Abstract
Introduction The study of the structure of strictures of various etiologies is an open and uncertain issue of modern urology. Aim To evaluate the morphological and immunohistochemical structure of strictures of various etiologies. Materials and methods The study involved postoperative tissue of a pathologically altered urethra of 110 patients aged 23 to 74 years who underwent treatment at the University Clinic of Urology, Russian National Research Medical University. N.I. Pirogova (2014-2018) with Ds: urethral stricture. Morphological study: Van-Gieson staining; hemotoxylin - eosin. Immunohistochemical study: mouse monoclonal antibodies to muscle and connective tissue markers (Smooth Muscle Actin, Vimentin, Calponin) and inflammation markers (CD45R, CD58, CD138, CD20, CD3) were used as primary antibodies in all reactions. Results According to the revealed morphological changes, the material was divided into three groups: group I (n=27) - active inflammation; group II (n=33) - the predominant development of connective tissue with low activity of inflammation; group III (n=50) - mixed (chronic mild inflammation, an even amount of connective tissue). In a morphological study of idiopathic urethral strictures, it was noted that the multicolumnar epithelium was replaced by a multi-layer flat epithelium with a weakly pronounced keratinization. Inflammatory changes were mild, including the submucosal connective tissue and the spongy body. Spongiofibrosis is accompanied by a significant reduction in the vascular bed of both venous sinuses and arteries. The same changes were observed in the inflammatory genesis of urethral strictures. In the study of strictures with traumatic etiology, a restructuring of the cylindrical epithelium was observed. In cases with severe inflammation in the mucosa, the changes were atrophic-hyperplastic in nature with reactive cell atypia. Conclusion urethral Strictures in men have a specific etiological factor, but the pathogenesis of urethral lesions can be divided into: post-traumatic and post-inflammatory.
Published Version
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