Articular cartilage injuries are common in orthopedic clinics and are prone to occur in cases of joint sprains and localized external blows. Cartilage injuries can occur alone, in combination with subchondral bone injuries, or in combination with injuries to other structures of the joint, mainly ligaments. Because articular cartilage is a thin layer of tissue, and because it is not easily detected by many imaging studies, articular cartilage injuries are easily missed. Articular cartilage is the main body of the joint, and the ability of the joint to move smoothly is related to the very low frictional resistance of the normal articular cartilage surfaces. The loss of articular cartilage means that the joint is completely obsolete and can only be replaced. Therefore, the importance of articular cartilage is self-evident. Articular cartilage is one of the non-renewable tissues in the body, and in fact many of the tissues and structures that make up the human body are non-renewable, making it a natural law of life and death. Not only is articular cartilage not regenerable, but most cartilage injuries are difficult to repair, making articular cartilage injuries one of the most difficult problems in orthopedic clinical care. In many cases, doctors treat articular cartilage injuries with a simple2 joint debridement procedure. A debridement is the removal of broken cartilage fragments and flushing with large amounts of saline. For lesions of less than 1.5 cm of exposed subchondral bone, the surgeon often drills a hole with a special pointed awl or a fine keratome needle, which is called a “microfracture” procedure, in which mesenchymal stem cells from the bone marrow cavity migrate to the cartilage defect and eventually form fibrocartilage. The stimulated cartilage formed after microfracture is not the clear cartilage of normal joint surface and has poor wear resistance, so doctors can only comfort themselves that it is better than nothing. In order to prevent the loss of mesenchymal stem cells and to induce their differentiation into chondrocytes, many methods have been thought of, but unfortunately none of them are satisfactory. The method of osteochondral column transplantation for the treatment of articular cartilage damage was popular for a while. The principle of this method is to use a “tear-down” method, in which cartilage is grafted to the cartilage defect along with subchondral bone, because bone tissue heals more easily than cartilage, thus helping its own cartilage to heal with the surrounding normal cartilage. Instead of a single osteochondral graft, this method is usually done in a piecemeal fashion using multiple osteochondral columns, hence the term “mosaic osteochondral grafting”. Obviously, this method has a limited source of osteochondral bone for grafting and it is difficult to ensure that the individual osteochondral columns are on a single surface. Combined with the risk of non-healing and cartilage loss, osteochondral grafting has been on the decline over the years. The application of autologous chondrocytes to repair cartilage defects has been a dream of physicians and patients alike. In fact, 20 years ago, a small portion of a patient’s normal chondrocytes were removed and proliferated in culture to bring the chondrocyte count to the order of millions or even tens of thousands, and then these chondrocytes were transplanted into the cartilage defect site. Since the cultured chondrocytes are liquid and will flow everywhere, the so-called graft is actually injected into the cartilage defect and the surface of the defect is covered by periosteum and tightly sutured, which is the famous autologous chondrocyte transplantation technique (ACI). Due to the tendency of periosteal grafts to overproliferate and the limited source of periosteum, recent advances over the years have been mainly in the question of what to use as a replacement for periosteum. The most common replacement is collagen, and the latest advancement is the integration of chondrocytes into the collagen to make a cartilage scaffold, which is transplanted into the cartilage defect site, and over time the chondrocytes secrete type II collagen, which gradually replaces the type I collagen in the scaffold and heals firmly with the surrounding normal cartilage, which is known as scaffold-assisted cartilage transplantation (MACI).