Surgical removal of articular cartilage leads to loss of chondrocytes from cartilage bordering the wound edge

Background: A number of arthroscopic procedures that are used in the treatment of focal cartilage lesions or osteoarthritic joints, such as shaving, debridement, and laser abrasion, involve the removal of both diseased and healthy articular cartilage. The excision of such tissue has the effect of generating lesions within the articular cartilage. The fate of the chondrocytes that border such lesions has not been evaluated. The purpose of this investigation was to ascertain whether the surgical creation of lesions in articular cartilage induces irreversible loss of chondrocytes over time from tissue bordering the wound edge and to determine whether the synthetic activity of cells in this region is compromised. Methods: Partial-thickness defects of defined dimensions were created in the femoral condyle and/or trochlear groove of rabbits and miniature pigs. Cell volumes, cell volume densities, and numerical cell densities within tissue close to (within 100 pm) and remote from (control site) the wound edge were determined by quantitative histomorphometry at various time intervals up to six months after surgery. Rates of proteoglycan synthesis by cells in both regions were determined by quantitative autoradiography following S-35-sulphate labeling in vivo. Results: The surgical creation of partial-thickness lesions in articular cartilage induced a significant and long-term loss of cells from tissue near the wound edge. However, the surviving cell population maintained a normal rate of matrix proteoglycan deposition. Conclusions: This study illustrates that maintenance and remodeling of cartilage matrix close to wound edges in articular cartilage lesions is compromised, since fewer cells, with an unchanged metabolic activity rate, are left to sustain matrix domains. Clinical Relevance: The long-term benefits of arthroscopic treatments such as shaving, debridement, and laser abrasion may be deleteriously affected by their adverse biological effects on the cells and matrix of articular cartilage.