Department of Clinical Medicine and Surgery, Section of Dermatology, University of Naples Federico II, Naples, Italy
scarring. This suggests that these pathological scars are due to injury of this skin layer and the subsequent aberrant wound healing therein by persistent inflammation. The reticular layer of keloids and hypertrophic scars contains inflammatory cells, increased numbers of fibroblasts, and newly formed blood vessels. Hypertrophic scars are typically pink, raised, and firm, with thick hyalinised collagen bundles that remain within the borders of the original site of injury and collagen deposits (Figure 1). Hypertrophic and keloidal scars are more common in darker-skinned individuals and occur predominantly on the trunk.Prevention of Acne Scars Prevention of acne scar development can be lead by controlling skin inflammation during acne treatment. Inflammation plays a crucial role in acne scars formation. By examining biopsy specimens of acne lesions from the back of patients with severe scars and without scars, Holland et al found that the inflammatory reaction at the pilosebaceous gland was stronger and had a longer duration in patients with scars versus those without; in addition, the inflammatory reaction was slower in those with scars versus patients who did not develop scars. They showed a strong relationship between severity and duration of inflammation and the development of scarring, suggesting that treating early inflammation in acne lesions may be the best approach to prevent acne scarring.7 Among therapeutic options to control the inflammatory process in acne are topical retinoids that have shown high efficacy. Several clinical trials have demonstrated the efficacy of topical retinoids to prevent acne scars.8-9 Direct and indirect anti-inflammatory properties of topical retinoids are the molecular principle by which their activity is based on.Different authors focused on the molecular events involved in the scar formation, explaining the activity of topical retinoids in acne scarring prevention.10 They described the inflammatory pathways active in vivo in acne lesions, showing the hyperactivation of two important transcriptional factors: NFK-B e AP-1. In particular, NFK-B activation increases the expression of various cytokines (especially TNF alpha and IL-1) that are able to break out the inflammatory cascade with different mechanisms, especially through the recruitment of circulating inflammatory cells. These cells, when "attracted" by these mediators, migrate from the circulation through the vessel wall reaching the inflammatory site. All these events contribute significantly to the histological damage occurring in the pilo-sebaceous unit, contributing to the appearance of disfiguring scars in patients suffering from acne (Figure 2).AP-1 is a transcriptional factor able to modulate different genes and activate the expression of different Metalloproteinases (MMPs) such as MMP-1, MMP-3, MMP-9. These types of MMPs seem to be particular represented in the dermis and they are involved in extracellular matrix degradation, a crucial event in acne scars formation. The activities of NFK-B and AP-1 on molecular pathways involved in scarring events explain why the anti-inflammatory effect of retinoids is so important for their efficacy in acne scars prevention.11 It has also been demonstrated that retinoids are able to reduce free fatty acids amounts in microcomedones, promoting the correct barrier function of infundibular wall by an indirect antinflammatory activity. Retinoic
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