K Murata1, N Kanemura2, T Kokubun3, T Fujino4, Y Morishita4, K Onitsuka4, S Fujiwara4, A Nakajima4, D Shimizu3, K Takayanagi3. 1. Graduate Course of Health and Social Services, Graduate School of Saitama Prefectural University, Saitama, Japan; Department of Physical Therapy, School of Health and Social Services, Saitama Prefectural University, Saitama, Japan. 2. Department of Physical Therapy, School of Health and Social Services, Saitama Prefectural University, Saitama, Japan. Electronic address: kanemura-naohiko@spu.ac.jp. 3. Department of Physical Therapy, School of Health and Social Services, Saitama Prefectural University, Saitama, Japan. 4. Graduate Course of Health and Social Services, Graduate School of Saitama Prefectural University, Saitama, Japan.
Abstract
OBJECTIVE: Joint instability induced by anterior cruciate ligament (ACL) transection is commonly considered as a predisposing factor for osteoarthritis (OA) of the knee; however, the influence of re-stabilization on the protection of articular cartilage is unclear. The aim of this study was to evaluate the effect of joint re-stabilization on articular cartilage using an instability and re-stabilization ACL transection model. DESIGN: To induce different models of joint instability, our laboratory created a controlled abnormal joint movement (CAJM) group and an anterior cruciate ligament transection group (ACL-T). Seventy-five Wistar male rats were randomly assigned to the CAJM (n = 30), ACL-T (n = 30), or no treatment (INTACT) group (n = 15). Cartilage changes were assessed with soft X-ray analysis, histological and immunohistochemistry analysis, and real-time polymerase chain reaction (PCR) analysis at 2, 4, and 12 weeks. RESULTS: Joint instability, as indicated by the difference in anterior displacement between the CAJM and ACL-T groups (P < 0.001), and cartilage degeneration, as evaluated according to the Osteoarthritis Research Society International (OARSI) score, were significantly higher in the ACL-T group than the CAJM group at 12 weeks (P < 0.001). Moreover, joint re-stabilization maintained cartilage structure (thickness [P < 0.001], surface roughness [P < 0.001], and glycosaminoglycan stainability [P < 0.001]) and suppressed tumor necrosis factor-alpha (TNF-α) and caspase-3 at 4 weeks after surgery. CONCLUSION: Re-stabilization of joint instability may suppress inflammatory cytokines, thereby delaying the progression of OA. Joint instability is a substantial contributor to cartilage degeneration.
OBJECTIVE:Joint instability induced by anterior cruciate ligament (ACL) transection is commonly considered as a predisposing factor for osteoarthritis (OA) of the knee; however, the influence of re-stabilization on the protection of articular cartilage is unclear. The aim of this study was to evaluate the effect of joint re-stabilization on articular cartilage using an instability and re-stabilization ACL transection model. DESIGN: To induce different models of joint instability, our laboratory created a controlled abnormal joint movement (CAJM) group and an anterior cruciate ligament transection group (ACL-T). Seventy-five Wistar male rats were randomly assigned to the CAJM (n = 30), ACL-T (n = 30), or no treatment (INTACT) group (n = 15). Cartilage changes were assessed with soft X-ray analysis, histological and immunohistochemistry analysis, and real-time polymerase chain reaction (PCR) analysis at 2, 4, and 12 weeks. RESULTS:Joint instability, as indicated by the difference in anterior displacement between the CAJM and ACL-T groups (P < 0.001), and cartilage degeneration, as evaluated according to the Osteoarthritis Research Society International (OARSI) score, were significantly higher in the ACL-T group than the CAJM group at 12 weeks (P < 0.001). Moreover, joint re-stabilization maintained cartilage structure (thickness [P < 0.001], surface roughness [P < 0.001], and glycosaminoglycan stainability [P < 0.001]) and suppressed tumor necrosis factor-alpha (TNF-α) and caspase-3 at 4 weeks after surgery. CONCLUSION: Re-stabilization of joint instability may suppress inflammatory cytokines, thereby delaying the progression of OA. Joint instability is a substantial contributor to cartilage degeneration.
Authors: Yusuke Hagiwara; Felix Dyrna; Andrew F Kuntz; Douglas J Adams; Nathaniel A Dyment Journal: Ann N Y Acad Sci Date: 2019-10-09 Impact factor: 5.691
Authors: Joao Pedro Garcia; Lizette Utomo; Imke Rudnik-Jansen; Jie Du; Nicolaas P A Zuithoff; Anita Krouwels; Gerjo J V M van Osch; Laura B Creemers Journal: Cells Date: 2021-02-27 Impact factor: 6.600