The underlying mechanism of seborrheic dermatitis (SD) is poorly understood but major scientific progress has been made in recent years related to microbiology, immunology and genetics. In light of this, the major goal of this article was to summarize the most recent articles on SD, specifically related to underlying pathophysiology. SD results from Malassezia hydrolysation of free fatty acids with activation of the immune system by the way of pattern recognition receptors, inflammasome, IL-1β and NF-kB. M. restricta and M. globosa are likely the most virulent subspecies, producing large quantities of irritating oleic acids, leading to IL-8 and IL-17 activation. IL-17 and IL-4 might play a big role in pathogenesis, but this needs to be further studied using novel biologics. No clear genetic predisposition has been established; however, recent studies implicated certain increased-risk human leucocyte antigen (HLA) alleles, such as A*32, DQB1*05 and DRB1*01 as well as possible associations with psoriasis and atopic dermatitis (AD) through the LCE3 gene cluster while SD, and SD-like syndromes, shares genetic mutations that appear to impair the ability of the immune system to restrict Malassezia growth, partially due to complement system dysfunction. A paucity of studies exists looking at the relationship between SD and systemic disease. In HIV, SD is thought to be secondary to a combination of immune dysregulation and disruption in skin microbiota with unhindered Malassezia proliferation. In Parkinson's disease, SD is most likely secondary to parasympathetic hyperactivity with increased sebum production as well as facial immobility which leads to sebum accumulation. K E Y W O R D Sinflammasome, Malassezia, sebaceous glands, seborrheic dermatitis, systemic disease While the order of events is unclear regarding the pathophysiology of SD, it is agreed upon by most sources that the three main prerequisites are as follows: Malassezia colonization, lipid secretion by sebaceous glands and an underlying immune system susceptibility. [1,5,7,38] The pathogenesis can be categorized into five different phases.

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Psoriasis vulgaris is a common, inflammatory skin disease affecting approximately 3% of the population in the United States. The etiology of psoriasis and its associated comorbidities are complex and the result of complicated interactions between the skin, immune system, disease-associated susceptibility loci, and multiple environmental triggers. The modeling of human disease in vivo through the use of murine models represents a powerful, indispensable tool for investigating the immune and genetic mechanisms contributing to a clinical disease phenotype. Nevertheless, modeling a complex, multigenic disease like psoriasis in mice has proven to be extremely challenging and is associated with significant limitations. Over the last four decades, more than 40 unique mouse models for psoriasis have been described. These models can be categorized into three major types: acute (inducible), genetically engineered (transgenic), and xenograft (humanized). The purpose of this Research Techniques Made Simple article is to provide an overview of the common types of psoriasis-like mouse models currently in use and their inherent advantages and limitations. We also highlight the need for improved psoriasis mouse model systems and several key factors to be considered as this field of laboratory science advances.

Summary Background An epidemic of basal cell carcinoma (BCC) has led to a significant healthcare burden in white populations. Objectives To provide an update on incidence rates and tumour burden in an unselected, geographically isolated population that is exposed to a low level of ultraviolet radiation. Methods This was a whole‐population study using a cancer registry containing records of all cases of BCC in 1981–2017. We assessed BCC incidence according to age, residence and multiplicity and assessed trends using join‐point analysis. Age‐standardized and age‐specific incidence rates were calculated along with cumulative and lifetime risks. Results During the study period, the age‐standardized incidence rates increased from 25·7 to 59·9 for men, and from 22·2 to 83·1 for women (per 100 000). Compared with the single‐tumour burden, the total tumour burden in the population was 1·72 times higher when accounting for multiplicity. At the beginning of the study period, the world‐standardized rates in men and women were similar, but by the end of the study period the rates were 39% higher in women (83·1 per 100 000, 95% confidence interval 77·9–88·3) than in men (59·9 per 100 000, 95% confidence interval 55·6–64·2). This increase was most prominent in women on sites that are normally not exposed to ultraviolet radiation in Iceland: the trunk and legs. Conclusions This is the only reported population in which the incidence of BCC is significantly higher in women than in men. The period of notable increase in BCC lesions correlates with the period of an increase in tanning beds and travel popularity. The high multiplicity rates suggest that the total tumour burden worldwide might be higher than previously thought. What is already known about this topic? Basal cell carcinoma (BCC) is becoming an increasing healthcare burden worldwide, especially in white populations. Recent population studies have reported a rapid increase in incidence among younger individuals, especially women. What does this study add? Iceland is the only reported population in which the incidence of BCC is significantly higher in women than in men, and there does not seem to be a clear relationship between latitude and BCC incidence in Europe. Men might be comparatively protected in the northern low‐ultraviolet environment, with tanning beds and travel abroad likely playing important roles in the observed incidence increase, especially in women. The high multiplicity rates suggest that the total tumour burden worldwide might be higher than previously thought. Linked Comment: Pandeya. Br J Dermatol 2020; 183:799–800.

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Background The worldwide incidence of cutaneous squamous cell carcinoma (cSCC) is increasing. Objectives To evaluate the tumour burden of in situ and invasive cSCC in Iceland, where the population is exposed to limited ultraviolet radiation. Methods This whole-population study used the Icelandic Cancer Registry, which contains records of all in situ and invasive cSCC cases from 1981 to 2017. Incidence of cSCC was evaluated according to age, anatomical location, residence and multiplicity, and trends were assessed using joinpoint analysis. Age-standardized rates (WSR) and age-specific incidence rates per 100 000 person-years were calculated, along with cumulative and lifetime risks. Results Between 1981 and 2017, in situ cSCC WSR increased from 1Á2 to 19Á1 for men and from 2Á0 to 22Á3 for women. Invasive cSCC WSR rose from 4Á6 to 14 for men and from 0Á3 to 13Á2 for women. The average number of in situ cSCC lesions was 1Á71 per woman and 1Á39 per man. Women developed more in situ cSCCs than invasive cSCCs in almost all anatomical locations, whereas men developed more invasive cSCCs, mostly on the head and neck. The rates of in situ cSCC were higher in Reykjavik compared with rural areas. Furthermore, women more commonly developed multiple in situ lesions. For lip cSCCs, invasive lesions occurred more frequently than in situ lesions among both sexes. Joinpoint analysis showed that in situ cSCC in women exhibited the most rapid incidence increase. Conclusions cSCC has become an increasingly significant public health problem in Iceland. Tanning bed use and travelling abroad may contribute to skin cancer development. Public health efforts are needed to stem the behaviours leading to this rapid rise in cSCC.What is already known about this topic?• Cutaneous squamous cell carcinoma (cSCC) incidence is on the rise worldwide, posing a significant public health threat, especially in light-skinned populations.What does this study add?• Icelandic women were more likely to develop in situ cSCC, and men were more likely to develop invasive cSCC of the head and neck.

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