Abstract
Chondral or osteochondral defects are still controversial problems in orthopedics. Here, chondrocytes labeled with magnetic nanoparticles were cultivated on a biphasic, type II collagen–chitosan/poly(lactic-co-glycolic acid) scaffold in an attempt to develop cultures with trackable cells exhibiting growth, differentiation, and regeneration. Rabbit chondrocytes were labeled with magnetic nanoparticles and characterized by scanning electron microscopy (SEM), transmission electron (TEM) microscopy, and gene and protein expression analyses. The experimental results showed that the magnetic nanoparticles did not affect the phenotype of chondrocytes after cell labeling, nor were protein and gene expression affected. The biphasic type II collagen–chitosan/poly(lactic-co-glycolic) acid scaffold was characterized by SEM, and labeled chondrocytes showed a homogeneous distribution throughout the scaffold after cultivation onto the polymer. Cellular phenotype remained unaltered but with increased gene expression of type II collagen and aggrecan, as indicated by cell staining, indicating chondrogenesis. Decreased SRY-related high mobility group-box gene (Sox-9) levels of cultured chondrocytes indicated that differentiation was associated with osteogenesis. These results are encouraging for the development of techniques for trackable cartilage regeneration and osteochondral defect repair which may be applied in vivo and, eventually, in clinical trials.
Highlights
Articular cartilage defects related to congenital deficiency, trauma, or sports injury are common problems
The result showed that the incorporation ratio of magnetic nanoparticles reached a plateau when the concentration of magnetic nanoparticles exceeded 250 μg/mL
Transmission electron microscope (TEM) images, Figure 2C–E, from lower to higher magnification, where labeled cells are indicated by red arrows, showed no discernible structural alteration
Summary
Articular cartilage defects related to congenital deficiency, trauma, or sports injury are common problems. To date, repair of articular defects remains a significant challenge, since cartilage damage has a poor intrinsic capacity for healing [1]. The goal of treatment is to achieve regeneration of organized hyaline cartilage instead of fibrocartilage [2,3,4]. Various techniques exist for chondral or osteochondral defect treatment, including abrasion, drilling, microfracture, osteochondral autografts, osteochondral allografts, and chondrocyte transplantation, but the effectiveness of these varies [3,4]. Osteochondral autologous transplantation is the current treatment of choice for articular cartilage defect repair with proven long-term effectiveness [2,5]. Limited graft availability and donor site morbidity are still concerns
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