Abstract
To reveal the tissue, cellular, and molecular predictors leading to the development of chronic obstructive pulmonary disease (COPD) in smokers on the basis of a morphometric analysis of bronchial biopsy specimens. A cross-sectional study was conducted in 115 smokers aged 40 to 60 years (58.3±3.24 years) with a male predominance of 90.9%. Morphological examination of bronchial biopsy specimens was first made in the smoking patients with and without COPD. The smokers with COPD versus those without this condition were found to have a statistically significant increase in a number of indicators: the specific volume (SV) of the surface epithelium (p=0.017), SV of basal epitheliocytes (p=0.008), the height of the epithelium (p=0.001), and the thickness of the basal membrane (p=0.006) due to impaired regeneration processes in the bronchial epithelium and to fibrosis of the lamina propria of the bronchi with a concurrent increase in the total number of fibroblasts. The group of smokers with COPD, unlike the comparison group, showed signs of vascular remodeling and microcirculatory disorders as the increased connective tissue volumetric density of the lamina propria of the bronchi with predominant perivascular localization. This was followed by reductions in the relative volume of capillaries (p=0.016), in the SV of micropinocytic vesicles (p=0.005), and the size of Weibel-Palade bodies (p=0.004) in the endotheliocytes. In the COPD patients, the total density of cell infiltrate per mm2 of the lamina propria of the bronchi was statistically significantly (p<0.001) greater than that in the comparison group at the expense of neutrophils, lowly and moderately granulated basophils, macrophages, plasma cells with a simultaneous rise in their interepithelial forms. Compensatory structural changes without signs of bronchial wall remodeling were recorded in the smokers without signs of bronchial disease. The smokers with the examined nosological entity were observed to have morphological signs of hemodynamic disorders, as well as perivascular fibrosis, atrophy, and squamous cell metaplasia of the bronchial epithelial lining.
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