{'fraction_non_alphanumeric': 0.01870657402458578, 'fraction_numerical': 0.012292891501870658, 'mean_word_length': 5.591549295774648, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Morphological Studies on the Ageing and Osteoarthritis of the Articular Cartilage in C57 Black Mice

Purpose. To study the cause and mechanism of joint degeneration in osteoarthritis, through histopathological and ultrastructural-histochemical experiments on the articular cartilage of the knees of the C57 black mouse. Methods. 192 C57 black mice and a control group of 64 C57BL/6J mice were used in this study. The left and right knee articular capsules of the joints were removed and stained. Each articular cartilage sample was examined and osteoarthritic changes were assessed using a transmission electron microscope. The severity of osteoarthritis in the knee joint cartilage of C57 black mice was histologically assessed using a classification system described by Okabe, based on Maier's system. Results. The incidence and the severity of osteoarthritis gradually increased with age; the incidence increased from 20% at 2 months to 80% at 16 months. Irreversible changes appeared at an advanced stage, and the process of degeneration was quite similar to that in human osteoarthritis. Through transmission electron microscopy, we observed poorly developed Golgi apparatus, markedly increased intracellular microfilaments, decreased proteoglycan granules, and broken collagen networks in all stages of osteoarthritis. By contrast, Golgi apparatus and other organelles were well developed in histologically normal mice of all ages. Proteoglycan granules, which mainly consisted of keratan sulphate, were observed; collagen networks were maintained. Conclusion. Disturbed protein transport and sugar synthesis in chondrocytes, caused by the deficient development of the Golgi apparatus, could result in degenerative changes in articular cartilage. The structure and function of the matrix were maintained mainly because of the continued presence of keratan sulphate.