Journal of

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Background and Aim: Demodex is a common mite and ectoparasite in humans and animals. The existence of Demodex folliculorum and Demodex brevis in human skin can have a role in some inflammatory skin diseases such as acne, rosacea, and dermatitis. This study aimed to identify the prevalence of Demodex ectoparasite in women and its possible association with skin lesions.

Methods: Fifty women with skin lesions (case group) and 50 women without skin lesions (control group) were selected and evaluated by clinical and
laboratory tests. The study was approved by the Ethics Committee and the volunteers provided written informed consent. The skin scrapings were investigated by placing in a 10% potassium hydroxide (KOH) and lactophenol solutions and were analyzed under microscope to detect the Demodex.

Results: Twenty-two out of 50 patients (with acne, rosacea, dermatitis, and eczema) had Demodex folliculorum infestation (44%). The highest levels of infestation were observed in women aged 20-30 years (22%) and the infestation of Demodex was only confirmed in 10 cases (20%) out of the 50 subjects in the control group.

Conclusion: The rate of Demodex in patients with skin lesions was much higher than healthy subjects. There was a significant association between Demodex and skin lesions (sig.=0.023, P<0.05). The authors suggest that Demodox treatment should be considered in the therapeutic strategy of some inflammatory skin diseases.

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Background and aim: Human dermal fibroblasts (HDFs) are key regulators of skin homeostasis through extracellular matrix remodeling. Polydeoxyribonucleotides (PDRN) and magnesium ascorbyl phosphate (MAP) are recognized as skin regenerative agents, but their molecular effects on HDFs are not fully elucidated. This study aimed to investigate the effects of PDRN and MAP on cellular proliferation and type I collagen gene expression in HDFs.
 

Methods: The HDF cell line was treated with PDRN and MAP, and cell viability was evaluated using the MTT assay at 24, 48, and 72 hours. Based on viability outcomes, optimal concentrations of PDRN (100 ng/ml) and MAP (250 µg/ml) were selected. Seventy-two hours post-treatment, the expression levels of KI-67 and COL1A1 genes were analyzed via qPCR (P<0.05).
 

Results: Cell viability analyses demonstrated significant time- and dose-dependent responses for both PDRN and MAP. At the molecular level, independent treatments with PDRN and MAP upregulated KI-67 gene expression, confirming an enhanced cellular proliferative capacity. Conversely, in a divergent manner, COL1A1 gene expression was downregulated under these exact treatment conditions.
 

Conclusion: PDRN and MAP induce a divergent response in HDFs; while promoting mitogenic activity, they simultaneously suppress fibrogenesis and COL1A1 expression. This cellular reprogramming underscores the therapeutic potential of these compounds in anti-fibrotic strategies and scarless wound healing. However, in vivo studies are required to conclusively validate these findings.