Abstract
Localized cartilage lesions in early osteoarthritis and acute joint injuries are usually treated surgically to restore function and relieve pain. However, a persistent clinical challenge remains in how to repair the cartilage lesions. We expressed doublecortin (DCX) in human adipose-derived stromal/stem cells (hASCs) and engineered hASCs into cartilage tissues using an in vitro 96-well pellet culture system. The cartilage tissue constructs with and without DCX expression were implanted in the knee cartilage defects of rabbits (n = 42) and monkeys (n = 12). Cohorts of animals were euthanized at 6, 12, and 24 months after surgery to evaluate the cartilage repair outcomes. We found that DCX expression in hASCs increased expression of growth differentiation factor 5 (GDF5) and matrilin 2 in the engineered cartilage tissues. The cartilage tissues with DCX expression significantly enhanced cartilage repair as assessed macroscopically and histologically at 6, 12, and 24 months after implantation in the rabbits and 24 months after implantation in the monkeys, compared to the cartilage tissues without DCX expression. These findings suggest that hASCs expressing DCX may be engineered into cartilage tissues that can be used to treat localized cartilage lesions.
Highlights
In the United States, arthritis is the most common cause of disability[1]
We demonstrate that cartilage tissues engineered from human adipose-derived stromal/stem cells (hASCs) expressing DCX yield significantly better cartilage repair outcomes than cartilage tissues engineered from hASCs without DCX expression
The joint interzone develops into a joint through cavitation, in which the two chondrogenous layers re-differentiate into articular chondrocytes[39,40,41]
Summary
In the United States, arthritis is the most common cause of disability[1]. The most common form of arthritis is osteoarthritis and other forms include rheumatoid arthritis, gout, lupus, and fibromyalgia. Osteoarthritis (OA) affects over 32.5 million US adults according to the Centers for Disease Control and Prevention. OA has a complex and multifactorial (genetic, biological, and biomechanical) pathogenesis. About 20% to more than 50% of patients who suffer acute cartilage injuries may develop post-traumatic OA2. Articular cartilage lesions are common after acute joint trauma, which are usually treated clinically with microfracture, mosaicplasty (osteochondral autograft transfer), and autologous chondrocyte transplantation that is still being modified for improvement[3,4]. New strategies based on mesenchymal stem cells are being actively tested in humans and animals[5,6]
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