BackgroundHypertrophic scar following a burn is caused by the excessive deposit of collagen resulting in an exaggerated wound healing response. The burn patient complains of pain and itching over the scar, which can give rise to cosmetic and functional problems.ObjectiveThe aim of this study was to investigate the clinical and histological correlation of a hypertrophic burn scar for itching and pain sensations.MethodsThirty-eight patients underwent a scar release and skin graft. the modified Vancouver scar scale and the verbal numerical rating scale were recorded. All biopsies were taken from scar tissue (scar) and normal tissue (normal). Histologically, tissues were observed in the epidermis, the monocytes around the vessels, the collagen fiber, elastic fiber, and the mast cells.ResultsThe mean total score of MVSS was 8.4±2.7 (pliability 2.0±0.9; thickness 1.8±0.9; vascularity 2.0± 0.9; and pigmentation 2.1±0.9). Pain and itching were 2.4±2.0 and 2.9±3.0. Epidermis were 7.9±2.8 layers (scar) and 4.0±0.8 layers (normal). The collagen fibers were thin and dense (scar) and thicker and loose (normal). The elastic fibers were thin and nonexistent (scar) and thin and loose (normal). Mast cells were 11.2±5.8/high power field (scar) and 7.4±4.1 (normal).ConclusionAs the scar tissue thickens, the itching becomes more severe. The stiffness of the scar with the pain appeared to be associated with the condition of the tissue. The correlation between clinical and histological post-burn hypertrophic scars will help further studies on the scar. This helped with the development of the base material for therapeutic strategies.

We demonstrated semiquantitative differences in neuropeptides in the skin of AD patients. In addition, topical tacrolimus reduced the levels of neuropeptides in the tissues of AD patients.

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It is known that DNA hypomethylation of aryl hydrocarbon receptor repressor (AhRR), one of the epigenetic markers of environmental pollutants, causes skin diseases. However, the function and mechanisms are still unknown. We aimed to determine whether AhRR is hypomethylated in PBMC of psoriasis patients, as well as to examine the expression of psoriasis-related inflammatory cytokines and antimicrobial peptides after 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) treatment in HaCaT cells overexpressing or silencing AhRR. AhRR was determined by qPCR, Western blot, immunohistochemistry, and immunocytochemistry in skin tissue and HaCaT cells. DNA methylation of AhRR was performed by Infinium Human Methylation450 BeadChip in PBMC of psoriasis patients and methylation-specific PCR (MSP) in HaCaT cells. NF-κB pp50 translocation and activity were performed by immunocytochemistry and luciferase reporter assay, respectively. We verified AhRR gene expression in the epidermis from psoriasis patients and healthy controls. AhRR hypomethylation in PBMC of psoriasis patients and pAhRR-HaCaT cells was confirmed. The expression level of AhRR was increased in both TCDD-treated HaCaT cells and pAhRR-HaCaT cells. NF-κB pp50 translocation and activity increased with TCDD. Our results showed that AhRR was hypomethylated and overexpressed in the lesional skin of patients with psoriasis, thereby increasing AhRR gene expression and regulating pro-inflammatory cytokines through the NF-κB signaling pathway in TCDD-treated HaCaT cells.