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Updated: Jun 17, 2026
Standardized Histomorphometric Evaluation of Osteoarthritis in a Surgical Mouse Model
Published on: May 6, 2020
Synovial transcriptomic biomarkers predict structural severity in equine osteochondral fragment-induced experimental
Hannah Chernavsky1,2, Lynn M Pezzanite1,3,2, Steven Dow1,3,2
1Orthopaedic Research Center, Translational Medicine Institute, Department of Clinical Sciences, Colorado State University, Fort Collins, CO.
Objective:
Develop a global joint score (GJS) reflecting equine osteoarthritis (OA) structural severity and identify clinical or molecular parameters predicting disease severity.
Methods:
A retrospective analysis was performed using data from horses (n = 104; 58 females and 46 geldings; 2 to 5 years old) undergoing experimental OA induction via surgical osteochondral fragment creation in the middle carpal joint and high-speed treadmill exercise over 70 days. Longitudinal measures included subjective lameness examinations (lameness, effusion, and flexion), synovial fluid (SF) and serum glycosaminoglycan (GAG), SF prostaglandin E2, and SF cell and synovium gene expression (mRNA sequencing, n = 8). All samples were collected every 14 days except synovium, which was collected on days 0 and 70. Macroscopic and histopathologic data (day 70) were combined creating a GJS characterizing structural severity. Clinical parameters, biochemical markers, and transcriptomic alterations were modeled against the GJS to identify diagnostic methods predicting severity of OA progression.
Results:
Subjective lameness examinations and GAG and PGE2 concentrations did not predict OA severity. In contrast, subsets of genes (46 in SF cells and 8 in synovium) demonstrated high predictive value with GJS, coupled with significant endpoint expression changes.
Conclusions:
Single clinical markers are not strong predictors of disease severity due to the heterogeneity of OA. Gene expression and transcriptomic biomarkers may be more sensitive predictors of disease severity.
Clinical Relevance:
This study provides preliminary evidence toward the identification of target genes and pathways to further elucidate the pathophysiology of early OA and potential therapeutic targets, advancing our understanding of the molecular underpinnings of joint disease.
