Abstract
This study aimed to explore changes in nanoscale elastic modulus of the synovium using atomic force microscopy (AFM) in addition to investigate changes in synovial histomorphology and secretory function in osteoarthritis (OA) in a rat anterior cruciate ligament transection (ACLT) model. Sprague-Dawley rats were randomly assigned to sham control and ACLT OA groups. All right knee joints were harvested at 4, 8, or 12 weeks (W) after surgery for histological assessment of cartilage damage and synovitis in both the anterior and posterior capsules. AFM imaging and nanoscale biomechanical testing were conducted to measure the elastic modulus of the synovial collagen fibrils. Immunohistochemistry was used to visualize the expression of interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), and matrix metalloproteinase-3 (MMP-3) in the synovium. The OA groups exhibited progressive development of disease in the cartilage and synovium. Histopathological scores of the synovium in the OA groups increased gradually. Significant differences were observed between all OA groups except for the posterior 4W group. The synovial fibril arrangement in all OA groups was significantly disordered. The synovial fibrils in all ACLT OA groups at each time point were stiffer than those in the sham controls. OA rats displayed a significantly higher expression of IL-1β and MMP3 in the anterior capsule. In summary, synovial stiffening was closely associated with joint degeneration and might be a factor contributing to synovitis and increased production of proinflammatory mediators. Our data provided insights into the role of synovitis, particularly stiffening of the synovium, in OA pathogenesis.
Highlights
Osteoarthritis (OA) is the most common joint disease worldwide and a leading cause of pain and disability [1]
It was clear that the 4W, 8W, and 12W anterior cruciate ligament transection (ACLT) OA groups represented early, middle, and late stages of OA, respectively
The ACLT model has been shown to be an important tool in OA pathological research
Summary
Osteoarthritis (OA) is the most common joint disease worldwide and a leading cause of pain and disability [1]. Especially anterior cruciate ligament rupture, can eventually lead to posttraumatic OA. This common arthritic disease has been characterized by marked changes in the structure and function of the articular cartilage. In contrast to earlier viewpoints, joint failure in OA is perceived as being the result of a complex interactive pathological process in multiple articular tissues including the cartilage, synovium, meniscus, muscle, and cortical and subchondral bone [3]. It is still debated as to which tissue structures undergo change initially as OA progresses. Increasing evidence from both experimental and clinical studies suggests that inflammation, especially synovitis, plays an important role in the pathologic process of OA [4]. Histological changes of the synovium are often accompanied by increased vascularity, inflammatory molecule expression, and immune cell infiltration [6]
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