Open AccessSTRUCTURE OF THE KNEE ARTICULAR CARTILAGE AFTER THE FEMUR AND TIBIA EXTRA-ARTICULAR INJURY
Author(s) -
А. S. Tkachenko,
O. S. Maksymova,
Oleksii Volodymyrovych Korenkov,
Andrii Andriiovych Voznyi,
Геннадій Федорович Ткач
Publication year - 2021
Publication title -
wiadomości lekarskie
Language(s) - English
Resource type - Journals
eISSN - 2719-342X
pISSN - 0043-5147
DOI - 10.36740/wlek202108115
Subject(s) - chondrocyte , tibia , anatomy , cartilage , articular cartilage , femur , medicine , patella , osteoarthritis , pathology , surgery , alternative medicine
The aim: To study the microscopic, ultramicroscopic, and histomorphometric features of the knee articular cartilage in rats with an extra-articular injury of the femur and tibia.Materials and methods: 60 white laboratory rats divided into three groups (I – control; II – animals with traumatic femur injury; III – animals with traumatic tibia injury) were used for the study. The light microscopy was performed by Olympus BH-2 microscope (Japan), transmission electron microscopy – by JEM-1230 microscope (Japan). SPSS software (version 17.0) was used for mathematical analysis.Results: The more pronounced morphological changes were observed in the articular cartilage of the proximal tibial epiphysis after mechanical tibial injury. The thickness of the articular cartilage was 27.89 % less than in the control. The chondrocyte number in the superficial zone was lower by 8.94 %, intermediate zone – by 14.23 %, and deep zone – by 21.83%, compared to control. Herewith, the histological changes were mostly detected in the intermediate and deep zones of the articular cartilage of both bones. Also, some chondrocytes had deformed nuclei, hypertrophied organelles, numerous inclusions, and residual glycogen granules.Conclusion: The extra-articular mechanical trauma of the lower limb bones leads to pathological changes in the knee articular cartilage. The structural changes include the articular cartilage thickening, the decrease in chondrocyte number, as well as chondrocyte rearrangement due to degenerative-dystrophic processes.