I am a postgraduate researcher at the University of Leeds. I have completed my master's degree in the Erasmus Tribos program at the University of Leeds, University of Ljubljana, and University of Coimbra and my bachelor's degree in Mechanical Engineering from VTU in NMIT, India. I am an editor and social networking manager at TriboNet. I have a YouTube channel called Tribo Geek where I upload videos on travel, research life, and topics for master's and PhD students.
Cartilage Lubrication
Cartilage degeneration is due to osteoarthritis (OA) which is commonly seen in aging populations. This degeneration occurs due to the deterioration of the mechanical and tribological properties of articular cartilage (AC), primarily caused by lubrication failure. Understanding the causes of these failures and finding solutions could have significant economic and societal benefits, improving quality of life.
Figure 1. A schematic illustration of the zones of healthy and OA cartilage. In OA, the AC undergoes structural changes resulting in the loss of its mechanical and tribological properties.
Effectively addressing cartilage degeneration, especially in OA, requires a deep understanding of the lubrication process within AC. The frictional properties of AC largely rely on proper lubrication, but pathological changes in synovial joints make the AC surface softer and more permeable, disrupting its natural self-lubricating abilities. These changes, influenced by joint mechanics and aging, initially hinder joint lubrication, causing pain. Without proper medical treatments this deterioration worsens, eventually leading to the complete breakdown of AC and severe joint dysfunction, often requiring surgery. Mechanical stresses often initiates this degeneration, leading to surface damage like microcracks and peeling of the AC’s outer layer. Moreover, the infiltration of synovial fluid enzymes into the AC can degrade its matrix, softening the tissue and contributing to OA. These disruptions not only affect joint lubrication but also interfere with the AC’s nutritional pathways by compromising its health and function. Both the mechanical and physiological roles of AC are essential for proper lubrication, but these functions are often impaired, undermining the cartilage’s self-lubricating capabilities.
Figure 2. The human gait cycle, with the possible lubrication mechanism at the cartilage interface to support the load and the arrow shows the movement of fluid
Applying classical lubrication theories to synovial joints reveals that no single theory can fully explain their complex tribological behavior. This complexity arises from the biological nature of synovial joints, which respond differently to varying velocities, loads, and motions. It is clear that synovial joints rely on a combination of multiple lubrication mechanisms rather than just one. However, in OA, where the AC surface is damaged, the joint’s normal functioning is disrupted, often leading to a dependence on only one or two lubrication mechanisms due to physical limitations.
Friction at the AC interface is primarily governed by lubrication, which is sensitive to changes in forces and relative velocities over time. As loads increase, the ability of interstitial fluid to support the joint decreases, causing the solid extracellular matrix to bear most of the compressive and frictional loads. In such cases, boundary lubrication—focused on solid–solid interactions—becomes crucial. However, in OA, initial cartilage damage leads to surface irregularities, matrix breakdown, and progressive wear, as classified in the K-L grading system. This damage intensifies from grade 1 to 4, negatively affecting lubrication properties. The reduced effectiveness of interstitial fluid lubrication forces the joint to rely more on boundary lubrication. Understanding the role of synovial fluid components like hyaluronic acid, lubricin, and phospholipids in boundary lubrication is essential for developing therapies to enhance AC lubrication. Such insights are crucial for identifying treatments that can help restore joint function in the early stages of OA.
To understand these lubrication mechanisms in detail, check the reference
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