Striae distensae: assessment of a combined treatment on fibroblasts and an in vivo study

Introduction Stretch marks or Striae Distensae (SD) appear clinically as parallel streaks, perpendicular to the lines of tension in the skin. SD evolves into two clinical phases, an initial inflammatory phase or striae rubrae (SR) and a chronic phase or striae albae (SA). Fibroblasts appear to play a key role in the pathogenesis of stretch marks. The results of studies explaining the etiology of SD are discordant, which is why we have tried to analyze the phenotype and function of fibroblasts in initial and old lesions and compare them with those in healthy skin (NS) of the same patient. Currently, there is no cure for SA. The non-ablative fractional laser can achieve satisfactory results, but only on the initial lesions (SRs). The goals of this study were: to describe and analyze fibroblasts from stretch marks and the differences between SRF and SAF compared to fibroblasts from healthy tissue from the same donor (NSF); to test innovative treatments (sodium ascorbate and PrP) on cell cultures of fibroblasts from SA (SAF) in vitro; performing an in vivo study using PRP + nanofat combined treatment. Material and methods In order to characterize the SMF, the expression of alpha smooth muscle actin (alpha SMA) was investigated. Type I collagen expression was measured in SAF, before and after adding different PrP concentrations and sodium ascorbate in the culture medium. The products tested were: Standard PrP 1% and 5%, PrP concentrated 1% and 5%, sodium ascorbate (100µg / M), PrP standard 1% and 5% + sodium ascorbate (100µg / M), PrP concentrated 1% and 5% + sodium ascorbate (100µg / M), no treatment (control). For the in vivo study, the products tested were: PRP, PRP 20% + nanofat 80%, nanofat. Results were processed through statistical analysis models using the Student's t-test. Results A significant increase in alpha SMA (P <0.001) was observed in SRF. SAF treated with PrP and sodium ascorbate showed a resumption of their metabolic activity by an increase in collagen type I production and cell proliferation. After 24 hours of incubation with PrP 1% and PrP 5% + Sodium ascorbate, cell viability was increased by 140% and 151% and by 156 and 178% after 48 hours respectively compared to the control. Regarding the in vivo study: the PrP and the nanofat contributed to increasing the biosynthesis of collagen in the treated areas significantly compared to the control. A greater effect was observed for AS treated with the combined PrP-Nanofat treatment (p <0 .0001). Conclusion Our study shows that a biologically mediated improvement of SMF metabolic activity is possible. Our promising results require further trials to be able to confirm the reproducibility of these combined treatments, particularly in vivo.