The effects of systemic ozone application and hyperbaric oxygen therapy on knee osteoarthritis: an experimental study in
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ORIGINAL PAPER
The effects of systemic ozone application and hyperbaric oxygen therapy on knee osteoarthritis: an experimental study in rats Onur Yılmaz 1
&
Ali Bilge 1
&
H. Yener Erken 1
&
Tolgahan Kuru 1
Received: 29 June 2020 / Accepted: 3 November 2020 # SICOT aisbl 2020
Abstract Objective To evaluate the effects of systemic medical ozone (O3) application and hyperbaric oxygen (HBO) therapy on surgically induced knee osteoarthritis (OA) in a rat model. Materials and methods We performed anterior cruciate ligament transection (ACLT) in order to create experimental OA in the right knees of 27 male rats. The left knee joints of all rats were sham-operated without ACLT as the negative control group. The rats were randomly assigned into three groups: (1) control group, which received no treatment; (2) O3 group, which received intraperitoneal 30 μg medical O3; (3) HBO group, which received HBO therapy for 60 minutes twice a day. We sacrificed the rats on the tenth week after the operation. We evaluated the degree of OA using Mankin scores. Results As a result of histopathological examination, the mean Mankin scores in the right knees with ACLT were 8.17 ± 2.12 in the control group, 6.22 ± 1.56 in the HBO group, and 4.72 ± 1.30 in the O3 group. The differences between the O3 group and the HBO group and the O3 group and the control group were found to be statistically significant (p 0.001, p 0.039, respectively). There was no difference between the HBO group and the control group (p 0.086). Conclusions The results of the present study show that systemic medical O3 application was more effective than HBO therapy and may reduce development of cartilage damage and prevent OA formation. Keywords Hyperbaric Oxygen . Osteoarthritis . Ozone
Introduction Osteoarthritis (OA) is a degenerative joint disease characterized by progressive cartilage degeneration, subchondral bone changes, osteophyte formation, and low-grade synovitis. The main physiopathology of OA is a dynamic process which is a
Level of evidence: 2 * Onur Yılmaz [email protected] Ali Bilge [email protected] H. Yener Erken [email protected] Tolgahan Kuru [email protected] 1
Faculty of Medicine, Orthopedics and Traumatology, Çanakkale Onsekiz Mart University, Canakkale, Turkey
result of disruption of the normal balance between destruction and construction of the joint cartilage and the subchondral bone [1, 2]. Changes in the articular cartilage occur as a consequence of this process. Additionally, all joint-related tissues such as subchondral and metaphyseal bone, synovium, ligaments, joint capsule, and joint-related muscles are affected by joint degeneration [1, 2]. Many proinflammatory mediators are released in the pathogenesis of OA including reactive oxygen species (ROS), such as nitric oxide (NO) and hydrogen peroxide (H2O2) [3]. The development and progression of OA are associated with constant exposure to oxidants, as in other degenerative diseases [3]. NO production in the early phase of OA can lead to chondrocyte apoptosis. B
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