The International Association for the Study of Pain (IASP) has previously designated the "Global Year Against Pain in the Joints" to highlight a major health burden. One of the most common causes of joint pain is Osteoarthritis (OA). In fact, 20% of chronic pain worldwide is associated with OA. The most commonly affected joints are the knees, hips, fingers, and toes, with the condition being most prevalent in people over the age of 65.
The symptoms of OA generally progress with age and activity, although the underlying cause of the condition and its exact progression is multifactorial. The most common symptoms include:
Previously, OA was thought simply to be caused by general mechanical wear and tear of the joints. However, it is now recognized as a complex degenerative disease of the joints with numerous risk factors. Major factors contributing to the development of OA include:
Excess weight is the main risk factor second to age. Research suggests that excess fat tissue produces pro-inflammatory adipokines (cell-signaling proteins secreted by fatty tissue). An excess of these molecules induces inflammation, which can cause direct joint damage. Increased mechanical loading due to excess weight also contributes to accelerated cartilage breakdown.
Research has identified numerous genes that may be associated with an increased susceptibility to OA. Primary gene candidates include those coding for collagen, structural proteins, and inflammatory molecules. While single genes alone may not be enough to infer an increased risk, the interactions between genetics and environmental factors, such as obesity, account for a significant portion of OA risk.
Overuse of the joints, prior injuries, and muscular imbalances all lead to accelerated cartilage breakdown. Research shows that this is not simply due to physical wear; increased levels of inflammatory and degradative molecules have been detected in patients with joint and ligament injuries, giving rise to an extra level of localized tissue damage.
Unfortunately, there is no permanent cure for OA. Contrary to popular belief, however, the symptoms of OA are not inevitable. Various medical treatments and management strategies exist that aim to alleviate pain, improve mobility and function, and slow the progression of the disease.
Over-the-counter analgesic medications include paracetamol, which has specifically demonstrated effectiveness for people with OA, and non-steroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen. For stronger pain relief during severe phases, opioid medications may be precisely prescribed by a doctor.
Exercise is one of the most effective ways to manage OA. While it may initially be uncomfortable, light exercise has actually been shown to reduce pain long-term. Strengthening the muscles around the affected joint reduces the structural load, while increasing joint flexibility helps to regain motion. Exercise is also highly beneficial for weight loss and maintenance. A physiotherapist can develop an individualized exercise program to help manage your symptoms.
Injection therapy can help to significantly reduce OA pain. Commonly injected agents include corticosteroids and hyaluronic acid. There is also growing clinical evidence to support the use of Platelet-Rich Plasma (PRP) and targeted Botox injections to settle joint inflammation. In cases of severe, refractory OA pain where conservative treatments have failed, invasive surgery remains an option, including joint replacement and bone realignment.
An occupational therapist can assist with reducing the burden of home and work activities by developing ways to reduce associated joint stress. Additionally, assistive devices are available to support joint stability, and studies suggest that certain dietary supplements, such as chondroitin and Vitamin D, may help support overall joint health.
If you are struggling with chronic joint pain or osteoarthritis, please speak to your General Practitioner about a formal referral to our specialized team. Contact Hunter Pain Specialists on (02) 4985 1800 or visit our official Contact Us page.