Articular cartilage: Why does it need movement?



As clinicians we often see patients with degenerative joints. Part of our advice is to keep active and keep those joints moving. However sometimes we don’t always fully understand the rationale for the advice we give. This blog is all about articular cartilage and why we should continue to encourage patients to ‘keep on moving’.

Let’s start with a brief rundown on the anatomy and physiology of articular cartilage as this provides the basis for understanding the need for movement. As we know, articular cartilage is present on the ends of bones and is responsible for providing resistance to compressive forces, distributing load, and together with synovial fluid, allowing the near frictionless movement of the surfaces of the articulating joint. Cartilage is made up of cells called chondrocytes, which are contained in an extracellular matrix consisting of cross-linked type II collagen fibres. The presence of type IX collagen fibres help to increase strength and stability of the collagen network. Imbedded within the collagen network are aggregating proteoglycans – large macromolecules that are capable of attracting and binding water. When they bind with water the cartilage creates an internal pressure that allows it to resist mechanical loads. Compression forces cause the water to be displaced within the extracelluar matrix, allowing it to spread the load over a greater surface area. In addition, some water is displaced from the surface of the articular cartilage, which provides a lubricating film. When the compressive forces are removed, the water returns to the articular cartilage.

As articular cartilage is avascular, diffusion from the synovial fluid is a major means by which cartilage obtains nutrients. Synovial fluid is the plasma ultrafiltrate produced by the synovial membrane and consists of water and nutrients. The displacement of water in and out of cartilage during loading assists in increasing the rate at which the chondrocytes receive nutrients (Handley, 1995). O’Hara et al (1990) showed that loading and fluid movement may influence the rate at which larger solutes such as growth factors, hormones and enzymes are able to be transported to the cells. They also suggested that loading and movement assists nutrition by increasing production of synovial fluid, and aid in the removal of waste products via the synovial membrane. So in summary, movement is essential for the health of cartilage.

From a practical point of view, the need for movement and loading is clearly demonstrated by seeing what happens to immobilised joints. In patients who have sustained a spinal cord injury, there is progressive atrophy of the articular cartilage over time (Vanwanseele et al 2002). Studies on animals have shown that immobilisation can cause altered proteoglycan synthesis and softening of the cartilage (Vanwanseele et al., 2002). This is due to the detrimental effects immobilisation has on the ability of cartilage to obtain nutrients and stay healthy.

Furthermore, despite the progressive breakdown of articular cartilage in osteoarthritic joints, studies have revealed the beneficial effects of cyclical loading. It has been consistently shown that weight-bearing exercise improves pain and function in patients with osteoarthritis of the knee (Fransen et al 2001, Roddy et al 2005).

The moral of the story is clear – when dealing with patients with articular damage such as arthritis, it is important that appropriate exercise programmes are prescribed in order to reduce disease progression. Complete rest is rarely an appropriate option. While high impact activities may not be the best idea, measured and progressive loading can go a long way to improving pain and function in these patients.


Fransen, M., McConnell, S., & Bell, M. (2001, April 23). Exercise for osteoarthritis of the hip or knee. Cochrane Database of Systematic Reviews, 2001(3)

Garstang, S.V., & Stitik, T.P. (2006). Osteoarthritis: epidemiology, risk factors, and pathophysiology. American Journal of Physical Medicine & Rehabilitation, 85(11 Suppl), S2-11.

Grad, S., Lee, C.R., Wimmer, M.A., & Alini, M. (2006). Chondrocyte gene expression under applied surface motion. Biorheology. 43(3-4), 259-269.

Handley, C.J. (1995). Physiological responses to injury: synovial joint structures. In M. Muluga (Ed.), Sports Physiotherapy: Applied Science and Practice. London: Churchill Livingstone.

Huber, M., Trattnig, S., & Lintner, F. (2000). Anatomy, biochemistry, and physiology of articular cartilage.Investigative Radiology, 35(10), 573-580.

Kerin, A., Patwari, P., Kuettner, K., Cole, A., & Grodzinsky, A. (2002). Molecular basis of osteoarthritis: biomechanical aspects. Cellular & Molecular Life Sciences, 59(1), 27-35.

O’Hara, B.P., Urban, J.P., & Maroudas, A. (1990). Influence of cyclicloading on the nutrition of articular cartilage. Annals of the Rheumatic Diseases, 49(7), 536-539.

Roddy, E., Zhang, W., & Doherty, M. (2005). Aerobic walking or strengthening exercise for osteoarthritis of the knee? A systematic review. Annals of the Rheumatic Diseases, 64(4), 544-548.

Vanwanseele, B., Eckstein, F., Knecht, H., Stussi, E., & Spaepen, A. (2002). Knee cartilage of spinal cord-injured patients displays progressive thinning in the absence of normal joint loading and movement. Arthritis & Rheumatism, 46(8), 2073-2078.

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