HISTOLOGICAL AND MORPHOLOGICAL CHANGES IN THE SYNOVIAL MEMBRANE IN EXPERIMENTAL MODELS OF OSTEOARTHRITIS

Osteoarthritis (OA) is a leading cause of disability globally, affecting over 500 million individuals and imposing substantial socioeconomic burdens. The synovial membrane, integral to joint function, undergoes critical histological and morphological transformations that perpetuate OA pathology. This study delineates these changes in experimental rodent models, employing advanced histological, immunohistochemical, and morphometric techniques to achieve high scientific rigor. Induction via monoiodoacetate (MIA) or anterior cruciate ligament transection (ACLT) revealed temporal progression: early synovitis with inflammatory infiltration, mid-stage hyperplasia and angiogenesis, and late fibrosis with pannus formation. Quantitative metrics, including synovial thickness (up to 3.75-fold increase) and fibrosis scores (peaking at 2.5), were statistically validated (p<0.001). Histological stains (H&E, Masson’s trichrome) and immunohistochemistry (CD68, VEGF) corroborated extracellular matrix remodeling and macrophage dominance. Morphological analyses via atomic force microscopy (AFM) indicated elevated elastic modulus in OA synovium, aligning with recent biomechanical studies. Integrating tables, histological images, and diagrams, this research highlights the synovium's role in OA's vicious cycle, offering insights for targeted therapies like anti-cytokine biologics. Amid rising OA prevalence due to aging populations, these findings enhance preclinical models' translational value, addressing gaps in synovium-focused interventions. The study's expanded scope, incorporating multi-modal assessments, underscores its timeliness in advancing OA management strategies.

Hali tarjima qilinmagan