RESUMEN
BACKGROUND: Therapies for postacne scarring act through modulation of elastin and collagen, and collagen III might therefore represent a biomarker of treatment effectiveness. PATIENTS AND METHODS: Patients (n = 70) with postacne scars and individuals without scars (n = 56) were included in this case-control study. Patients were treated with Dermaroller microneedling, trichloroacetic acid chemical reconstruction, punch excision, or scar subcision. Scar severity was graded immediately before and after treatment with a photographic quartile scale and the ECCA scale. Serum levels of collagen III were measured in control individuals and in patients, before treatment, 1 month after the first treatment session, and 4 months after the final session. RESULTS: Circulating levels of collagen III were significantly higher in patients with postacne scarring (24.1 ± 12.5) before treatment than in control individuals (2.6 ± 0.8). Circulating levels of collagen in patients were significantly lower 4 months posttreatment (14.3 ± 8.1) than at baseline. The mean percentage change in serum collagen III was positively correlated with both the mean percentage improvement by photographic evaluation (r = .530, P < .000) and the mean percentage change in the ECCA scale (r = .632, P < .000). CONCLUSION: Circulating collagen III is a biomarker for improvement of postacne scarring following different therapies.
Asunto(s)
Acné Vulgar/terapia , Cicatriz/terapia , Colágeno Tipo III/sangre , Piel/patología , Acné Vulgar/complicaciones , Adolescente , Adulto , Biomarcadores/sangre , Estudios de Casos y Controles , Cáusticos/administración & dosificación , Cicatriz/sangre , Cicatriz/diagnóstico , Cicatriz/etiología , Colágeno Tipo III/metabolismo , Punción Seca , Femenino , Humanos , Hipertrofia/diagnóstico , Hipertrofia/etiología , Hipertrofia/terapia , Masculino , Fotograbar , Índice de Severidad de la Enfermedad , Piel/diagnóstico por imagen , Piel/efectos de los fármacos , Piel/metabolismo , Resultado del Tratamiento , Ácido Tricloroacético/administración & dosificación , Adulto JovenRESUMEN
BACKGROUND AND AIMS: Hypertrophic scar is a form of abnormal wound healing process in which tissue repair regulating mechanism is disrupted. Transforming growth factor ß1 has a particular importance in the fibrotic scarring response. Treatment of hypertrophic scar included many chemical, physical, and surgical options. Fractional CO2 laser devices have gained acceptance as a way for managing hypertrophic scar. Aims of this study are: (a) to determine the clinical and histopathological effects of fractional CO2 laser on hypertrophic scar, (b) to evaluate the expression pattern of transforming growth factor-ß1 (TGF-ß1) as an important fibrogenic factor before and 6 months after fractional CO2 laser treatment. PATIENTS AND METHODS: Forty patients of hypertrophic scar were selected, each patient was treated by four sessions with 1 month apart with fractional CO2 laser. Vancouver Scar Scale (VSS) was used to assess the patients before and after laser treatment. Skin biopsy was taken from eight cases before and 3 months after four fractional CO2 laser sessions and four normal skin control biopsies. All were assessed by hematoxylin-eosin (H&E), Masson's trichrome, Van Gieson and immunohistochemical (IHC) staining with TGF-ß1. The epidermal thickness was assessed before and after treatment by image analyzing system software. RESULTS: There was statistically significant difference in VSS before and after fractional CO2 laser (P > 0.001). The epidermal thickness showed significant increase after laser treatment (P > 0.001), and there was also thinning in stratum corneum and replacement of the irregular collagen bands with organized new collagen fibrils as demonstrated by H&E and the other special stains. The study also showed significant decrease in TGF-ß1 expression after laser therapy (P = 0.008). CONCLUSION: Fractional CO2 laser could be considered as a good way for hypertrophic scar management. It normalizes dermal collagen as imaged by histopathological picture and the change in TGF-ß1 expression.