Mucosal Epithelial Preservation of Free Nasal Grafts Depending on the Recipient Site

xlomafota13 shared this article with you from Inoreader Mucosal Epithelial Preservation of Free Nasal Grafts Depending on the Recipient Site Via The Laryngoscope Objectives/Hypothesis Reconstruction of mucosal defects using free mucosal grafts has become a common procedure during endoscopic sinus surgery. Epithelialization of mucosal grafts affects postoperative complications and outcomes, which could be influenced by different recipient tissue. However, morphological changes occurring in the grafts transplanted over different tissues remain unexplored. Study Design An animal study. Methods Free mucoperichondrial grafts were prepared from the nasal septum of rabbits; the cartilage group had reconstruction on the nasal septal cartilage, and the perichondrium group had reconstruction on the contralateral perichondrium. The nasal septum was removed after 1 and 4 weeks of reconstruction, and the graft was histologically evaluated. Results After 1 week of reconstruction, the mucosal epithelium of grafts in the cartilage group disappeared, whereas the columnar epithelium of grafts was preserved in the perichondrium group. After 4 weeks of reconstruction, the mucosal defect site was covered with mucosal epithelium in both groups. However, while squamous epithelium was mostly observed in the cartilage group, columnar epithelium containing the healthy ciliary and goblet cells was observed in the perichondrium group. Statistically significant differences were detected in the parameters of epithelial morphology between the two groups, which were higher in the perichondrium group. Conclusions In the reconstruction of mucosal defects using free mucosal grafts, difference in recipient tissue affects the graft epithelial morphology. Level of Evidence NA Laryngoscope, 2021 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Small plaque psoriasis re‐visited: A type of psoriasis mediated by a type‐I interferon pathway

xlomafota13 shared this article with you from Inoreader Small plaque psoriasis re‐visited: A type of psoriasis mediated by a type‐I interferon pathway Via Experimental Dermatology Abstract TNFα-inhibitor-induced psoriasis is mediated by the type-I interferon pathway, of which IFNα, LL37 and IL-36γ are major players. A subset of patients treated with TNFα inhibitors develop small plaque psoriatic lesions. Small plaque psoriasis is similarly observed in patients on immune-checkpoint inhibitors (ICI), and with concurrent systemic lupus erythematosus (SLE) or positive antinuclear antibody (ANA). Small plaque psoriasis is also the predominant phenotype in Asian populations. The association between small plaque psoriasis morphology in various clinical scenarios and the type-I interferon pathway has not been previously studied. A cross-sectional study was conducted of patients who developed small plaque psoriasis and had a biopsy for diagnostic clarification between 2009 to 2017. We obtained skin specimens from 14 adults with small plaque psoriasis; 4 patients taking anti-TNFα treatment, 4 patients with antecedent SLE, 3 patients with concurrent ANA positivity and 3 p atients taking ICI. Controls included three patients with chronic plaque psoriasis. Histology confirmed psoriasiform epidermal hyperplasia with focal lichenoid and spongiotic features. Immunohistochemical analysis revealed higher expression of IFNα-induced MXA, LL37, IL-36γ in all clinical scenarios of small plaque psoriasis compared to chronic plaque psoriasis. There was decreased CD8 T-cell migration to the epidermis and variability in the number of LAMP3+ cytoplasmic dendritic cells in the dermis of small plaque psoriasis. The findings suggest that small plaque psoriasis is a unique type of psoriasis with a distinct morphology and immune-phenotype, primarily mediated by the type-I interferon pathway. Associating morphology and disease pathogenesis, may help identify therapeutic targets for better disease control. View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.