preprints.org > biology and life sciences > biochemistry and molecular biology > doi: 10.20944/preprints202409.0446.v1

Preprint Brief Report Version 1 This version is not peer-reviewed

Version 1 : Received: 15 August 2024 / Approved: 5 September 2024 / Online: 5 September 2024 (11:02:11 CEST)

Cartilage microfracturation is a surgical technique specifically designed to address chondral defects, which are injuries to the cartilage that covers the ends of bones in joints. These defects can result from traumatic injuries, degenerative conditions such as osteoarthritis, or congenital abnormalities. The primary objective of microfracture surgery is to promote the regeneration of functional cartilage tissue, thereby restoring joint function, alleviating pain, and enhancing mobility. The procedure involves creating small, controlled perforations, or microfractures, in the subchondral bone plate beneath the damaged cartilage. This process, performed with precision to minimize damage to surrounding healthy tissue, penetrates the subchondral bone to reach the bone marrow, which is rich in mesenchymal stem cells (MSCs). MSCs are multipotent cells capable of differentiating into various cell types, including chondrocytes, which are essential for cartilage production. The microfractures provide an access pathway for MSCs, allowing them to migrate from the bone marrow to the defect site. Once at the site, these stem cells differentiate into chondrocytes and initiate the formation of new cartilage tissue. This newly formed tissue helps fill the defect, aiming to restore the smooth surface of the cartilage and improve the joint's structural integrity. Understanding the molecular processes involved in cartilage repair is crucial for optimizing rehabilitation strategies and improving clinical outcomes. These processes include the regulation of various signaling pathways that control stem cell migration, differentiation, and extracellular matrix (ECM) synthesis. Growth factors such as transforming growth factor-beta (TGF-β), bone morphogenetic proteins (BMPs), and fibroblast growth factors (FGFs) play pivotal roles in these pathways, guiding MSCs in their transformation into functional cartilage cells. Additionally, the role of the ECM, composed primarily of collagen type II and proteoglycans like aggrecan, is paramount in providing structural support and biochemical signals. The ECM supports the newly differentiated chondrocytes and helps maintain the cartilage's mechanical properties. Matrix metalloproteinases (MMPs) and their inhibitors, tissue inhibitors of metalloproteinases (TIMPs), are crucial in ECM remodeling, ensuring the balance between synthesis and degradation of the matrix to support tissue repair and integrity. Angiogenesis and vascularization are also critical aspects of the molecular repair process. The initial phase of cartilage repair often includes transient vascularization facilitated by vascular endothelial growth factor (VEGF), ensuring that the newly formed tissue receives adequate nutrients and oxygen. However, as the repair tissue matures, it transitions back to an avascular state characteristic of healthy articular cartilage, which is essential for maintaining its mechanical properties and longevity. Rehabilitation strategies following microfracture surgery are meticulously crafted to facilitate recovery and functional restoration. These strategies include early mobilization techniques, controlled mechanical loading, biological augmentation, nutritional support, and advanced therapeutic modalities. Early mobilization with gentle passive range-of-motion exercises promotes synovial fluid circulation within the joint, preventing adhesions and joint stiffness, and delivering essential nutrients and growth factors. Controlled mechanical loading through gradual weight-bearing activities helps condition the repaired tissue, stimulating chondrocyte proliferation and ECM production while ensuring proper integration and function. Biological augmentation, including platelet-rich plasma (PRP) and hyaluronic acid (HA), supports cartilage repair by enhancing cellular activities and ECM formation. PRP, rich in growth factors, promotes cell proliferation and matrix synthesis, while HA injections improve joint lubrication, reduce pain, and provide a scaffold for new tissue growth. Nutritional support, including amino acids, vitamins, minerals, glucosamine, chondroitin sulfate, and antioxidants, plays a vital role in collagen synthesis and overall cartilage maintenance, protecting chondrocytes from oxidative stress and modulating inflammation. Advanced therapeutic modalities such as low-intensity pulsed ultrasound (LIPUS), pulsed electromagnetic fields (PEMF), photobiomodulation therapy, and cryotherapy offer additional benefits by enhancing chondrocyte activity, reducing inflammation, and promoting ECM production. These modalities work through various molecular mechanisms, such as activating signaling pathways and modulating gene expression, to improve the quality and durability of the repaired cartilage. By comprehensively understanding the molecular and practical aspects of cartilage repair, clinicians can develop more effective treatment plans that optimize cartilage healing and improve patient outcomes. The integration of molecular insights with advanced rehabilitation techniques holds the promise of revolutionizing cartilage repair, offering hope for those suffering from debilitating joint conditions. This review aims to bridge the gap between molecular biology and clinical practice, providing a roadmap for optimizing cartilage repair strategies and ensuring long-term success for patients.

knee joint; cartilage; molecular biology; biochemistry

Biology and Life Sciences, Biochemistry and Molecular Biology

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