Abstract
Subchondral bone lesions, as the crucial inducement for accelerating cartilage degeneration, have been considered as the initiating factor and the potential therapeutic target of knee osteoarthritis (KOA). Acupotomy, the biomechanical therapy guided by traditional Chinese meridians theory, alleviates cartilage deterioration by correcting abnormal mechanics. Whether this mechanical effect of acupotomy inhibits KOA subchondral bone lesions is indistinct. This study aimed to investigate the effects of acupotomy on inhibiting subchondral bone resorption and to define the possible mechanism in immobilization-induced KOA rabbits. After KOA modeling, 8 groups of rabbits (4w/6w acupotomy, 4w/6w electroacupuncture, 4w/6w model, and 4w/6w control groups) received the indicated intervention for 3 weeks. Histological and bone histomorphometry analyses revealed that acupotomy prevented both cartilage surface erosion and subchondral bone loss. Further, acupotomy suppressed osteoclast activity and enhanced osteoblast activity in KOA subchondral bone, showing a significantly decreased expression of tartrate-resistant acid phosphatase (TRAP), matrix metalloproteinases-9 (MMP-9), and cathepsin K (Ctsk) and a significantly increased expression of osteocalcin (OCN); this regulation may be mediated by blocking the decrease in osteoprotegerin (OPG) and the increase in NF-κB receptor activated protein ligand (RANKL). These findings indicated that acupotomy inhibited osteoclast activity and promoted osteoblast activity to ameliorate hyperactive subchondral bone resorption and cartilage degeneration in immobilization-induced KOA rabbits, which may be mediated by the OPG/RANKL signaling pathway. Taken together, our results indicate that acupotomy may have therapeutic potential in KOA by restoring the balance between bone formation and bone resorption to attenuate subchondral bone lesions.
Highlights
Cartilage degeneration is the most typical pathological feature of knee osteoarthritis (KOA) [1]; the critical role of subchondral bone lesions in KOA has gradually become an area of focus in recent years [2, 3]
Clinical studies have confirmed that inhibiting subchondral bone lesions can effectively relieve cartilage erosion [8, 9], which implied that subchondral bone was a potential therapeutic target for protecting cartilage and treating KOA
In the 4w model group, the content of proteoglycan decreased in the cartilage, which was manifested by the partial deletion of Safranin O staining
Summary
Cartilage degeneration is the most typical pathological feature of knee osteoarthritis (KOA) [1]; the critical role of subchondral bone lesions in KOA has gradually become an area of focus in recent years [2, 3]. Increasing evidence implies that subchondral bone lesions may be the initiating factor in KOA [4, 5]. In the early-stage KOA, due to the abnormal activation of osteoclasts [11] in the subchondral bone, bone remodeling is mainly characterized by hyperactive bone resorption [12]. Osteoprotegerin (OPG)/NF-κB receptor activated protein ligand (RANKL) is the critical pathway to regulate bone remodeling [13, 14], which is mainly realized by regulating osteoclast activity. OPG can inhibit osteoclast activity by blocking the binding of RANK and RANKL [16]. Studies confirmed that bone resorption can be effectively alleviated by regulating OPG/RANKL pathway [17, 18]
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callMore From: Evidence-based complementary and alternative medicine : eCAM
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
