CARTILAGE DEFECTS

Orthopaedic clinical problem

Chondrocytes are metabolically active cartilage cells that are responsible for developing, maintaining, and repairing the surrounding extracellular matrix

Cartilage defects can arise from daily wear, acute injury, degenerative conditions, or disease, resulting in pain, inflammation, and impaired joint function

Due to its avascular nature, articular cartilage has low metabolic activity, limited regenerative ability, and minimal self-healing capacity, making it especially difficult to repair

Injury triggers a cascade of biochemical and mechanical events that accelerate degeneration, potentially progressing to osteoarthritis (OA) and ultimately necessitating joint replacement if left untreated

PATHOPHYSIOLOGY

Early diagnosis and intervention with RECARTA can reduce the progression of cartilage defects

Microfracture has been considered the first choice cartilage repair over the last 20 years

LIMITATIONS OF CURRENTLY USED TECHNIQUES

  • 42.1% reoperation rate at 2.63 years

    • fibrocartilage

    • subchondral sclerosis and cysts

    • intralesional osteophytes

    • severe bone marrow edema

  • Failure rates

    • 11 – 27% within the first 5 years

    • 6 – 32% at long-term follow-ups

  • >3.6cm² – predictive of additional surgical intervention in the future

  • Still lack of

    • standardized clinical evaluations

    • rehabilation protocols

    • radiological assessments

Reference: 1. W. Widuchowski, J. Widuchowski, T. Trzaska, Articular cartilage defects: Study of 25,124 knee arthroscopies, The Knee, Volume 14, Issue 3. 2007. 2. Orth P, Gao L, Madry H. Microfracture for cartilage repair in the knee: a systematic review of the contemporary literature. Knee Surg Sports Traumatol Arthrosc. 2020. 3. Weber, Alexander & Locker, Philip & Mayer, Erik & Cvetanovich, Gregory & Tilton, Annemarie & Erickson, Brandon & Yanke, Adam & Cole, Brian. Clinical Outcomes After Microfracture of the Knee: Midterm Follow-up. Orthopaedic Journal of Sports Medicine. 2018.