Abstract
Cartilage neoangiogenesis holds a prominent role in osteoarthritis (OA) pathogenesis. This study aimed to assess the efficacy bevacizumab, an antibody against vascular endothelial growth factor and inhibitor of angiogenesis, in a rabbit OA model. Animals were divided into four groups: one receiving a sham intra-articular knee injection and three groups undergoing 5, 10, and 20 mg intra-articular bevacizumab injections. The effect of the antibody on articular cartilage and synovium was assessed through histology and quantified with the Osteoarthritis Research Society International (OARSI) scores. Immunohistochemistry was performed to investigate type 2 collagen, aggrecan, and matrix metalloproteinase 13 (MMP-13) expression. Bevacizumab treatment led to a significant reduction of cartilage degeneration and synovial OA changes. Immunohistochemistry revealed significantly lower cartilage MMP-13 expression levels in all experimental groups, with the one receiving 20 mg bevacizumab showing the lowest. The antibody also resulted in increased production of aggrecan and type 2 collagen after administration of 5, 10, and 20 mg. The group treated with 20 mg showed the highest levels of type 2 collagen, while aggrecan content was even higher than in the healthy cartilage. Intra-articular bevacizumab has been demonstrated to effectively arrest OA progression in our model, with 20 mg being the most efficacious dose.
Highlights
Osteoarthritis (OA) is a degenerative joint disorder affecting more than 10% of individuals older than 60 years of age
The results showed a significant increase in aggrecan expression in all animals articular cartilage of the four groups
The total Osteoarthritis Research Society International (OARSI) score for articular cartilage (Figure 1B) demonstrated a statistically significant difference between the OA group and all treatment groups
Summary
Osteoarthritis (OA) is a degenerative joint disorder affecting more than 10% of individuals older than 60 years of age. It is characterized by escalating joint pain and stiffness progressively leading to disability, with a significant burden on patients’ overall functionality and quality of life, as well as on healthcare expenditure [1]. Main risk factors comprise aging, female gender, genetics, and alterations of joint biomechanics. Major pathologic characteristics include articular cartilage damage and thinning, which are associated with chondrocyte hypertrophy, tissue inflammation [4], and extracellular matrix (ECM) disruption [5]. Articular cartilage vascular ingrowth has been demonstrated to foster tissue calcification, periarticular osteophyte formation, and sprouting of sympa-
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