Морфологія / Morphologia / Morfologìâ

Retrospective analysis of the morphofunctional architectonics and pathohistological transformation of the myocardium: from the molecular norm to regenerative potential in remodelling and ischaemia (literature review)

2026-06-02T10:10:14+03:00

Introduction. Myocardial viability depends on the spatial organization of subcellular structures (ion clusters, nanodomains), whose disorganization of which causes rhythm disturbances even before the appearance of histological signs of necrosis. This makes an in-depth study of cardiac microarchitecture critically important for clinical practice. Aim. To systematize modern histological, ultrastructural, and immunohistochemical criteria for evaluating the myocardium in normal conditions, during adaptive remodeling, ischemia, and inflammation, as well as to analyze the regenerative potential of the tissues. Methods. A systematic review was conducted, resulting in the selection of 25 sources from the PubMed, Scopus, and Web of Science databases spanning 1990–2026 (with a focus on the last 5 years) using the keywords: myocardium, histology, pathology. Results. Normal myocardial architecture is maintained by intercalated discs and ankyrins, which serve as molecular "anchors" for ion channels. During hypoxia, ankyrin proteolysis disrupts this stability. In ischemia, ultrastructural changes (mitochondrial swelling) are recorded as early as 30 minutes. For the ultra-early verification of true ischemia and necrosis, specific immunohistochemical markers (C9 complex, SIRT1) are utilized, and the local tissue loss of troponin C is monitored. Post-necrotic remodeling culminates in irreversible collagen scarring involving myofibroblasts (α-SMA expression). Surviving muscle "bridges" within the scar can generate arrhythmias. Simultaneously, regeneration faces the connexin-43 (Cx43) paradox: although differentiated progenitor cells express it, the excessive extracellular matrix physically isolates cardiomyocytes, blocking electrical contacts. Conclusion. The early verification of ischemia and inflammation relies on electron microscopy and specific markers (C9, CD3). Overcoming barriers in regenerative medicine requires comprehensive histomatrix analysis to combat fibrosis and restore conduction.

The ultrastructure of the gingival epithelial layer in adults

2026-06-02T10:32:56+03:00

Relevance. Periodontal diseases remain one of the most common problems in modern dentistry, which necessitates a detailed study of the morphofunctional state of the gums as the first biological barrier against pathogenic factors. Detailing the norms of the ultrastructural structure of the gums in adults is the foundation for studying the evolution of pathological processes and developing criteria for evaluating the effectiveness of the latest protocols for treating gum disease. The aim was to study the features of the ultrastructural organisation of cell components of the epithelial layer of the gums in adults. Methods. Transmission electron microscopy was used to study the soft tissues of the periodontium in clinically healthy individuals. Results and conclusion. A gradient increase in the electron density of keratinocytes was detected in the direction from the basement membrane to the surface layers, reflecting the dynamics of specific cellular metamorphosis. These changes are determined by the morphofunctional heterogeneity of the ultrastructural organisation of cells in different layers of the gingival epithelium. The cells of the basal layer are characterised by their high functional activity, as evidenced by the presence of a well-developed synthetic apparatus. In the cells of the spinous layer, against the background of a decrease in synthetic functions, a clearly formed apparatus of intercellular connections is observed. Epithelial cells of the granular layer are characterised by the onset of keratinisation processes and preparation for programmed cell death. The architectonics of the stratum corneum is the determined result of a cascade of metabolic and structural changes occurring in the keratinocytes of the basal, spinous and granular layers.

Morphological features and functional state of the pulmonary nitric oxide system in guinea pigs with experimental allergic alveolitis

2026-06-02T10:44:05+03:00

The use of Freund’s complete adjuvant (FCA) is a versatile method for the experimental modelling of a wide range of immune-mediated and autoimmune disorders, including allergic alveolitis. Nitric oxide acts as a key regulator of metabolism and the immune response in such processes, exhibiting pronounced vasoactive, mediatory and cytotoxic activity. Due to the instability of the free radical NO, it is advisable to assess the functional state of this system by determining the levels of its stable metabolites (nitrites and nitrates) in biological substrates. The aim of the study is to determine the characteristics of the dynamics of morphological changes in the lungs and the levels of stable NO metabolites in an experimental model of allergic alveolitis (EAA). Methods. An experimental model of EAA was established in 39 guinea pigs weighing 180–230 g, which were administered 0.2 ml of Freund’s adjuvant intramuscularly into the hind leg. The experimental protocol involved six intravenous injections of 0.2 ml of an inactivated BCG vaccine suspension at 10-day intervals, starting from the 14th day after the initiation of immunisation. Results and conclusion. The results of morphological studies revealed a series of progressive changes in the microstructure of the lungs in EAA, which initially manifested as marked hyperaemia of the vascular bed and were subsequently accompanied by damage to the respiratory compartment in the form of thickening of the interalveolar septa, oedema of respiratory epithelial cells and macrophage infiltration. In later stages of the study, the formation of epithelioid granulomas was observed. Individual groups of alveoli in the pulmonary acini were in a state of atelectasis, indicating a local absence of the surfactant complex due to dysfunction of secretory alveolar cells. Biochemical analysis of lung tissue revealed elevated levels of nitric oxide (NO) derivatives, confirming its role as a pathogenetic link in the development and progression of immunopathological changes of the delayed-type hypersensitivity type, characteristic of experimental allergic alveolitis.

Assessment of indicators of myocardial fibrosis in experimental type 2 diabetes mellitus and with administration of L-arginine and N-acetyl-L-cysteine

2026-06-02T10:54:19+03:00

Background. The study is devoted to diffuse myocardial fibrosis in type 2 diabetes mellitus and the possibilities of its correction with the help of L-arginine and N-acetylcysteine. The work evaluates the potential of these compounds to modify already formed structural changes in the heart and the possibility of preventing further damage in conditions of insulin resistance and metabolic overload. Aim. To evaluate the morphological effects of L-arginine and N-acetyl-L-cysteine on interstitial and perivascular components of myocardial fibrosis in experimental type 2 diabetes mellitus (T2DM) in Wistar rats. Methods and Results. The study was conducted on 42 Wistar rats (18-20 months old). T2DM was induced by a high-fat diet combined with streptozotocin (30 mg/kg). The animals were divided into groups: control, T2DM without correction, T2DM treated with L-arginine (1.5 g/kg), and T2DM treated with N-acetyl-L-cysteine (1.5 g/kg) for 2 weeks. Masson's trichrome staining and immunofluorescence analysis for collagen type 1 were performed. T2DM was found to increase interstitial fibrosis by 3.94 times and perivascular fibrosis by 2.24 times compared to the control group. The content of collagen type 1 increased by 492 %. L-arginine administration led to a further increase in interstitial fibrosis (1.21 times) and collagen type 1 content (by 18 %). N-acetyl-L-cysteine treatment promoted a 0.74-fold reduction in interstitial fibrosis but was accompanied by a 44 % increase in collagen type 1 expression. Conclusions. Experimental T2DM forms pronounced diffuse myocardial fibrosis dominated by the interstitial component and collagen type 1 accumulation. L-arginine does not exhibit a fibroprotective effect in this model. N-acetyl-L-cysteine partially reduces interstitial fibrosis but does not prevent the pathological expression of collagen type 1.

Giant saccular aneurysm of the intracranial vertebral artery: clinico-morphological case

2026-06-02T12:03:18+03:00

Background. Giant vertebrobasilar aneurysms are rare and prognostically unfavorable lesions of the central nervous system. They are characterized by a pseudotumorous course, progressive mass effect, brainstem compression, and a high risk of fatal outcomes. Despite advances in endovascular treatment, periprocedural complications remain an important clinical problem. Objective. To increase physicians’ awareness of the clinical course, morphogenesis, and complications of giant intracranial vertebral artery aneurysms. Methods. A clinico-morphological case of giant saccular aneurysm of the intracranial (V4) segment of the right vertebral artery in a 57-year-old man was analyzed. Spiral computed tomography, cerebral angiography, endovascular coil embolization, and pathological examination findings were evaluated. Macroscopic assessment of the aneurysmal sac, thrombotic masses, and brain changes was performed. Results. The patient developed progressive neurological deficit with bulbar syndrome and alternating sensory disturbances. Neuroimaging revealed a giant vertebral artery aneurysm with severe mass effect. Subtotal endovascular coil embolization was performed. Pathological examination demonstrated an aneurysmal sac measuring 65×50×45 mm filled with mural thrombi at different stages of organization. Brainstem compression and displacement, cerebral edema, and cerebellar tonsillar herniation through the foramen magnum were identified. Death resulted from progressive compression of the vital medullary centers. Conclusions. Giant intracranial vertebral artery aneurysms are associated with severe pseudotumorous manifestations and a high risk of fatal complications. Endovascular treatment may increase the mass effect because of thrombosis within the aneurysm. Comprehensive pathological examination is essential for understanding tanatogenesis and improving diagnostic and therapeutic strategies.

Morphological markers of testicular degeneration in pediatric undescended testes: the role of fibrosis and angiodysplasia

2026-06-02T12:15:54+03:00

Background. An undescended testis is associated with high risks of male infertility and tumors. Since degenerative changes in the undescended testis progress with age, studying the morphological markers of gonadal degeneration (specifically fibrosis and the state of the vascular bed) is important for understanding the pathogenesis of testicular regression and optimizing surgical tactics in children. Objective. To determine the morphological markers of testicular tissue degeneration in pediatric undescended testis and to evaluate the role of fibrosis and angiodysplasia in the progression of hypoplasia based on the study of intraoperative biopsies. Methods. A histological study of 42 biopsies of undescended testes in boys aged 1 to 17 years was conducted. The material was obtained during orchidopexy for rudimentary forms (n=31), orchiectomy for torsion (n=5), and biopsy for suspected tumor (n=6). The diameter of the seminiferous tubules, the state of the basement membrane, the number of Sertoli cells, the tubular fertility index (TFI), as well as the state of the interstitium and blood vessels were evaluated. Results. A severe degree of testicular hypoplasia was diagnosed in 76.2% of cases. Fibrosis was detected in 80.95% of the samples, and dystrophic calcification in 28.57%. Three key morphological signs of degeneration were established: 1) persistence of mesenchyme-like fibrous tissue with signs of chondroid differentiation; 2) pronounced angiodysplasia (malformed vessels, thinning or absence of muscular layers of the wall, arteriovenous anastomoses); 3) chronic inflammation (perivascular lymphohistiocytic infiltrates). The TFI value critically decreased depending on the patients' age against the background of quantitative and qualitative disorders of Leydig cells. Conclusion. Destructive changes in the germinal epithelium occur even under conditions of a mild degree of hypoplasia. The leading markers of parenchymal degeneration of the undescended testis are progressive interstitial fibrosis, the persistence of embryonic mesenchyme, and severe angiodysplasia. These processes, combined with Leydig cell dysfunction, cause a critical decrease in fertility potential and can serve as predictors of malignant transformation.