Meniscus Tear
Eleanor Hayes
Why your meniscus is worth keeping
Meniscus removal accelerates cartilage degeneration; landmark trials found arthroscopic surgery no better than physiotherapy for degenerative tears, the predominant presentation.
London Cartilage Clinic
Insights
Explore expert articles on cartilage care, regenerative treatments, and practical recovery advice from our specialist team.
Explore
Explore
Knee Cartilage Repair
Eleanor Hayes
ChondroFiller injection for knee injury versus wear-and-tear OA
ChondroFiller injection regenerates tissue in focal cartilage defects with intact surrounding borders, but cushions the joint in diffuse wear-and-tear osteoarthritis where those borders are eroded.
ChondroFiller / Liquid Cartilage
Eleanor Hayes
ChondroFiller or Cingal for your knee cartilage
ChondroFiller addresses focal cartilage defects by recruiting the patient's own repair cells into a collagen scaffold; Cingal reduces osteoarthritis pain and stiffness through lubrication and anti-inflammatory effects, without repairing tissue.
ChondroFiller / Liquid Cartilage
Eleanor Hayes
Long-Term Joint Preservation with ChondroFiller Top-Ups
Articular cartilage lacks blood supply and cannot self-repair; structural damage often advances asymptomatically. The ChondroFiller Lifetime Programme intercepts this through annual MRI surveillance and preventative injections every two years, designed to prevent progression to joint replacement.
Cartilage Repair
Eleanor Hayes
Single-treatment ACI as one-stage cartilage repair
Traditional cartilage repair requires two surgeries weeks apart, during which harvested cells undergo dedifferentiation; STACi consolidates the entire process into one sitting by performing laboratory preparation within the operating theatre.
Cartilage Repair
Eleanor Hayes
Why microfracture and ChondroFiller injection outcomes diverge
Microfracture repairs peak at 12–18 months then deteriorate as fibrocartilage fails; ChondroFiller injection improves through year three as a collagen scaffold recruits the patient's own chondrocytes. Three mechanisms explain the divergence: tissue durability, secondary bone damage unique to microfracture, and incompatible patient populations.