Review of Lasers and Energy-Based Devices for Skin Rejuvenation and Scar Treatment With Histologic Correlations.

BACKGROUND: Lasers and energy-based devices (EBD) are popular treatments for skin rejuvenation and resurfacing. Achieving desired outcomes and avoiding complications require understanding the effects of these devices at a histologic level. Currently, no comprehensive review summarizing the histologic effects of laser and energy-based treatments exists. OBJECTIVE: To describe how lasers and EBD alter skin histology and improve the overall understanding of these devices. MATERIALS AND METHODS: A PubMed search was conducted for studies with histologic analysis of fractional picosecond laser, fractional radiofrequency microneedling, nonablative lasers, and ablative lasers. RESULTS: Fractional picosecond lasers induce intraepidermal and/or dermal vacuoles from laser-induced optical breakdown. Fractional radiofrequency microneedling delivers thermal energy to the dermis while sparing the epidermis, making it safer for patients with darker skin phototypes. Fractional nonablative lasers induce conical zones of coagulation of the epidermis and upper dermis. Ablative lasers vaporize the stratum corneum down to the dermis. Traditional ablative lasers cause diffuse vaporization while fractional ablative lasers generate columns of tissue ablation. CONCLUSION: Lasers and EBD are effective for skin resurfacing and rejuvenation and have different mechanisms with disparate targets in the skin. Safe and effective use of devices requires understanding the histologic laser-tissue interaction.

Systemic comorbidities of rosacea: practice gaps among dermatologists.

Rosacea is a chronic inflammatory skin condition that is associated with multiple systemic comorbidities, with the strongest evidence linking rosacea to hypertension, dyslipidemia, inflammatory bowel disease, and anxiety and depression. To assess dermatologists' awareness of and screening practices for rosacea comorbidities, we developed a survey that was distributed to attendings and residents across four academic dermatology departments in Massachusetts. A total of 73 dermatologists with varying experience participated in the study. Findings demonstrated significant knowledge and practice gaps among academic dermatologists in managing systemic comorbidities in rosacea. In addition, dermatologists' awareness of rosacea comorbidities was negatively correlated with number of years out of residency training, highlighting the need to address this knowledge gap through increased continuing medical education. Importantly, we observed a low screening frequency despite a high awareness of the association between rosacea and ocular comorbidities, suggesting that additional financial, institutional, or practice barriers likely contribute to the low screening rate.

Pleomorphic dermal sarcoma in a man with HIV: report with next-generation sequencing analysis and review of the atypical fibroxanthoma/pleomorphic dermal sarcoma spectrum.

Atypical fibroxanthoma (AFX) is a rare cutaneous fibrohistiocytic tumor that typically arises on chronically sun-damaged skin, such as the head and neck, as a nondescript ulcerated papule, nodule, or tumor. The clinical prognosis is usually favorable and metastasis is rare. Pleomorphic dermal sarcoma (PDS), or undifferentiated pleomorphic sarcoma, is a recently introduced diagnostic moniker for AFX-like tumors with more aggressive clinical and histologic features such as necrosis and vascular invasion. The exact relationship between AFX and PDS has been debated. Diagnosis of these tumors is generally based on immunohistochemical staining to exclude other mimics. A wholly specific marker for this tumor does not exist, leading to diagnostic ambiguity in certain cases. Herein, we present a case of pleomorphic dermal sarcoma in a 53-year-old man with human immunodeficiency virus that displayed patchy S100 staining concerning for melanoma upon hospital pathology review. Next-generation sequencing analysis confirmed a mutation pattern consistent with published molecular signatures of AFX/PDS. In discussing this case, we review the current understanding of AFX/PDS and discuss diagnostic pitfalls, as well as emphasize on how next-generation sequencing techniques might improve accuracy in the diagnosis of tumors in the spectrum of AFX/PDS.

Basal Cell Carcinoma with Osteoma Cutis.

Osteoma cutis is the formation of bone within the skin. It can present as either primary osteoma cutis or secondary osteoma cutis. Secondary osteoma cutis is more common and is associated with inflammatory, infectious, and neoplastic disorders, including basal cell carcinoma. A 79-year-old Caucasian man without underlying kidney disease or calcium abnormalities presented with a basal cell carcinoma with osteoma cutis on the chin. Basal cell carcinoma with osteoma cutis has seldom been described; however, the occurrence of this phenomenon may be more common than suggested by the currently published literature. The preferred treatment is surgical excision-with or without using Mohs micrographic technique. When the histopathologic examination reveals bone formation in the skin, clinicians should consider the possible presence of an adjacent malignancy, such as a basal cell carcinoma.

Edema Bullae Mimicking Disseminated Herpes Zoster.

Edema bullae typically forms at the site of skin swelling during acute states of volume overload, most commonly during renal or cardiac failure. Herpes zoster is a reactivation of latent varicella zoster virus that typically presents as painful vesicles in a dermatomal distribution. In immunocompromised individuals, disseminated herpes zoster skin manifestations may occur with several lesions in multiple dermatomes or widespread individual lesions or both, even visceral organs can be involved. Additionally, many conditions are known to mimic the lesions and distribution of herpes zoster. A 53-year-old immunosuppressed male with a history of renal transplant presented with dermatomal and non-dermatomal, disseminated herpes zoster that was confirmed by polymerase chain reaction testing. After one week of intravenous antiviral therapy during which his virus infection-associated lesions were resolved, new blisters developed near the insertion site of a peripheral venous line located on a previously uninvolved yet swollen upper extremity. The varicella zoster virus disease was initially suspected, but lab studies and skin biopsy of a blister excluded progressive or persistent viral infection and established a diagnosis of acute edema bullae. The blisters resolved following removal of the peripheral catheter. Acute edema bullae should be added to the list of mimickers of disseminated varicella zoster virus infection.

Erythrodermic Psoriasis in a Man with Monoclonal B-cell Lymphocytosis.

Erythroderma is characterized by erythema involving greater than 90% of the body surface area and may be caused by several etiologies, including erythrodermic psoriasis. Psoriasis is an autoimmune skin and systemic condition characterized by erythematous and scaly plaques. Monoclonal B-cell lymphocytosis is an asymptomatic hematological disorder diagnosed by elevated, small, clonal B-cell counts in the peripheral blood. The characteristics of a 71-year-old man with new onset of erythrodermic psoriasis and concurrent monoclonal B-cell lymphocytosis are presented. The simultaneous development of these two conditions raises the possibility that they may share a related pathogenesis.

Hydrogen sulfide suppresses oxidized low-density lipoprotein (ox-LDL)-stimulated monocyte chemoattractant protein 1 generation from macrophages via the nuclear factor κB (NF-κB) pathway.

This study was designed to examine the role of hydrogen sulfide (H2S) in the generation of oxidized low-density lipoprotein (ox-LDL)-stimulated monocyte chemoattractant protein 1 (MCP-1) from macrophages and possible mechanisms. THP-1 cells and RAW macrophages were pretreated with sodium hydrosulfide (NaHS) and hexyl acrylate and then treated with ox-LDL. The results showed that ox-LDL treatment down-regulated the H2S/cystathionine-ß-synthase pathway, with increased MCP-1 protein and mRNA expression in both THP-1 cells and RAW macrophages. Hexyl acrylate promoted ox-LDL-induced inflammation, whereas the H2S donor NaHS inhibited it. NaHS markedly suppressed NF-κB p65 phosphorylation, nuclear translocation, DNA binding activity, and recruitment to the MCP-1 promoter in ox-LDL-treated macrophages. Furthermore, NaHS decreased the ratio of free thiol groups in p65, whereas the thiol reductant DTT reversed the inhibiting effect of H2S on the p65 DNA binding activity. Most importantly, site-specific mutation of cysteine 38 to serine in p65 abolished the effect of H2S on the sulfhydration of NF-κB and ox-LDL-induced NF-κB activation. These results suggested that endogenous H2S inhibited ox-LDL-induced macrophage inflammation by suppressing NF-κB p65 phosphorylation, nuclear translocation, DNA binding activity, and recruitment to the MCP-1 promoter. The sulfhydration of free thiol group on cysteine 38 in p65 served as a molecular mechanism by which H2S inhibited NF-κB pathway activation in ox-LDL-induced macrophage inflammation.

LIN28 binds messenger RNAs at GGAGA motifs and regulates splicing factor abundance.

LIN28 is a conserved RNA-binding protein implicated in pluripotency, reprogramming, and oncogenesis. It was previously shown to act primarily by blocking let-7 microRNA (miRNA) biogenesis, but here we elucidate distinct roles of LIN28 regulation via its direct messenger RNA (mRNA) targets. Through crosslinking and immunoprecipitation coupled with high-throughput sequencing (CLIP-seq) in human embryonic stem cells and somatic cells expressing exogenous LIN28, we have defined discrete LIN28-binding sites in a quarter of human transcripts. These sites revealed that LIN28 binds to GGAGA sequences enriched within loop structures in mRNAs, reminiscent of its interaction with let-7 miRNA precursors. Among LIN28 mRNA targets, we found evidence for LIN28 autoregulation and also direct but differing effects on the protein abundance of splicing regulators in somatic and pluripotent stem cells. Splicing-sensitive microarrays demonstrated that exogenous LIN28 expression causes widespread downstream alternative splicing changes. These findings identify important regulatory functions of LIN28 via direct mRNA interactions.