there is no satisfactory prevention or treatment option for hypertrophic scars (HSs), which is mostly due to not completely comprehending the mechanisms underlying their formation. That is why the apprehension of regular and controlled physiological processes of scar formation is of utmost importance when facing hypertrophic scarring, its pathophysiology, prevention, and therapeutic approach. When treating HSs and choosing the best treatment and prevention modality, physicians can choose from a plethora of therapeutic options and many commercially available products, among which currently there is no efficient option that can successfully overcome impaired skin healing. This article reviews current therapeutic approach and emerging therapeutic strategies for the management of HSs, which should be individualized, based on an evaluation of the scar itself, patients’ expectations, and practical, evidence-based guidelines. Clinicians are encouraged to combine various prevention and treatment modalities where combination therapy that includes steroid injections, 5-fluorouracil, and pulsed-dye laser seems to be the most effective. On the other hand, the current therapeutic options are usually empirical and their results are unreliable and unpredictable. Therefore, there is an unmet need for an effective, targeted therapy and prevention, which would be based on an action or a modulation of a particular factor with clarified mechanism of action that has a beneficial effect on wound healing. As the extracellular matrix has a crucial role in cellular and extracellular events that lead to pathological scarring, targeting its components mostly by regulating bone morphogenetic proteins may throw up new therapeutic approach for reduction or prevention of HSs with functionally and cosmetically acceptable outcome.