How Bone and Cartilage Changes Lead to Osteoarthritis

This article explores three subchondral mineralized tissues - calcified cartilage, subchondral cortical bone, and subchondral trabecular bone - and their rate of progression of Osteoarthritis (OA). Burr hypothesized that the changes in the bone’s thickness and density has a direct correlation in the development of OA. Burr aims to learn how the tissues affect the function of the joints; how cartilage is broken down; and solutions for slowing down OA progression. His research highlights the importance of finding treatments and therapies to treat mineralized tissues and implement early preventative measures to slow the development of OA; develop methods for treating OA; and solutions for altering bone and cartilage properties.

Figure 1 shows the density of minerals changes on the calcified cartilages while monitoring the health of the calcified cartilage, subchondral cortical bone, and subchondral trabecular bone. Micro-CT scanners measure the density, the health of affected tissues, and mineralization of the tissues, while maintaining the health and conditions of the joints. The figure shows the calcified cartilage and a higher mineral density on the subchondral bone showing that the increase in mineral density adds stiffness to the joints and cartilage deterioration, evidencing that mineral density does contribute to OA’s progression and does lead to the morphology of various tissues within the joint.

Figure 2 shows two scenarios of a hip joint. On the left, is a healthy hip joint that has smooth cartilage that acts like a cushion between the bones, allowing movement without pain. In contrast, the X Ray on the left is an arthritic hip joint that has worn-down cartilage, joint space narrowing, and calcified subchondral cortical bone. This means the bones (femoral head and acetabulum) rub against each other, causing pain and swelling. This wear and tear make it hard to move your hip and can lead to stiffness and discomfort during everyday activities. Over time, the joint may also develop bony growths, making the situation worse and increasing the pain.

Figure 6 shows an experiment called impulsive loading model to see the effects of applying weight (loading) to weight bearing joints and what it does to articular cartilage. It turns out, after applying 1.5 times the body of weight of the rabbit for 40 minutes/day, 5 times a week for 3 to 9 weeks will result in complete cartilage loss within 6-9 months even after the load is no longer applied. What happens is the articular cartilage gets calcified, and the tidemark rides up into it making the cartilage thin and eventually eroding it completely.

Osteoarthrosis is a condition where the cartilage that cushions your joints gradually begins to wear down. This leads to changes in the bone under the cartilage (called subchondral cortical bone), the cartilage itself, which can become thickened and calcified. Normal cartilage is not supposed to be calcified; rather it has the ability to absorb shock. As the cartilage breaks down, the bones may start to rub against each other, causing pain, stiffness, and swelling in the affected joint. Inflammatory processes may also occur, causing further damage and discomfort. Many experiments have been done to show that if we apply excessive stress to our load bearing joints, they begin to undergo this condition which progresses and cannot be reversed.

Burr, D.B. (2004) Anatomy and physiology of the mineralized tissues: Role in the pathogenesis

of osteoarthritis. International Cartilage Repair Society., 12, S20-S30. 1016/j.joca.2003.09.016