Experimental Dermatology最新文献

Folliculitis decalvans (FD) and lichen planopilaris (LPP) are classified as neutrophilic and lymphocytic cicatricial alopecias respectively. FD and LPP have distinctive clinical, trichoscopic and histopathological features. Cases with concomitant or sequential features of both forms of primary cicatricial alopecia (PCA) have been described since 2020, and the term folliculitis decalvans and lichen planopilaris phenotypic spectrum (FDLPPPS) has been proposed. This study aimed to describe the clinicopathological features and response to treatment of patients who developed FDLPPPS in childhood. A retrospective review of patients with FDLPPPS with an age of onset of ≤ 18 years seen in three dermatology clinics in Australia and one in Lebanon from August 2020 to February 2024 was conducted. Fourteen patients (10 females and four males) with a mean (SD) age of onset of 12.4 (4.4) years were identified. Five patients had genetic or congenital abnormalities, and two patients were sisters. Scalp symptoms included itch (n = 8), pain or tenderness (n = 5) and flaking (n = 1), with clinical signs of crusting (n = 12), erythema (n = 10) and pustules (n = 3). Seven patients presented with a solitary plaque and seven with multiple plaques, most commonly affecting the vertex scalp (n = 13). Histopathological examination showed a perifollicular lymphocytic infiltrate and concentric lamellar fibrosis in 13 and 14 cases respectively. Keratosis pilaris (KP) or one of its variants was observed in eight cases. Treatment led to disease stabilisation in seven cases, but hair loss progressed in six cases. FDLPPPS is an aggressive form of primary cicatricial alopecia that can rarely begin in childhood. Given the clinical features and association with KP or its variants in a significant proportion of our patients, we hypothesise that FDLPPPS may be a sequela of a disorder of keratinisation.

The Mueller matrix has the capability of providing the complete polarisation information about the response of a medium to the incident polarised light. In this work, we report that the anisotropic structures of non-stained melanoma slices can be identified directly through the Mueller elements. It is observed that the elements M₁₂, M₂₂ and M₂₄ show a high degree of similarity with the three polarisation parameters (the x-y linear diattenuation, the x-y linear depolarization and the ±45° linear birefringence), with PSNR values of 33.4 dB, 35.7 dB and 40.0 dB, respectively. From images of M₁₂, M₂₂ and M₂₄, the cell nuclei and intercellular stroma in the melanoma dermis can be identified with higher contrast. The values of these elements are specific: for the cell nuclei, M₂₂ ranges from −0.75 to −0.27 and M₁₂ ranges from −0.12 to −0.04; for the extracellular matrix, M₂₂, M₁₂ and M₂₄ fall within −0.16 and −0.07, 0.06 and 0.16 and 0.09 and 0.57, respectively. Finally, a theoretical analysis is presented to explain the observations. The results obtained in this is helpful for clinic applications of Mueller matrix images where a method of interpreting measured Mueller matrices rapidly and accurately is essential.

Acne and hidradenitis suppurativa (HS) are inflammatory disorders of the pilosebaceous unit that exhibit distinct clinical manifestations, indicating that they likely differ in their underlying pathophysiology. Microbial dysbiosis is implicated in both diseases, yet direct comparisons using unified methods and analyses incorporating the oral microbiome are lacking. In this study, we collected lesional and nonlesional skin, buccal mucosa and faecal samples from 28 HS patients, 29 acne patients and 40 healthy controls, and profiled microbial communities using 16S rRNA V3–V4 sequencing with qPCR validation. HS lesions showed a pronounced enrichment of anaerobic Gram-negative taxa, including Prevotella, Porphyromonas and Fusobacterium, whereas acne lesions were dominated by Cutibacterium and Pseudomonas. Oral microbiome diversity was increased in both diseases, with HS showing distinct enrichment of Prevotella and Veillonella. HS patients also exhibited reduced gut microbial diversity. Correlation analyses revealed coordinated microbial alterations across the oral–gut–skin axis, and qPCR confirmed elevated concentrations of key anaerobes in HS. By directly comparing acne and HS across multiple anatomical sites, our study helps differentiate general inflammatory microbiome changes from those more specific to HS. The findings also suggest a potential oral–gut–skin microbial axis that may contribute to the chronic and destructive phenotype of HS, providing insights that could inform future microbiome-targeted therapeutic approaches.

Real-world data on the long-term effectiveness of dupilumab in moderate-to-severe atopic dermatitis (AD) remains limited, particularly concerning regional disparities in improvement and the outcomes of extended dosing interval regimens. To evaluate the anatomical region-specific responses to dupilumab and the long-term effectiveness under extended dosing-interval regimens. This retrospective cohort study included moderate-to severe AD patients treated with dupilumab. Eczema Area and Severity Index (EASI)-75/90, Numerical Rating Scale (NRS) ≤ 1, and regional EASI reductions were assessed at 6/12/18 months. Patients reaching EASI-75 switched to extended dosing (every 3/4 weeks), with long-term effectiveness and influencing factors evaluated. 108 patients were included. Percentage reductions in EASI scores from baseline at 4, 6 and 12 months were as follows: head/neck: 58.52%, 82.36% and 89.36%; trunk: 77.95%, 85.82% and 94.68%; upper limbs: 77.11%, 86.49% and 95.45%; and lower limbs: 66.34%, 84.03% and 90.34%, respectively. EASI-75/90 and NRS ≤ 1 responses increased over 18 months, reaching 100%/96.97% and 96.97% respectively. No significant differences in effectiveness were observed between the every-three-weeks and every-four-weeks dosing groups. Dupilumab demonstrates sustained, region-specific effectiveness in moderate-to-severe AD, with delayed but progressive improvement in head and neck region(s). Patients achieving EASI-75 with stable disease can safely transition to every-three-weeks or every-four-weeks dosing regimens.

Abnormal activation of keloid fibroblasts (KFs) within a hypoxic microenvironment is a hallmark of keloid pathogenesis. However, the precise molecular mechanisms by which hypoxia drives fibroblast dysfunction remain insufficiently understood. This study aimed to investigate the role of Stanniocalcin 2 (STC2), a hypoxia-responsive glycoprotein, in modulating keloid fibroblast behaviour under hypoxic conditions and to elucidate its upstream and downstream regulatory networks. We found the expression of STC2 was significantly upregulated in keloid tissues and primary KFs, with expression levels positively correlating with clinical severity, as assessed by the Vancouver Scar Scale. Mechanistically, hypoxia induced STC2 expression via hypoxia-inducible factor-1α. Functional assays revealed that STC2 silencing under hypoxia markedly reduced KF proliferation, migration and extracellular matrix remodelling, as evidenced by downregulation of fibrosis-associated markers including collagen I, α-SMA, MMP2 and MMP9. These inhibitory effects were accompanied by attenuation of ERK and AKT signalling pathway activation. Thus, targeting STC2 disrupts pro-fibrotic signalling and may represent a promising therapeutic strategy for the clinical management of keloid scars by modulating the aberrant hypoxic microenvironment.