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Osteoarthritis Cartilage. 2017 Feb;25(2):297-308. doi: 10.1016/j.joca.2016.10.011. Epub 2016 Oct 15.

Controlling joint instability delays the degeneration of articular cartilage in a rat model.

Author information

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.

KEYWORDS:

Articular cartilage; Caspase-3; Joint instability; Osteoarthritis; Tumor necrosis factor alpha

PMID:
27756697
DOI:
10.1016/j.joca.2016.10.011
[Indexed for MEDLINE]
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