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Old houses have creaky doors, and old bodies have creaky joints. Both are caused by the degradation of the joints. With doors, the lubrication from the hinges may have degraded, or the hinge may be out of alignment, causing the grinding of metal on metal. Our joints, including knees, are similar. The joints degrade, often from misalignment, causing pain and deformation. Unfortunately, we can’t pick up a replacement knee at the local hardware store. The most common condition causing joint degradation is osteoarthritis (OA). It affects around 20% of the global population, 500 million people. 

At its most basic, osteoarthritis is when joints start breaking down. It can affect different joints, but the knees are the most likely to be affected. Cartilage, the strong and flexible tissue that protects your joints and bones, breaks down in osteoarthritis. This causes joint pain, swelling, and loss of function (including range of motion) for the affected joint and may exacerbate comorbidities like diabetes and heart trouble. Women are more likely than men to have osteoarthritis and tend to have more severe symptoms. One major risk factor is obesity, which puts extra stress on joints like the knees and hips. They say age is just a number, but it is also a significant risk factor for OA. The risk of osteoarthritis peaks in a person’s ’60s. The incidence of osteoarthritis has more than doubled in the last 30 years, largely due to the aging global population. A big danger of OA is physical damage caused to the joint affected. This is called a biomechanical abnormality and could be due to a joint that is misaligned or has suffered prolonged abuse. Other risk factors for developing OA include metabolic syndrome, genetics, and trauma, such as torn ligaments.

So what causes osteoarthritis? A lot of things! Cartilage is broken down, but many things may cause this. Outside of the joint, changes in bone, ligament, and muscle can cause stress or degradation. Inside the joint, inflammation, and cell death can lead to failure of the support structures. Inside joints are chondrocytes, the only type of cell in healthy cartilage. They normally spend their whole lives building and maintaining cartilage. They are so dedicated to their job that they become embedded in the structure of cartilage and die in place. With osteoarthritis, stressors (including the risk factors above) can cause chondrocytes to lament the poor work/life balance and start acting irrationally. Some chondrocytes degrade and stop supporting the cartilage (often by dying), and some go into overdrive, becoming larger and further destabilizing our cartilage structure. This causes the cartilage to shrink, and bones can start grinding against each other resulting in joint degradation. This is very painful and can reduce the quality of life dramatically.

What can be done? One of the most important steps is to stop biomechanical abnormalities. Physiotherapy may help fix misalignments. Weight loss, lifestyle changes, and assistive walking devices can help reduce stress on joints. Surgery may be needed to replace or rebuild joints. Unfortunately, there are no approved medications that can cure osteoarthritis. Some anti-inflammatory medications may provide some relief, and are often prescribed. Luckily, the future is looking bright. Researchers are looking at new ways to target osteoarthritis, including next-generation anti-inflammatory medications, metabolic therapies, and even therapies that may rebuild cartilage through medication! In the future, we might not need to pick up a new knee at the hardware store, we might be able to build a new one on-site!

Staff Writer / Editor Benton Lowey-Ball, BS, BFA

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References:

Goldring, M. B., & Otero, M. (2011). Inflammation in osteoarthritis. Current opinion in rheumatology, 23(5), 471. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3937875/

Gu, Y. T., Chen, J., Meng, Z. L., Ge, W. Y., Bian, Y. Y., Cheng, S. W., … & Peng, L. (2017). Research progress on osteoarthritis treatment mechanisms. Biomedicine & Pharmacotherapy, 93, 1246-1252. https://doi.org/10.1016/j.biopha.2017.07.034

He, Y., Li, Z., Alexander, P. G., Ocasio-Nieves, B. D., Yocum, L., Lin, H., & Tuan, R. S. (2020). Pathogenesis of osteoarthritis: risk factors, regulatory pathways in chondrocytes, and experimental models. Biology, 9(8), 194. https://www.mdpi.com/2079-7737/9/8/194

Poole, A. R., Guilak, F., & Abramson, S. B. (2007). Etiopathogenesis of osteoarthritis. Osteoarthritis: diagnosis and medical/surgical management, 4, 27-49. https://www.sciencedirect.com/science/article/abs/pii/S0025712508001223?via%3Dihub

Long, H., Liu, Q., Yin, H., Wang, K., Diao, N., Zhang, Y., … & Guo, A. (2022). Prevalence trends of site‐specific osteoarthritis from 1990 to 2019: findings from the Global Burden of Disease Study 2019. Arthritis & Rheumatology, 74(7), 1172-1183. https://doi.org/10.1002/art.42089