Sensory nerves only temporarily protect the unstable canine knee joint from osteoarthritis. evidence that sensory nerves reprogram the central nervous system after cruciate ligament transection

Authors

  • B. L. O'connor PhD,

    Corresponding author
    1. Professor of Anatomy, Indiana University School of Medicine
    2. Department of Anatomy and the Rheumatology Division, Indiana University School of Medicine, the Indiana University Multipurpose Arthritis and Musculoskeletal Disease Center, and the Indiana University Specialized Center of Research in Osteoarthritis, Indianapolis.
    • Department of Anatomy, Indiana University School of Medicine, 635 Barnhill Drive, Indianapolis, IN 46202–5120
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  • D. M. Visco PhD,

    1. Visiting Assistant Professor, Department of Anatomy, Indiana University School of Medicine (current address: Miles Inc., Institute for Bone and Cartilage Metabolism, 400 Morgan Lane, West Haven, CT 06516)
    2. Department of Anatomy and the Rheumatology Division, Indiana University School of Medicine, the Indiana University Multipurpose Arthritis and Musculoskeletal Disease Center, and the Indiana University Specialized Center of Research in Osteoarthritis, Indianapolis.
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  • K. D. Brandt MD,

    1. Professor of Medicine and Head, Rheumatology Division, Indiana University School of Medicine; Director, Indiana University Multipurpose Arthritis and Musculoskeletal Disease Center; and Director, Indiana University Specialized Center of Research in Osteoarthritis
    2. Department of Anatomy and the Rheumatology Division, Indiana University School of Medicine, the Indiana University Multipurpose Arthritis and Musculoskeletal Disease Center, and the Indiana University Specialized Center of Research in Osteoarthritis, Indianapolis.
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  • M. Albrecht BS,

    1. Rheumatology Division, Indiana University School of Medicine
    2. Department of Anatomy and the Rheumatology Division, Indiana University School of Medicine, the Indiana University Multipurpose Arthritis and Musculoskeletal Disease Center, and the Indiana University Specialized Center of Research in Osteoarthritis, Indianapolis.
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  • A. B. O'connor BA

    1. Department of Anatomy, Indiana University School of Medicine.
    2. Department of Anatomy and the Rheumatology Division, Indiana University School of Medicine, the Indiana University Multipurpose Arthritis and Musculoskeletal Disease Center, and the Indiana University Specialized Center of Research in Osteoarthritis, Indianapolis.
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Abstract

Objective. The slow rate at which articular cartilage degrades in dogs after transection of the anterior cruciate ligament (ACLT) has been attributed to capsular thickening and buttressing by osteophytes. We investigated the roles of the peripheral and central nervous systems in protecting knee joints with chronic ACL deficiency from breakdown.

Methods. Five groups of dogs were studied; all were killed 72 weeks after left knee surgery. Group A had ACLT, group B had ACLT followed 52 weeks later by ipsilateral L4–S1 dorsal root ganglionectomy (DRG), group C had DRG followed 2 weeks later by ACLT, group D had sham DRG followed 2 weeks later by ACLT, and group E had DRG followed 2 weeks later by sham ACLT.

Results. Group E dogs did not develop knee pathology. All cruciate-deficient knees were lax at the end of the study. The osteoarthritis (OA) that developed in groups A, B, and D was comparable (P > 0.05), and was significantly greater than that in group E (P < 0.05). Group C developed much more severe OA than any of the other groups (P < 0.05).

Conclusion. Ipsilateral sensory input is temporarily important in protecting the unstable joint from rapid breakdown. Over time, the central nervous system apparently acquires the ability to protect the unstable joint without continued ipsilateral sensory input.

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