Articular cartilage is the shiny white cartilage at the end of bones that provides the smooth gliding surface of our joints. Articular cartilage is avascular and, therefore, has essentially no ability to heal once damaged. Damage to articular cartilage can occur due to a variety of factors, including trauma, degenerative joint disease, or other factors such as osteochondritis dissecans. Once damaged, studies have shown that defects in articular cartilage continue to grow and eventually lead to more generalized cartilage loss, resulting in osteoarthritic changes within the joint. While articular cartilage cannot be seen on plain X-ray, advancements in MRI technology have enabled more detailed evaluation of articular cartilage, which has aided in earlier diagnosis and more effective treatment.
When discussing treatment of articular cartilage lesions with my patients, I often use a civil engineering analogy comparing articular cartilage to a city street. A solitary pothole in an otherwise intact street can be repaired. However, when damage is more widespread, there is little choice but to resurface the street, which, in this analogy, would equate to some degree of arthroplasty or joint replacement/resurfacing.
Treatment of articular cartilage defects must account for the size of the defect, health of the underlying subchondral bone, meniscal and ligament pathology, and any potential limb alignment abnormalities. Historical treatment options were limited, but are still utilized today; the most common is chondroplasty, which includes simple debridement and stabilization of lesions. While chondroplasty does not restore the function of articular cartilage, it can provide relief of mechanical symptoms related to the cartilage lesions.
Microfracture is another common surgical treatment in which multiple punctures are created within the subchondral bone at the base of localized cartilage lesions. These puncture sites bleed, filling the cartilage defect with a collection of blood and marrow components that ultimately form a fibrocartilage replacement that fills in the articular cartilage defect. However, this fibrocartilage is an inferior form of cartilage that tends to break down over time. Occasionally, an overly robust response of the subchondral bone to microfracture can lead to formation of an osteophyte within the chondral lesions. Unlike the fibrocartilage replacement of microfracture, osteochondral autologous transplantation/transfer (OAT) fills defects with true articular cartilage. During OAT, small plugs of articular cartilage and underlying bone are harvested from non-weight-bearing areas of the joint and are transferred to the site of the articular cartilage defect. Osteochondral autologous transfer is limited by the size of the lesion due to the finite availability of osteochondral plugs that can be harvested before additional morbidity to the joint ensues.
While traditional surgical treatment options for localized articular cartilage defects were limited, recent technological advancements have led to a variety of additional treatment options that have added to the armamentarium of surgeons who treat articular cartilage pathology. Several of these innovative procedures utilize allograft tissue. Particulated juvenile cartilage allows for placement of morselized allograft hyaline cartilage within an articular cartilage defect, providing 10 times the density of chondrocytes than average adult cartilage. Osteochondral allografts come in various sizes, from disc-like membranes to osteochondral plugs analogous to that of OAT. Osteochondral allografts are particularly helpful when there is pathology of the native underlying subchondral bone. Unlike OAT, osteochondral allografts can be used to treat lesions of various sizes, including large lesions, due to the lack of graft harvest from the native joint. Finally, adjuncts to traditional microfracture with cartilage and extracellular matrix allografts or platelet-rich plasma propose to produce a more anatomic hyaline cartilage than the fibrocartilage that is formed with microfracture alone.
Autologous chondrocyte implantation (ACI) is a two-staged procedure that allows the regrowth of a patient’s cartilage cells for articular cartilage defects specific to the knee. A small biopsy of cartilage is taken from a non-weight-bearing portion of the knee at an initial diagnostic arthroscopy. The cartilage biopsy is then sent to a lab that replicates the chondrocytes and implants them evenly throughout a membrane. During a second procedure, the membrane is placed within the chondral defect and secured. Over a period of months, the membrane is incorporated in the patient’s knee and the patient can regrow their own cartilage that fills the previous defect. Like osteochondral allografts, ACI can be utilized to repair large defects. An additional benefit of ACI is that it can be shaped to fit irregular surfaces, such as the undersurface of the patella, where it can be difficult for osteochondral allografts to match the anatomic contours.
Articular cartilage defects have limited ability to heal on their own and will continue to grow in size and number when left untreated. While traditional treatment options were limited, recent technological developments have provided a variety of treatment options, including a variety of allograft options as well as the ability for patients to regrow their cartilage through ACI. When considering surgical treatment, the physician must consider other anatomic aspects of the patient, including limb alignment, meniscal and ligament pathology, and condition of the subchondral bone. When all patient factors are carefully considered and the appropriate surgical treatment option is chosen, innovative therapies can effectively treat a once inauspicious diagnosis.
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This article appeared in the Summer 2025 issue of Scripts.
