Abstract
Osteoarthritis (OA) is the most prevalent joint disease worldwide, making it a major cause of pain and disability. Identified as a chronic and progressive disease, effective treatment at the early stages of OA has become critical to its management. Jintiange (Jtg) capsules are a traditional Chinese medicine produced from multiple organic components of various animal bones and routinely used to treat osteoporosis in China. However, the effect of Jtg on subchondral bone and cartilage degeneration in OA remains unknown. The purpose of the present study was to investigate the biomolecular role and underlying mechanisms of Jtg in OA progression. Herein, we found that Jtg inhibited receptor activator of nuclear factor-κB ligand (RANKL)-induced osteoclast formation and it functions through the NF-κB signaling pathway. Jtg also inhibited chondrocyte apoptosis via reducing the reactive oxygen species concentration in these cells. Moreover, in vivo evaluation revealed that Jtg significantly attenuates subchondral bone remodeling and cartilage destruction in anterior cruciate ligament transection (ACLT) mouse models. Taken together, our data demonstrate that Jtg inhibits osteoclast differentiation in subchondral bone and chondrocyte apoptosis in cartilage, supporting its potential therapeutic value for treating OA.
Highlights
Osteoarthritis (OA), the most common chronic and degenerative joint disease globally, greatly threatens the quality of life of millions of people, especially the elderly
bone marrow macrophages (BMMs) remained viable when treated with Jtg at concentrations ranging from 1.25 to 40 mg/L, and the BMMs were incubated with macrophage colony stimulating factor (M-CSF) (30 ng/ml) and RANKL (50 ng/ml) to induce osteoclast differentiation
MRI revealed that more bone marrow lesions occur in the osteochondral junctions of OA patients which is likely a result of the increased remodeling of the subchondral bone in these joints and acts as a predictor of cartilage degeneration (Maas et al, 2015)
Summary
Osteoarthritis (OA), the most common chronic and degenerative joint disease globally, greatly threatens the quality of life of millions of people, especially the elderly. OA affects approximately 10% of men and 18% of women aged >60 years (Bijlsma et al, 2011; Litwic et al, 2013). Joint stiffness or deformity, and even disability at the end stages are commonly reported in studies from around the world as typical symptoms of OA (Hochberg et al, 2013; Riegger and Brenner, 2020). Existing pharmacotherapies focus on pain relief with no effective disease-modifying effects. Joint replacement surgery is routinely performed to improve joint function for end-stage OA patients, but the economic cost and complications associated with this type of intervention should not be ignored (Arden et al, 2021). There is a growing need to investigate and identify effective early-stage OA treatment schemes targeting underlying pathogenesis
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