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Osteoarthritis
Published in Nicole M. Farmer, Andres Victor Ardisson Korat, Cooking for Health and Disease Prevention, 2022
Diets rich in fruits and vegetables are thought to be beneficial to health due to the presence of flavonoids, polyphenols widely distributed in the fruits and vegetables. The range of foods containing flavonoids includes tea, citrus foods, herbs, and some commonly consumed vegetables such as celery. With regard to OA, there are particular categories of flavonoids that are protective of chondrocytes and joint damage. Flavones, a category of flavonoids located predominately in the leaves and in the outer parts of plants (Ewald et al., 1999) contain apigenin and luteolin. Often, apigenin and luteolin are found together in the same plant foods, such a parsley and celery. In a study of human chondrocytes, micromolar (µM) amounts of apigenin and lutein were found to prevent expression of joint destroying MMPs (Davidson et al., 2018). Pharmacokinetic studies in humans show that absorption of apigenin and luteolin from parsley or celery leads to serum levels in the µM range (Hostetler et al., 2017). Thus, it is logical to preclude that consumption of foods such as parsley, spinach, and celery which contain both apigenin and luteolin may be helpful for OA.
Introduction and Review of Biological Background
Published in Luke R. Bucci, Nutrition Applied to Injury Rehabilitation and Sports Medicine, 2020
Cartilage is an underprivileged tissue, and chondrocytes are underprivileged cells from a nutritional supply viewpoint. Without a direct supply of nutrients from blood vessels or lymphatics, and without direct neural support, chondrocytes are destined to an anaerobic metabolism. Chondrocytes manufacture and are immobilized in lacunae in hyaline cartilage, fibrocartilage, elastic cartilage, and epiphyseal cartilage. Chondrocytes are responsible for formation, maintenance, and repair of articular cartilage. Like fibroblasts, chondrocytes have the ability to proliferate, but this ability is much more restricted than fibroblasts. The complex interplay of cytokines on chondrocyte functions is beginning to be unraveled, showing that chondrocytes are much more responsive than previously thought. Chondrocytes are able to produce large amounts of collagen and PGs in spite of poor oxygen tension, limited nutrient supply, and anaerobic metabolism. Type II collagen, other minor collagens, reticular fibers, elastin, hyaluronan, proteoglycans, a host of noncollagenous matrix proteins, and even degradative enzymes, cytokines, and eicosanoids are produced by chondrocytes.
Animal Models of Articular Cartilage Defect
Published in Yuehuei H. An, Richard J. Friedman, Animal Models in Orthopaedic Research, 2020
Yuehuei H. An, Richard J. Friedman
Morphologically, articular cartilage is composed of four layers.1 (1) The superficial layer, about 10% of the cartilage thickness, is composed of mainly thin collagen fibers oriented along the outer surface of the joint. The lower part of the layer contains flattened chondrocytes aligned parallel to the surface. The load-bearing ability of the cartilage depends largely upon the integrity of this layer. (2) The intermediate layer is composed of vertically oriented collagen fibers and small spherical chondrocytes. The columnar orientation is less marked than in the deep layer. (3) The third or deep layer composed of large collagen fibers and larger chondrocytes. The collagen fibers are oriented mainly perpendicularly to the joint surface. The large chondrocytes form chondrons, which are composed of several chondrocytes surrounded by matrix and an outer layer of collagen/proteoglycan capsule.2 The chondrons lie in columns oriented in vertical direction. (4) The fourth or deepest layer, about 10% of the cartilage thickness, is the calcified cartilage, which joins together the cartilage and subchondral bone and provides growth and remodeling of underlying bone tissue. Collagen fibers are arranged in vertical bundles with bridging fibrils in between. There is a basophilic line called “tidemark,” aggregates of mineral associated with matrix vesicles, separating the uncalcified cartilage from the calcified layer. The total thickness of articular cartilage of femoral condyles of human and common animal subjects are listed in Table 1.
Omentin-1 promotes mitochondrial biogenesis via PGC1α-AMPK pathway in chondrocytes
Published in Archives of Physiology and Biochemistry, 2023
Zhigang Li, Yao Zhang, Fengde Tian, Zihua Wang, Haiyang Song, Haojie Chen, Baolin Wu
The chondrocyte produces and maintains the extracellular matrix (mainly collagen and proteoglycans) in cartilages, which determines the mechanical distribution of joints. The mitochondrial numbers in chondrocytes are typically low, but their functions are cohesively associated with cartilage homeostasis (Martin et al.2012). The mitochondrial dysfunction of chondrocytes has been linked to several mechanisms that have led to cartilage degradation in osteoarthritis (OA) (Blanco et al.2011). The mitochondria in chondrocytes are critical in the matrix production of chondrocytes to maintain its balanced dynamics (Blanco et al.2004). One of the primary regulators of mitochondrial biogenesis is the transcriptional factor peroxisome-PGC-1α. PGC-1α enhances mitochondrial biogenesis by targeting other regulators; including NRF1 and mitochondrial transcription factor A (TFAM) (Scarpulla 2008). NRF-1 activates the expression of key factors in regulating cellular respiration, mitochondrial DNA replication and transcription. TFAM directly binds to mitochondrial DNA and is required for the maintenance of mitochondrial DNA. Activation of PGC-1α is regulated by the protein kinase AMPKα (Wan et al.2014). PGC-1α has been proposed as a therapeutic target of OA (Wang et al.2015).
Senkyunolide A inhibits the progression of osteoarthritis by inhibiting the NLRP3 signalling pathway
Published in Pharmaceutical Biology, 2022
Minglei Shao, Dongwei Lv, Kai Zhou, Haijun Sun, Zhitao Wang
Chondrocytes are the unique stationary cells in the bone and joint system, and undergo a large number of changes during OA progression, such as proliferation and secretion (Charlier et al. 2019). The key role of chondrocytes is to maintain anabolic and catabolic homeostasis in the extracellular matrix (ECM) (Si et al. 2017). The aberrant apoptosis, inflammatory response of chondrocytes is related to the matrix degradation and cartilage destruction in OA (Wang et al. 2017). Interleukin-1β (IL-1β), a pro-inflammatory cytokine, can trigger inflammation and the production and secretion of catabolic factors, and play an important part in the pathogenesis of OA (Wang F et al. 2019). Inflammation and loss of ECM are increasingly considered to be important driving factors of OA cartilage damage (Chan et al. 2015; Wang et al. 2020). Therefore, exploring the mechanism of chondrocyte dysfunction will help to provide an understanding of the pathogenesis of OA.
Study on the poroelastic behaviors of the defected articular cartilage
Published in Computer Methods in Biomechanics and Biomedical Engineering, 2022
Yuqin Sun, Ningning Wang, Jianhao Yu, Yang Yan, Hao Dong, Xiaogang Wu, Meizhen Zhang, Yanqin Wang, Pengcui Li, Xiaochun Wei, Weiyi Chen
As the sole cellular component in cartilage tissue, the main responsibility of chondrocytes is to maintain the stability of the extracellular matrix (Benders et al. 2013). However, this stability is destroyed when the cartilage is defective, and chondrocytes needs to remodel it to find a new balance (Peng et al. 2021). A significant reduction in the synthesis of proteoglycans was observed in human osteoarthritis samples, which resulted in changes of the permeability and elastic modulus of the cartilage matrix. In turn, changes of the structure and composition of the extracellular matrix affect the fluid flow inside the tissue, which causes the chondrocytes to behave abnormally. It has been found that during the development of osteoarthritis, the elastic modulus of the extracellular matrix decreases (Armstrong and Mow 1982; Kiviranta et al. 2008) and the permeability increases (Nieminen et al. 2004; Knecht et al. 2006). Thus, different elastic modulus E (0.4, 0.5, 0.6, and 0.69 MPa) and permeability k (3 × 10−18m2, 4 × 10−18m2, 5 × 10−18m2, 6 × 10−18m2) were simulated. The average values of p and v around the defect under different parameters are shown in Figures 16 and 17. On the whole, the p and v show the opposite trend, that is, when the p increases, the v decreases instead. The softening of the solid matrix and the increase in permeability both lead to a decrease in p and an increase in v.