## 1 Introduction  
Articular cartilage is a highly specialized connective tissue that overlies the surface of bones in diarthrodial joints [1, 2]. It provides a smooth, lubricated surface to minimize friction during articulation and distributes mechanical forces across the joint capsule to protect the underlying subchondral bone [1; 3]. While articular cartilage functions to absorb compressive loads, applied mechanical stress contributes to gradual wear, tears, and injuries to the joint [2; 4]. However, articular cartilage exhibits a poor intrinsic healing capacity for self-repair, as it is avascular, aneural and alymphatic [1; 2; 5]. Without targeted therapies and repair treatment strategies, articular cartilage damage can contribute to gradual tissue deterioration, debilitating pain, joint inflammation, and ultimately complete degradation in the pathogenesis of osteoarthritis (OA) [2; 6]. The poor regenerative capacity of articular cartilage necessitates effective treatment methods to initiate joint healing and repair. Transplantation of cartilage osteochondral grafts, autologous or allogeneic depending on lesion size, is a common operative treatment to repair cartilage defect areas [7; 8]. However, a significant challenge remains with the integrative repair properties at the graft-host tissue interface, as proper surgical implantation and integration to the subchondoral bone are critical toward restoring normal load distribution across the joint [9; 10]. Osteochondral grafts may also undergo central necrosis and appearance of subchondoral cyst-like resorption areas, which may contribute to graft mechanical instability, poor cartilage nutrition, and ultimately graft failure [10]. Several cell-based treatments, including autologous chondrocyte implantation (ACI) and mesenchymal stem cell (MSC) delivery therapies, have emerged as surgical options for cartilage repair [11]. Both procedures seed cells that directly participate in defect healing and regulate cartilage metabolism by producing extracellular matrix (ECM) molecules that are critical for native function, including collagens, proteoglycans, and glycosaminoglycans (GAGs) [12; 13]. However, ACI and MSC delivery to defect lesions in the joint possess clinical limitations, including risk of further injury to healthy cartilage during autologous harvest, the need for two-step surgical techniques, cellular immune rejection following implantation, and graft hypertrophy [14; 15]. Instead of surgical interventions, natural repair processes via direct migration or selective homing of native target cells to defect sites in the cartilage surface hold potential as alterative treatment strategies [13; 16]. Articular cartilage is composed of chondrocytes, embedded within a dense extracellular matrix of collagens and proteoglycans [1; 5]. However, native chondrocytes have limited metabolic activity, proliferation, and biosynthesis, contributing to poor healing response following joint injury [1; 17]. Therefore, in order to address poor tissue integration and limited chondrocyte migration, fibroblast-like synovioocytes (FSL) that exhibit chondrogenic potential may serve as a cell-based strategy to promote in vitro cartilage repair. FLS are derived from the adjacent synovium, the specialized connective tissue membrane that envelops the diarthordial joint [18; 19; 20]. Synovium-derived cells have been directly implicated in both the native repair response as well as degradation of articular cartilage [21], thus providing a promising target for the development of novel strategies aimed toward preventing structural changes to the joint and treating clinical symptoms, especially in the development of early OA [22].