Osteoarthritis (OA) is the most common lifestyle disease in people over the age of 65. More common than high blood pressure and diabetes. For this reason, researchers have been working tirelessly to better understand OA. And some recent discoveries have turned some commonly held beliefs about OA on their head and have big implications for both treatment and prevention of the disease.
Historically, OA has been considered to be the non-inflammatory “wear and tear” arthritis. It was always thought that joints essentially had a used by date. If you used your joint too much, the cartilage would wear out. We now know this to be false, and understand that joints actually need movement and load to be healthy – but I will go into a bit more detail on this later.
The early research on OA often compared it to its cousin, Rheumatoid Arthritis (RA). There are stark differences between the two, particularly in the amount of inflammation they both present with. RA is an auto-immune disease which is characterised by large amounts of inflammation creating red, hot joints with lots of swelling. OA when compared to RA, only ever had minute amounts of inflammation, so inflammation was never thought to play a significant role in the disease. However, recent research has identified many ongoing immune system processes in OA joint, implicating chronic low-grade inflammation as a driver in the onset and progression of the disease.
The Immune System
The immune system is our body’s defence system. Researchers have identified two distinct parts to the immune system. The selective and specialised “Adaptive Immune System”. And the more general and primitive “Innate Immune System”. The adaptive immune system will target specific pathogens or altered body cells, whereas the innate system is charged with the first line defence against foreign bodies and the response to tissue injuries. A degree of innate immune system response including tissue inflammation is normal following small joint overload or injury. But when the inflammatory process fails to completely resolve within the joint and becomes chronic, it can be a catalyst for the OA process.
Several things have been identified by scientists that can stimulate the innate immune system to go on the offensive like this. Among others, obesity, poor (inflammatory) diet and chronic lack of sleep have all been linked to an aggressive innate immune system.
Obesity is one of the leading causes of OA. The fatty cells within the body contain large amounts of inflammatory mediators called adipokines. Levels of adipokines have been associated with OA incidence and severity. The more fatty tissue we have, the more adipokines. This combined with more weight through the load bearing joints can create the perfect storm for OA to develop and progress.
Individuals consuming a diet scoring high on the Dietary Inflammatory Index (DII) have been shown to have a higher prevalence of OA. The DII is a tool that was developed to measure the inflammatory potential of an individuals’ diet. In previous research, higher DII levels have been associated with higher blood serum levels of pro-inflammatory proteins called Interleukin 6 (IL-6) and Tumour Necrosis Factor (TNF). Both catalysts in the OA process if higher levels are maintained over a long period of time.
Sleep deprivation and OA commonly go hand in hand. Historically it was thought that joint pain at night was mainly responsible for insomnia in people with OA. But more recent research has blurred these lines a little. They are now thought to coexist in people with OA creating a vicious cycle, both stimulating each other – sleep deprivation increasing the pain felt with OA, and the increased pain providing more sleepless nights. Research into sleep deprivation as driver in the onset and progression of OA is in its infancy, but early studies are already showing a strong link.
How can we treat or prevent OA?
The discoveries around the inflammatory nature of OA have opened the door to new therapies, and also given researchers insight into why some already well-established therapies might be successful. New therapies targeting inflammation including “Disease Modifying OA Drugs” (DMOADs), and supplements including Curcumin are showing promise in early trials. Improving sleep quality with techniques such as Cognitive Behavioural Therapy (CBT) and meditation are also in the early stages of evaluation, but are showing some benefits for people with sleep disturbance as a co-morbidity. But the strongest evidence is still around a combination of education, exercise and weight loss.
Exercise has the strongest evidence of any intervention currently available for OA. As I noted previously, we now understand joints need movement and load to be healthy. As joint cartilage doesn’t have a blood supply, it actually relies on joint movement and exercise for its health. As we move, joint fluid is pushed in and out of the cartilage making it healthier.
Reduce Levels of inflammatory
Exercise has also been shown to reduce levels of the inflammatory mediators stimulating the innate immune system – reducing pain and the progression of OA. Other benefits of exercise include improved mental health, and improved confidence with movement that science also tells us can reduce the experience of pain with OA.
The benefits of weight loss for OA are twofold. Firstly, losing weight can reduce the load through a weight bearing joint by a substantial margin. Secondly, reduction of the volume of adipokines can reduce overall systemic inflammation in the body. Scientific studies have shown that reducing weight as little as 5-10% can improve symptoms significantly.
The way we think about OA has changed in recent years. Inflammation is now considered to play a large role in the onset and progression of the disease. Reducing inflammatory behaviours, maintaining a healthy weight and exercising regularly can be great ways to reduce pain and slow the progression of OA, but also potentially prevent it from developing.