Dermatoscopic Features of Naevi During Pregnancy-A Mini Review

Changes in melanocytic naevi and development of new naevi have been reported in pregnant women. The association between pregnancy and melanoma is a controversial topic. We conducted this review to identify the dermatoscopic changes that occur in naevi during pregnancy that could facilitate in distinguishing benign from suspicious lesions. Medline, Scopus, and Embase datasets were reviewed for clinical studies on dermatoscopic characteristics of melanoma and naevus in pregnancy. Six cohort studies with a total of 258 patients with 1,167 skin lesions that were examined fulfilled the conditions to be included in the review. None of the patients developed melanoma. Development of new naevi, when reported, was observed in less than half of the participants. The most frequent observed dermatoscopic change among the studies was the increase in the number of dots. Development of new vessels, hypo- and hyperpigmentations and changes in the pigment network were common described changes. The included studies were heterogeneous not allowing head-to-head comparisons between them. Robust and larger studies of dermatoscopic evaluation of naevi in pregnant women are needed to determine high-risk dermatoscopic characteristics

The role of ultraviolet radiation and tyrosine stimulated melanogenesis in the induction of oxidative stress alterations in fair skin melanocytes

Melanocytes are producing melanin after UV irradiation as a defense mechanism. However, UV-induced damage is involved in melanoma initiation, depending on skin phototype. Melanocytes seem to be extremely susceptible to free radicals. Their main enzymatic antioxidants are superoxide dismutase and catalase. Aim: To study how melanin synthesis modulates the activity of the oxidative stress defense enzymes and cell proliferation after UV induced cell damage. Methods: Normal human melanocyte cultures from fair skin individuals were exposed to high levels of L-tyrosine and irradiated, with 20, 30, 40 mJ/cm2 UVA, and respective UVB. Proliferation was measured using a MTS assay; viability was assessed by trypan blue exclusion dye method. Spectrophotometrical methods were used to determine total melanin content, the enzymatic activity of tyrosinase, superoxide dismutase and catalase. Results: Tyrosine had a negative effect on proliferation, enhanced with time elapsed. Overall, UV irradiation decreased proliferation. UVA increased proliferation relative to UVB in the cultures exposed for a longer time to high (2 mM) tyrosine concentration. There were no proliferation differences between UVA and UVB irradiation in lower tyrosine concentration exposed melanocytes. Both, UV irradiation and tyrosine increased melanogenesis. Exposure of the melanocytes to increased levels of tyrosine in medium (0.5 mM and 1 mM) and UV irradiation enhanced the activity of superoxide dismutase and catalase. The enzymes showed a high activity rate in melanocytes while exposed for a short time to 2 mM tyrosine, but their activity was dramatically decreased with longer tyrosine exposure and UV irradiation. Conclusion: Our data indicate that in low phototype melanocytes, melanogenesis, either following UV irradiation, or tyrosine exposure, especially in high concentrations, was detrimental for the cells by reducing the activity of catalase and superoxidedismutase, the natural antioxidants. UVA was more efficient in stimulating the activity of superoxide dismutase and catalase but also in depleting the reserves of the enzymatic defense against oxidative stress, especially catalase, than UVB. This physiologic response to UV light can be considered as an adjunctive risk factor for people with low phototype for developing a melanoma, when exposed to UV irradiation

Can vitamins improve periodontal wound healing/regeneration?

Periodontitis is a complex inflammatory disorder of the tooth supporting structures, associated with microbial dysbiosis, and linked to a number if systemic conditions. Untreated it can result in an irreversible damage to the periodontal structures and eventually teeth loss. Regeneration of the lost periodontium requires an orchestration of a number of biological events on cellular and molecular level. In this context, a set of vitamins have been advocated, relying their beneficial physiological effects, to endorse the biological regenerative events of the periodontium on cellular and molecular levels. The aim of the present article is to elaborate on the question whether or not vitamins improve wound healing/regeneration, summarizing the current evidence from in vitro, animal and clinical studies, thereby shedding light on the knowledge gap in this field and highlighting future research needs. Although the present review demonstrates the current heterogeneity in the available evidence and knowledge gaps, findings suggest that vitamins, especially A, B, E, and CoQ10 , as well as vitamin combinations, could exert positive attributes on the periodontal outcomes in adjunct to surgical or nonsurgical periodontal therapy

A Recurrent Case of Targetoid Hemosiderotic Hemangioma: A Case Report and a Comprehensive Review of the Literature

Targetoid hemosiderotic hemangioma is an acquired vascular malformation of unknown origin. We report the case of a 31-year-old man with a recurrent and spontaneous regressive targetoid hemosiderotic hemangioma. Diagnosis relied on clinical and histological findings. Physical examination revealed presence of an approximately 2 cm targetoid lesion located on the left arm, and associated with pain after pressure. No trigger agent (trauma, insect sting) was reported. Dermoscopy showed a group of red lacunae centrally, encircled by an intermediate yellow circular homogenous area and a red violaceous homogenous ring in the periphery. The histopathological examination and the immunohistochemical staining of the lesion were characteristic for a hemangioma-like proliferation of vessels in the upper part of the dermis, similar to a targetoid hemosiderotic angioma. We also review epidemiological, clinical, and histopathological findings in 6 similar cases presented in the literature. Spontaneous regression and recurrence have rarely been described in this type of skin lesion

An Animal Model of Cutaneous Cyst Development Enables the Identification of Three Quantitative Trait Loci, Including the Homologue of a Human Locus (TRICY1)

Brief Summary Using inbred BN and LE/Stm rats susceptible and resistant, respectively, to chemically induced cutaneous cyst development we were able to further unveil the genetic architecture of inherited multiple cyst formation. N-methyl-N-nitrosourea-treated (BN x LE) F2 intercross rats proved to develop differential numbers of cutaneous cysts, demonstrating epidermal, trichilemmal and verrucous keratinization types. Male rats developed significantly more cysts per animal than females. QTL interval mapping yielded three loci on rat chromosomes 1, 8 and 11 (Ccd1, Ccd2, Ccd3) linked to cutaneous cyst formation. Ccd2 proved to be homologous to the human TRICY1 region which could further be narrowed down by genome comparison in both species. It contains 11 genes with evidence of expression in human keratinocytes.Non peer reviewe

Junctional Epidermolysis Bullosa: Allelic Heterogeneity and Mutation Stratification for Precision Medicine

Junctional epidermolysis bullosa (JEB) is a hereditary blistering disease caused by reduced dermal-epidermal adhesion due to deficiencies of one of the proteins, laminin-332, type XVII collagen, integrin α6β4 or integrin α3. Significant progress has been achieved in the development of therapies for EB, such as bone-marrow transplantation, local or systemic injections with fibroblasts or mesenchymal stromal cells, readthrough of premature termination codons, or exon skipping. These were tailored in particular for dystrophic EB, which is caused by type VII collagen deficiency and have not yet reached broad clinical practice. Recently, pioneering combined gene and stem cell therapy was successful in treating one boy with junctional EB. Beside these exclusive approaches, no specific therapy to amend the major clinical features, skin and mucosal blistering and non-healing wounds is available to date. Here we extend the mutational spectrum of junctional EB, provide a stratification of COL17A1 mutations and discuss potential molecular therapeutic approaches

Research Techniques Made Simple: Analysis of Autophagy in the Skin.

Autophagy is required for normal skin homeostasis and its disordered regulation is implicated in a range of cutaneous diseases. Several well-characterized biomarkers of autophagy are used experimentally to quantify autophagic activity or clinically to correlate autophagy with disease progression. This article discusses the advantages and limitations of different approaches for measuring autophagy as well as the techniques for modulating autophagy. These include analysis of endogenous LC3, a central autophagy regulatory protein, and measurement of LC3 flux using a dual-fluorescent reporter, which provides a quantitative readout of autophagy in cell culture systems in vitro and animal models in vivo. Degradation of SQSTM1/p62 during autophagy is proposed as an alternative biomarker allowing the analysis of autophagy both experimentally and clinically. However, the complex regulation of individual autophagy proteins and their involvement in multiple pathways means that several proteins must be analyzed together, preferably over a time course to accurately interpret changes in autophagic activity. Genetic modification of autophagy proteins can be used to better understand basic autophagic mechanisms contributing to health and disease, whereas small molecule inhibitors of autophagy regulatory proteins, lysosomal inhibitors, or activators of cytotoxic autophagy have been explored as potential treatments for skin disorders where autophagy is defective. [Abstract copyright: Copyright © 2020 The Authors. Published by Elsevier Inc. All rights reserved.