Stress-induced sebaceous hyperactivity is a key driver of acne and seborrheic dermatitis; however, research investigating the pathway-specific mechanisms through which stress exerts its effects and the suppression of sebum production via targeting stress signaling remains relatively limited. In this study, we investigated whether Camellia nitidissima flower extract (CNF) could counteract stress-induced sebaceous dysfunction and its underlying mechanisms. Using a cortisone-stimulated SZ95 human sebocyte model, we evaluated lipid accumulation, cortisol production, signaling pathway activation, and apoptotic markers. CNF treatment dose-dependently suppressed cortisone-induced lipid production, reducing triglyceride, cholesterol, and free fatty acid levels by up to 35.44%, 38.02%, and 46.39%. Mechanistically, CNF inhibited 11β-HSD1 expression (17.17% reduction) and cortisol secretion (32.84% decrease), thereby blocking local cortisol reactivation. This upstream interception subsequently attenuated PI3K/Akt/mTOR hyperphosphorylation, downregulated lipogenic transcription factors (SREBP-1, PPARγ, LXRα, C/EBP-α) and their target enzymes (FAS, ACC, DGAT). Beyond lipid synthesis inhibition, CNF reversed cortisone-induced apoptosis resistance by reducing the Bcl-2/Bax ratio and suppressing PCNA-mediated hyperproliferation, thereby decreasing sebocyte number. These findings demonstrate that CNF exerts dual oil-control effects: reducing lipid production per cell and reducing lipid-producing cell abundance. Collectively, CNF represents a promising multi-target botanical agent for managing stress-related sebaceous disorders and cosmetic sebum regulation.

Introduction: Seborrheic dermatitis (SD) is a lipid-dependent inflammatory dermatosis in which sebaceous activity, Malassezia, barrier dysfunction and host inflammation interact. Whether scalp SD severity is associated with systemic lipid and liver-associated biochemical parameters remains unclear. Methods: In this exploratory cross-sectional observational study, we included 34 adults with clinically diagnosed scalp SD. Severity was assessed using a published 16-point scalp SD score and a study-specific 0-36 physician-assessed score. Fasting lipids, glucose, alanine aminotransferase (ALT), aspartate aminotransferase and gamma-glutamyl transferase (GGT) were recorded. The triglyceride/high-density lipoprotein cholesterol ratio and non-HDL cholesterol were calculated. Patients were stratified as having non-severe or severe disease according to the 16-point score. Results: Complete 16-point data were available in 33 patients: 15 with non-severe and 18 with severe scalp SD. Severe disease was associated with higher triglycerides (116.0 vs. 78.0 mg/dL; p = 0.004), triglyceride/high-density lipoprotein cholesterol ratio (2.57 vs. 1.23; p = 0.006), ALT (46.0 vs. 20.0 U/L; p = 0.028) and GGT (33.0 vs. 11.0 U/L; p = 0.003). The strongest correlations with the 16-point score were observed for GGT (rho = 0.745), triglycerides (rho = 0.634), ALT (rho = 0.572) and triglyceride/high-density lipoprotein cholesterol ratio (rho = 0.569; all p < 0.001). These prespecified associations remained significant after false-discovery-rate adjustment and after adjustment for age and BMI. The correlation pattern was strengthened using the 0-36 score and persisted after excluding one liver enzyme outlier. Conclusions: More severe scalp SD was associated with triglyceride-related lipid parameters and liver-associated enzymes, suggesting a broader lipid-liver metabolic phenotype. These findings require confirmation in larger controlled studies.

Kerion is an abscess caused by a fungal infection, commonly occurring on the scalp among children and rarely in adults. This report illustrates the case of a 12-year-old boy who presented with multiple plaques with crusty lesions on the scalp for 2 months, associated with purulent discharge and boggy swelling, initially misdiagnosed as seborrheic dermatitis. Following unsuccessful treatment, his condition was correctly diagnosed as kerion based on clinical appearance, history of contact with domestic animals and Wood's lamp examination findings. The diagnosis was delayed for 2 months, leading to a prolonged disease course. Complete resolution of symptoms and lesions was achieved with systemic antifungal treatment, although permanent scarring alopecia remained. The delay in diagnosis and treatment led to prolonged illness and alopecia.

Yeasts of the Malassezia genus are implicated in numerous skin conditions, including seborrheic dermatitis, pityriasis versicolor, and folliculitis. While ciclopirox olamine (CPO) and piroctone olamine (OCT) are effective anti-Malassezia agents, the activity of magnetized water against pathogenic yeasts remains unclear. The aim of this study was to examine the in vitro efficacy of magnetized saline water (MSW), alone or combined with CPO plus OCT, against three Malassezia species (M. furfur, M. globosa, and M. restricta) using broth microdilution to determine minimal inhibitory concentrations (MICs). A proof-of-concept study evaluating a shampoo containing MSW 30% + CPO 0.5% + OCT 1.0% in 20 patients with scalp seborrheic dermatitis (SSD) was subsequently conducted. Participants applied the shampoo four times per week for 12 weeks; efficacy was assessed by changes in a validated 16-point SSD severity score. The triple combination demonstrated additive-to-synergistic activity, with MIC values of 3.91 mg/L across all three species, representing a 2.0- to 4.0-fold MIC reduction compared to CPO + OCT alone, and synergy (FIC=0.31) for M. furfur. The total SSD score decreased by 33.9% after 12 weeks (p<0.001), with improvements in pruritus (49.0%), erythema (54.3%), and scaling (24.2%); all p values remained significant after Bonferroni correction (α=0.0125). These findings support MSW as a vehicle to potentiate the anti-yeast activity of CPO and OCT while reducing the chemical load, potentially offering a novel strategy for Malassezia-associated skin disorders. The open-label, single-arm design limits causal attribution, and larger controlled trials are needed.

Objective We aimed to evaluate the safety and efficacy of a cream (SDπ) containing S. fruticosa leaf extract rich in carnosic acid and carnosol in the treatment of facial seborrheic dermatitis (SD). Methods In this 12-year retrospective study, 10 patients (eight males, two females; age range, 40-78 years) with mild to very severe facial seborrheic dermatitis (mean baseline Seborrheic Dermatitis Area and Severity Index (SEDASI) score: 19; range, 10-60) applied SDπ cream once nightly as monotherapy. Follow-up ranged from 6 months to 5 years. Results All patients achieved complete disease clearance (SEDASI=0) within a mean of 7.7 days (range 3-15 days) with marked reduction in erythema, scaling, and rapid relief of pruritus. Remission persisted from 20 days to 10 months. Subsequent episodes responded to re-treatment in a shorter period (mean 4.8 days), while no relapses were observed during long-term maintenance therapy with nightly or alternate-night application. No local or systemic safety concerns were documented throughout treatment and the longitudinal follow-up period. Conclusions In this retrospective observational study, SDπ cream was associated with favorable clinical outcomes and good tolerability, suggesting that it may represent a promising natural topical monotherapy for facial seborrheic dermatitis. Although these findings are encouraging, prospective randomized controlled studies are required to confirm efficacy and long-term safety. To our knowledge, this work represents the first full-length retrospective report in the literature documenting the therapeutic role of S. fruticosa leaf extract rich in carnosic acid and carnosol in seborrheic dermatitis.

Background: Parkinson's disease (PD) is a progressive neurodegenerative disorder with a well- documented prodromal phase during which non-motor symptoms appear years before motor onset. Seborrheic dermatitis (SD) is a chronic inflammatory skin disease that is significantly more prevalent in PD patients than in the general population. The biological mechanisms underlying this association have not been integrated into a single framework. Objectives: This narrative review aims to synthesise the available evidence on the molecular, genetic, and pathophysiological mechanisms linking SD and PD. Methods: A literature search was conducted across PubMed/MEDLINE, Scopus and ScienceDirect, supplemented by manual searches in OMIM and GeneCards. Results: Four major biological links between SD and PD have been proposed. First, alpha-synuclein deposits are detectable in cutaneous nerve fibres and autonomic fibres innervating sebaceous glands in PD patients and their pattern has been associated with disease subtype and progression. Second, dysfunction in ceramide and sphingolipid metabolism, associated with variants in GBA1, LRRK2, and ZNF750, has been linked to impaired lysosomal function and skin barrier integrity in both brain and skin tissue. Third, Malassezia, a commonly associated organism and possible trigger in susceptible hosts, produces metabolites that activate neuroinflammatory pathways relevant to PD and PD patients show altered Malassezia species composition on their skin. Fourth, NLRP3 inflammasome activation, which can be triggered by ceramide accumulation and fungal metabolites, has been proposed as a shared inflammatory mechanism that may operate in both keratinocytes and dopaminergic neurons. Conclusions: SD and PD appear to share overlapping genetic, lipidomic, microbial, and neuroinflammatory features. These associations are consistent with, but do not yet prove, a common pathological basis rather than a coincidental one. SD may therefore represent a potential prodromal feature or risk marker of PD. Future research should examine whether targeted intervention in high-risk SD patients can delay or modify PD onset.

Pathological aggregation of α-synuclein (αSyn) is a hallmark of Parkinson's disease (PD), but increasing evidence indicates that αSyn deposits extend beyond the central nervous system to peripheral tissues, including the skin. In PD patients, cutaneous αSyn accumulation has been associated with seborrheic dermatitis (SD), a chronic inflammatory condition linked to sebocyte dysfunction and altered sebum production. Marked differences in sebum composition between PD patients and healthy controls have been described. We aimed to investigate whether pathological αSyn could contribute to dysregulated sebum production and composition by assessing key markers of sebocyte differentiation and lipogenesis in human sebaceous gland cells and skin biopsies from PD patients (n = 5) and matched controls (n = 5) without clinically recorded SD. O-αSyn exposure of immortalized sebaceous gland cells (SZ95) altered the transcriptional programs related to sebocyte differentiation, inflammation, metabolism, and lipogenesis. Consistently, protein markers of mid-to-late sebocyte differentiation were increased. Upregulation of PLIN2, together with elevated PPARγ, SREBP1, SCD1, and FADS2, indicated progression toward a mature and lipid-producing phenotype characterized by enhanced accumulation of neutral lipids within lipid droplets. Lipidomic profiling revealed remodeling of multiple lipid classes, with increases in triglycerides, ceramides, and selected phospholipids. Increased expression of PLIN2 and PPARγ was also observed in sebaceous glands from PD skin biopsies compared to controls. Collectively, our findings indicate that O-αSyn exposure is associated with molecular changes consistent with altered sebocyte differentiation and lipid remodeling. These results support a potential association between αSyn and lipid dysregulation in sebocytes and suggest that these cells may represent unrecognized peripheral targets of αSyn.