Ankle Osteoarthritis.

Area of Science:

• Orthopedics
• Rheumatology
• Molecular Biology

Background:

• Ankle osteoarthritis (OA) is a chronic, progressive joint disease, primarily caused by trauma.
• Post-traumatic ankle OA affects up to 40% of patients within 20 years, especially after bimalleolar or talus fractures.
• Limited cartilage regeneration, poor vascularity, and stem cell scarcity complicate ankle OA treatment.

Purpose of the Study:

• To update current scientific understanding of post-traumatic ankle OA.
• To focus on molecular signaling pathways, senescence, and chondrocyte apoptosis in ankle OA.
• To review epidemiology, pathophysiology, clinical aspects, and therapeutic targets for ankle OA.

Main Methods:

• Literature review of recent scientific evidence on post-traumatic ankle OA.
• Focus on changes in synovia, cartilage, and synovial fluid.
• Analysis of molecular signaling, senescence, and chondrocyte apoptosis.

Main Results:

• Post-traumatic ankle OA risk is high (up to 40% at 20 years), particularly after specific fracture types.
• Molecular pathways involving senescence and chondrocyte apoptosis are critical to OA development.
• Synovial changes, cartilage degradation, and synovial fluid alterations are key pathological features.

Conclusions:

• Effective treatment of ankle OA requires understanding its molecular underpinnings.
• Further research into senescence and apoptosis pathways may reveal novel therapeutic targets.
• Addressing the challenges of cartilage repair is essential for managing post-traumatic ankle OA.