Effect of Arterial Hypertension and Hyperlipidemia on the Remodeling of Articular Cartilage and the Development of Osteoarthritis (Experimental Study)

Autor: T. S. Kovalenko, G. I. Sukhanova, V. A. Nevzorova, M. A. Kabalyk
Rok vydání: 2020
Předmět:
Zdroj: Advances in Gerontology. 10:79-85
ISSN: 2079-0589
2079-0570
DOI: 10.1134/s2079057020010087
Popis: Osteoarthritis (OA) is a degenerative inflammatory disease of the synovial joints associated with age, cardiovascular comorbidity, and other factors. It is based on articular cartilage (AC) and subchondral bone (SCB) damage. Recent studies have shown that age-related changes, cardiovascular diseases, and OA may have a few common molecular mechanisms. At the same time, the conditions and the degree of influence of arterial hypertension (AH) and hyperlipidemia (HL) on joint tissues remain unclear. The goal of the study is to analyze the effect of AH and HL on the processes of cellular stress, AC remodeling, and OA development. An experimental study was carried out on 18 adult males of purebred guinea pigs (28–30 weeks old, weight 750–900 g). The first (AH model), second (HL model), and third (control) groups included six individuals each. The results of the study demonstrated that AH and HL directly affect the joint tissues and cause cellular stress, which is manifested in changes in the morphofunctional characteristics of chondrocytes. Changes in the cellular phenotype lead to the degradation of AC and SCB, as well as to the ectopic angioproliferation. However, cardiometabolic factors influence AC remodeling processes in different ways. Thus, during isolated AH, hypertrophic differentiation of chondrocytes, AC destruction, and a loss of cambial cells are observed. Cell death processes, pathological AC mineralization, and enhanced pathological angiogenesis are observed in HL. The greatest changes in AC are caused by the combination of AH and HL. A combination of cardiometabolic factors results in necrotic destruction of AC and SCB replacement with osteopod-like matrix.
Databáze: OpenAIRE
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