Human dermal fibroblast-derived extracellular matrix reduces postinflammatory hyperpigmentation after fractional carbon dioxide laser facial resurfacing in Asians.

BACKGROUND: Extracellular matrix (ECM) components promote the development of skin wounds by providing biological scaffolds and regenerative microenvironments. AIMS: To evaluate the beneficial effects of human dermal fibroblast-derived ECM after fractional carbon dioxide laser resurfacing in Asians. PATIENTS/METHODS: In this double-blind, randomized, vehicle-controlled, split-face study, 15 participants with features of facial skin aging were treated with a single session of fractional carbon dioxide laser, followed by the application of either ECM (ECM group) or placebo (control group). In vivo skin parameters were measured at baseline and after 4 and 12 weeks of treatment using the Antera 3D®, Cutometer® MPA580, Dermascan®, and Tewameter®. RESULTS: A total of 14 participants (mean age 45.1 ± 9.7 years) completed the study. The change in melanin level was significantly lower in the ECM group than in the control group at week 12 (p < 0.05). Transient increase in erythema level was observed at week 4 in the control group, and the change in the erythema level was greater in the control group than in the ECM group (p = 0.014). Though the ECM group showed improvements in the dermal density, texture, transepidermal water loss, marionette lines (volume, maximum depth, and average depth), and nasolabial folds (volume, maximum depth, and length), no significant differences were found between the two groups. Treatment-related adverse events were not reported. CONCLUSIONS: We suggest that human dermal fibroblast-derived ECM may be used as adjunctive therapy after fractional carbon dioxide resurfacing to prevent postinflammatory hyperpigmentation in Asians.

Oral administration of megestrol acetate can increase fat graft survival in a rat model.

Insufficient and inconsistent survival is a significant shortcoming of fat grafts. Reportedly, megestrol acetate (MA) could induce proliferation, migration, and adipogenic differentiation of adipose-derived stem cells in vitro. Thus, we tested whether MA could promote fat graft survival in a rat model. Twenty-eight Sprague-Dawley rats (8 weeks old, male) were divided into two groups: experimental (MA group, n = 14) and control (n = 14). The inguinal fat pad (1 g) was extracted en bloc and re-implanted under the scalp in both groups. MA (100 mg/kg/day) was administered orally for 14 postoperative days in the experimental group. After 6 weeks, the volume and weight of the grafted fat were measured. Histologic examination with hematoxylin and eosin (HE) and real-time polymerase chain reaction (PCR) for vascular endothelial growth factor (VEGF), fibroblast growth factor 2 (FGF2), and CCAAT/enhancer-binding protein alpha (C/EBP-α) were performed. Perilipin staining was performed to check the viability of grafted fat. Graft fat volume was greater in the MA group, compared with that in the control (P = 0.023). The MA group also had more viable cells, including more adipocytes, and less fibrosis or vacuoles than the control on HE and perilipin staining. MA upregulated the expression of FGF2 (P<0.001), VEGF (P = 0.008), and C/EBP-α (P = 0.002) at the second postoperative week. MA increased survival of grafted fat in an animal model. Increased vascularization and adipogenesis were related to these results. Further human clinical trials are necessary to evaluate adjunctive oral administration of MA after fat grafting to promote graft survival.