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The cartilage is solely composed of cells known as chondrocytes. Chondrocytes maintain the extracellular matrix (ECM) and produce the cartilage matrix. Surrounded by collagenous fibers, chondrocytes release substances to make cartilage strong yet flexible. In general, chondrocytes are found within intervertebral discs and in any form of articular cartilage. Chondrocytes play a crucial role in maintaining homeostasis within the acromioclavicular joints, which provide cushioning during joint movements. Like cells within other specialized tissues, chondrocytes distance themselves from each other by the cartilage matrix.[1] Chondrocytes are also responsible for chondral repair; due to their reconstructive nature, they respond to outside trauma in case of tissue damage. Because of their ability to heal degenerative conditions, chondrocytes are under active research for implantation and other reconstructive procedures.[2]

As mentioned earlier, chondrocytes maintain homeostasis between the creation and destruction of extracellular matrix components. Chondrocytes, influenced by external stimuli, polypeptide growth factors, and cytokines, create such components and the enzymes that break them down.[6] A disruption in homeostasis leads to osteoarthritis. Researchers are still unsure of the initial point of degradation. A microfracture from any trauma may cause the production of enzymes, leading to “wear” particle synthesis and its macrophage-caused destruction. Eventually, “wear” particle production inhibits the systematic degradation of such particles, mediating inflammation and influencing chondrocytes to secrete degradative enzymes. Collagen and proteoglycan metabolism yields particles that trigger the release of proinflammatory cytokines, such as TNF-alpha, IL-6, and IL-1. These cytokines can bind to chondrocyte receptors, which release metalloproteinases and inhibit type II collagen assembly, thereby promoting cartilage degradation. Homeostatic disruption increases the water content and decreases the proteoglycan content of the extracellular matrix (ECM). This modification weakens the collagen network due to reduced type II collagen synthesis and increases the breakdown of pre-existing collagen. Chondral apoptosis is also visible. Increased anabolic and catabolic activity is characteristic of patients with osteoarthritic cartilage. Compensatory mechanisms, such as increased production of matrix molecules (collagen, hyaluronate, and proteoglycans) and the spread of chondrocytes into deeper chondral layers, help maintain the integrity of the articular cartilage. Chondrocyte loss, however, along with changes in the extracellular matrix, predominates, leading to osteoarthritic conditions. Thinning cartilage, degrading cartilage thickness, and fibrillation of superficial layers are all caused by the initial degradations. These changes get worse over time, and articular cartilage thins to the point of complete destruction. This condition exposes the underlying subchondral bone plate and characterizes these changes as chondropathy.[7] Current investigations about the heterogeneity of cellular reaction patterns that characterize osteoarthritic cartilage degeneration highlighted apoptotic chondrocyte death and its underlying mechanisms.[8]