Elucidating the Role of Joint Disuse in the Development of Osteoarthritis Following Return to High-Impact Loading
Abstract
Joint unloading via hindlimb suspension is known to activate the tidemark within articular cartilage as well as ligament entheses. Our hypothesis that hind limb suspension in the mouse could be used to model unloading, thus providing a platform to understand how this perturbation can lead to degenerative joint disease. However initial studies failed to demonstrate evidence of tide mark activation may be related to how the histological studies were designed. Recent human clinical data using superimposition of PET and MRI data indicates that earliest abnormalities that precede articular cartilage pathology is mineralization activity in the perichondrial surfaces and the enthesis. Because our sectioning was sagittal through the condyles, most of these regions where this activity is located were not examined. Using the remaining tissue blocks from the experimental animals, frontal sections at increasing depth of the intact femur and tibial were analyzed using the cryohistological workflow. New embedding, staining and imaging processes were developed. With these changes, fluorescent mineralization lines indicative of appositional mineral deposition were readily observed in the articular cartilage, periarticular cartilage and articular cartilage prior to any evidence of the classic markers of cartilage degeneration observed in standard decalcified paraffin embedded tissues.
Document Details
- Document Type
- Technical Report
- Publication Date
- Jun 01, 2019
- Accession Number
- AD1114522
Entities
People
- David W Rowe
Organizations
- University of Connecticut Health Center