Interleukin-1β and methylprednisolone acetate demonstrate differential effects on equine deep digital flexor tendon and navicular bone fibrocartilage cells in vitro.
Authors: Z. Belacic, S. Sullivan, H. Rice, S. Durgam
Journal: American journal of veterinary research
Summary
# Editorial Summary Navicular disease remains one of the most challenging conditions to manage in equine practice, yet the cellular mechanisms underlying how intra-bursal corticosteroid injections affect the affected tissues are poorly understood. Belacic and colleagues examined how interleukin-1β (IL-1β), a key inflammatory cytokine implicated in navicular pathology, and methylprednisolone acetate (MPA)—the gold-standard intra-bursal corticosteroid—influence cells from both the deep digital flexor tendon (DDFT) and navicular bone fibrocartilage (NBF) using in vitro cell cultures from five sound horses. When exposed to IL-1β alone or combined with either 0.05 or 0.5 mg/mL MPA for 24 hours, NBF cells demonstrated significantly greater suppression of extracellular matrix gene expression compared with DDFT cells, indicating they are more vulnerable to inflammatory insult and steroid exposure. Moreover, whilst IL-1β triggered matrix metalloproteinase (MMP)-3 and MMP-13 release—enzymes that degrade cartilage and tendon—these destructive responses were considerably more pronounced in NBF cells, suggesting the navicular fibrocartilage is at higher risk of degenerative changes during inflammatory flares. These findings underscore that current intra-bursal corticosteroid protocols may require refinement to balance anti-inflammatory benefits against potential detrimental effects on navicular bone fibrocartilage biosynthesis, highlighting a critical knowledge gap in dosing regimens for horses with navicular disease.
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Practical Takeaways
- •Intrabursal corticosteroid injections may have differential protective effects on DDFT versus navicular bone tissues; current dosing protocols do not account for these tissue-specific responses
- •NBF cells appear more vulnerable to inflammatory insult than DDFT cells, suggesting navicular disease pathology may require distinct therapeutic approaches from flexor tendon conditions
- •Future corticosteroid regimens for navicular disease need to be refined based on tissue-specific cellular responses to balance inflammation control with preservation of fibrocartilage matrix synthesis
Key Findings
- •Navicular bone fibrocartilage (NBF) cells showed greater susceptibility to IL-1β-mediated extracellular matrix gene expression downregulation compared to DDFT cells
- •IL-1β significantly upregulated MMP-3 concentrations in DDFT cells only, while MMP-13 upregulation was greater in NBF cells
- •Methylprednisolone acetate combined with IL-1β did not prevent the catabolic effects on extracellular matrix gene expression in either cell type
- •Total glycosaminoglycan content changes differed between cell types in response to treatment conditions