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Acne Scars: Pathogenesis, Classification and Treatment

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Hindawi Publishing Corporation Dermatology Research and Practice Volume 2010, Article ID 893080, 13 pages doi:10.1155/2010/893080

Review Article Acne Scars: Pathogenesis, Classification and Treatment
Gabriella Fabbrocini, M. C. Annunziata, V. D’Arco, V. De Vita, G. Lodi, M. C. Mauriello, F. Pastore, and G. Monfrecola
Division of Clinical Dermatology, Department of Systematic Pathology, University of Naples Federico II, Via Sergio Pansini 5, 80133 Napoli, Italy Correspondence should be addressed to Gabriella Fabbrocini, gafabbro@unina.it Received 17 March 2010; Revised 7 September 2010; Accepted 28 September 2010 Academic Editor: Daniel Berg Copyright © 2010 Gabriella Fabbrocini et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Acne has a prevalence of over 90% among adolescents and persists into adulthood in approximately 12%–14% of cases with psychological and social implications. Possible outcomes of the inflammatory acne lesions are acne scars which, although they can be treated in a number of ways, may have a negative psychological impact on social life and relationships. The main types of acne scars are atrophic and hypertrophic scars. The pathogenesis of acne scarring is still not fully understood, but several hypotheses have been proposed. There are numerous treatments: chemical peels, dermabrasion/microdermabrasion, laser treatment, punch techniques, dermal grafting, needling and combined therapies for atrophic scars: silicone gels, intralesional steroid therapy, cryotherapy, and surgery for hypertrophic and keloidal lesions. This paper summarizes acne scar pathogenesis, classification and treatment options.

1. Introduction
Acne has a prevalence of over 90% among adolescents [1] and persists into adulthood in approximately 12%–14% of cases with psychological and social implications of high gravity [2, 3]. All body areas with high concentrations of pilosebaceous glands are involved, but in particular the face, back and chest. Inflammatory acne lesions can result in permanent scars, the severity of which may depend on delays in treating acne patients. The prevalence and severity of acne scarring in the population has not been well studied, although the available literature is usually correlated to the severity of acne [4]. 2133 volunteers aged 18 to 70 from the general population showed that nearly 1% of people had acne scars, although only 1 in 7 of these were considered to have “disfiguring scars” [5]. Severe scarring caused by acne is associated with substantial physical and psychological distress, particularly in adolescents.

2. Pathogenesis
The pathogenesis of acne is currently attributed to multiple factors, such as increased sebum production, alteration of

the quality of sebum lipids, androgen activity, proliferation of Propionibacterium acnes (P. acnes) within the follicle and follicular hyperkeratinization [6]. Increased sebum excretion contributes to the development of acne. Neutral and polar lipids produced by sebaceous glands serve a variety of roles in signal transduction and are involved in biological pathways [7]. Additionally, fatty acids act as ligands of nuclear receptors such as PPARs. Sebaceous gland lipids exhibit direct pro- and anti-inflammatory properties, whereas the induction of 5-lipoxygenase and cyclooxygenase-2 pathways in sebocytes leads to the production of proinflammatory lipids [8]. Furthermore, hormones like androgens control sebaceous gland size and sebum secretion. In cell culture, androgens only promote sebocyte proliferation, whereas PPAR ligands are required for the induction of differentiation and lipogenic activity [9]. On the other hand, keratinocytes and sebocytes may be activated by P. acnes via TLR, CD14, and CD1 molecules [10]. Pilosebaceous follicles in acne lesions are surrounded by macrophages expressing TLR2 on their surface. TLR2 activation leads to a triggering of the transcription nuclear factor and thus the production of cytokines/chemokines, phenomena observed in acne lesions. Furthermore, P. acnes induces IL-8 and IL-12 release from TLR2 positive monocytes [11].

2 All these events stimulate the infrainfundibular inflammatory process, follicular rupture, and perifollicular abscess formation, which stimulate the wound healing process. Injury to the skin initiates a cascade of wound healing events. Wound healing is one of the most complex biological process and involves soluble chemical mediators, extracellular matrix components, parenchymal resident cells as keratinocytes, fibroblasts, endothelial cells, nerve cells, and infiltrating blood cells like lymphocytes, monocytes, and neutrophils, collectively known as immunoinflammatory cells. Scars originate in the site of tissue injury and may be atrophic or hypertrophic. The wound healing process progresses through 3 stages: (1) inflammation, (2) granulation tissue formation, and (3) matrix remodeling [12, 13]. (1) Inflammation. Blanching occurs secondary to vasoconstriction for hemostasis. After the blood flow has been stopped, vasodilatation and resultant erythema replace vasoconstriction. Melanogenesis may also be stimulated. This step plays an important role in the development of postacne erythema and hyperpigmentation. A variety of blood cells, including granulocytes, macrophages, neutrophils lymphocytes, fibroblasts, and platelets, are activated and release inflammatory mediators, which ready the site for granulation tissue formation [14]. 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 [15]. (2) Granulation Tissue Formation. Damaged tissues are repaired and new capillaries are formed. Neutrophils are replaced by monocytes that change into macrophages and release several growth factors including platelet-derived growth factor, fibroblast growth factor, and transforming growth factors α and β, which stimulate the migration and proliferation of fibroblasts [16]. New production of collagen by fibroblasts begins approximately 3 to 5 days after the wound is created. Early on, the new skin composition is dominated by type III collagen, with a small percentage (20%) of type I collagen. However, the balance of collagen types shifts in mature scars to be similar to that of unwounded skin, with approximately 80% of type I collagen [17]. (3) Matrix Remodelling. Fibroblasts and keratinocytes produce enzymes including those that determine the architecture of the extracellular matrix metalloproteinases (MMPs) and tissue inhibitors of MMPs. MMPs are extracellular matrix (ECM) degrading enzymes that interact and form a lytic cascade

Dermatology Research and Practice

Acne scars subtypes

Icepick

Rolling

Boxcar

Skin surface

SMAS

Figure 1: Acne scars subtypes.

Figure 2: Icepick scars.

for ECM remodeling [18]. As a consequence, an imbalance in the ratio of MMPs to tissue inhibitors of MMPs results in the development of atrophic or hypertrophic scars. Inadequate response results in diminished deposition of collagen factors and formation of an atrophic scar while, if the healing response is too exuberant, a raised nodule of fibrotic tissue forms hypertrophic scars [19].

3. Morphology, Histology, and Classification
Scarring can occur as a result of damage to the skin during the healing of active acne. There are two basic types of scar depending on whether there is a net loss or gain of collagen (atrophic and hypertrophic scars). Eighty to ninety percent of people with acne scars have scars associated with a loss of collagen (atrophic scars) compared to a minority who show hypertrophic scars and keloids. 3.1. Atrophic Scars. Atrophic acne scars are more common than keloids and hypertrophic scars with a ratio 3 : 1. They have been subclassified into ice pick, boxcar, and rolling scars (Figure 1 and Table 1). With atrophic scars, the ice pick type represents 60%–70% of total scars, the boxcar 20%–30%, and rolling scars 15%–25% [20]. Icepick: narrow (2 mm), punctiform, and deep scars are known as icepick scars. With this type of scar, the opening is typically wider than the deeper infundibulum (forming a “V” shape) (Figure 2).

Dermatology Research and Practice
Table 1: Acne scar morphological classification (adapted from [20]). Acne Scars Subtype Icepick Rolling Boxcar Shallow 3 mm diameter Deep 3 mm diameter

3

Clinical Features Icepick scars are narrow (

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