This study evaluated early changes in full-thickness (FT) and partial-thickness (PT) articular cartilage defects created by arthroscopic surgery. The defects were of various configurations in a model (horse) that was weight-bearing immediately after surgery. The objectives were to evaluate recellularization and to examine the effect defect configuration had on adjacent cartilage cellularity and proteoglycan content. Thirty-six PT lacerations, FT lacerations, PT scrapes, PT craters, and FT craters were created in the antebrachiocarpal and intercarpal joints of eight adult horses. The configurations were lacerations by knife blade, scrapes by a curette, and craters created by motorized burr. Horses were euthanized one, three, and eight weeks after surgery. Histologic examination was performed using hematoxylin and eosin and safranin-O staining. All FT craters showed evidence of early repair. None of the lacerations showed evidence of early repair. One PT scrape and four PT craters bad fibrous tissue within the defect. All defects had degenerative changes in adjacent cartilage. Craters and scrapes had significantly worse degenerative changes than lacerations. Patients undergoing arthroscopic surgery who will be weight-bearing immediately after surgery should have full thickness crateriform debridement if a healing response is desired. Partial thickness debridement does not show evidence of repair. Degenerative changes in adjacent cartilage occurred in all defects and they are directly proportional to the amount of trauma and instrumentation used at surgery. Full thickness (FT) cartilage defects that penetrate the zone of calcified cartilage rely on hemorrhage from subchondral bone and the resultant fibrin clot to initiate repair. The fibrin clot acts as a matrix for cellular repair that results in formation of fibrous tissue. The quality of repair (i.e. fibrous tissue, fibrocartilage, or hyaline cartilage) relies on metaplasia of fibrous tissue. This mechanism of articular cartilage healing, referred to as extrinsic repair1,2 occurs after subchondral abrasion with motorized instrumentation;3,4,5 however, the quality and durability of repair tissue has been questioned.5,6,7 Partial thickness (PT) cartilage defects do not penetrate the zone of calcified cartilage and do not bleed. Healing of PT defects relies on mitotic activity of chondrocytes and increased metabolic activity adjacent to the defect to create intrinsic repair.2 Many investigators have shown the inability of PT defects to heal.3,8,9,10,18 It has recently been shown that PT defects may undergo further degeneration.3 The fibrin clot and other extrinsic factors released during hemorrhage in FT defects are reported to be important in initiating repair of articular cartilage.5 Mesenchymal cells from the subchondral bone initiate the recellularization process in FT defects.11,12,13 If PT defects are to heal with any degree of consistency then a “modified” extrinsic repair must occur or blood clot must attach to the defect and recellularization from synovial cells within the joint must take place. Early reparative changes in articular cartilage of other species have been documented. Most studies investigating articular cartilage healing in the horse are long-term studies evaluating the quality and durability of repair tissue. The purpose of this study was to investigate early recellularization of FT and PT defects created by arthroscopic surgery in articular cartilage located within the same joint surface in a model in which the operated horse was weight-bearing immediately after surgery. The objectives were to evaluate early recellularization and to examine the effect various types of defects had on adjacent cartilage cellularity and proteoglycan content at one, three, and eight weeks after surgery.