One of the most common causes of joint pain is Osteoarthritis (OA). It is one of the leading causes of chronic pain and disability worldwide. The most commonly affected joints are the knees, hips, ankles and hands (wrists, fingers). OA is most common in people over the age of 65.

Diagnosis & Symptoms

Diagnosis of OA is primarily based on symptom presentation, medical history, physical examination of joints and reflexes, as well as an assessment of physical function and ability. X-rays may be helpful as they can show cartilage loss and bone damage and/or spurs. If X-ray results aren’t limited, magnetic resonance imaging (MRI) may be performed. MRI can reveal non-bony damage, such as ligament or connective tissue damage.

The most common symptoms of OA are:

  • Stiffness / tension in the joint that is worse after resting;
  • Limited range of motion/mobility;
  • Clicking / crunching / scraping sounds or sensations in the joint;
  • Swelling (inflammation) within or around the joint;

Symptoms generally progress with age and activity.

What Causes OA?

The underlying cause of OA and symptom progression is multifactorial, depending on the patient and various contributing factors. Previously, it was believed simply to be caused by general mechanical wear and tear of the joints, however, it is now recognised as a degenerative disease of the joints with numerous risk factors.

Image by BruceBlaus (Own work) [CC BY-SA 4.0 (https://creativecommons.org/licenses/by-sa/4.0)], via Wikimedia Commons.

The major contributing factors include:

  • Weight: Research suggests that excess fat tissue produces proinflammatory adipokines (cell-signalling proteins that are secreted by fatty tissue). An excess of these molecules induces inflammation, which can cause joint damage. Increased mechanical loading due to excess weight also contributes to accelerated cartilage breakdown.
  • Genetics: Research has identified numerous genes that may be associated with an increased susceptibility to OA. Primary gene candidates include those coding for collagen and other structural proteins and inflammatory molecules. Single genes alone may not be enough to infer an increased risk of developing OA, however, the interactions between genes and environmental / lifestyle factors, such as obesity and diet, may account for a significant portion of OA risk.
  • Joint Injury & Overuse: Overuse of the joints, injuries and muscular imbalance, all lead to accelerated cartilage breakdown and are also risk factors for OA development. Research shows that this may not simply be due to cartilage damage and increased wear and tear. Increased levels of inflammatory and degradative molecules have been detected in patients with knee injuries, which can give rise to an extra level of joint damage.

Current Treatment Options

Whilst there is no cure for OA, the symptoms are avoidable. There are numerous treatments and management strategies available that aim to alleviate OA associated pain, improve mobility and function, and slow its progression. The effectiveness of treatments differs between patients and depend on the location and grade of OA.

Pharmaceuticals

Over-the-counter analgesic medications include paracetamol, which has specifically demonstrated effectiveness for people with OA, and nonsteroidal anti-inflammatory drugs (NSAIDS), such as ibuprofen. For stronger pain relief, opioid medications (i.e. oxycodone and tramadol) may be prescribed by a physician, however, they are often associated with side effects. Topical analgesics (i.e. NSAIDS or opioids) may provide relief without the systemic side effects associated with oral medications.

Nutraceuticals

Although research is somewhat limited, certain dietary supplements, such as chondroitin, glucosamine and Vitamin D, may help to reduce the progression or symptoms of OA.

Physical Therapy

Exercise is one of the most effective ways to manage OA. While it may be painful, light exercise has actually been shown to reduce pain. Strengthening the muscles around the affected joint can also reduce the pain. Increasing joint flexibility will help to regain motion in the joint. Exercise can also help with weight loss and maintenance. A physiotherapist can develop an individualised active exercise program to help a patient manage their OA. Studies also suggest that aquatic exercise may provide some benefit in terms of pain, disability and quality of life for OA of the knee or hip.

Injections & Surgery

Joint injections (intra-articular), such as corticosteroids and hyaluronic acid, may improve pain and function. There is growing evidence to also support the use of platelet-rich plasma (PRP) and Botox injections.

In cases of severe, refractory OA pain, invasive surgery is an option and includes joint replacement and bone realignment.

Management Strategies

An occupational therapist can assist with reducing the burden of home and work activities by developing ways to reduce the associated stress and pain. Assistive devices are also available to OA patients.


Clinical Trials

Genesis Research Services conducts clinical trials for a range of painful conditions. To view currently recruiting studies or register your interest for future studies, click here or call us on (02) 4985 1860.


 References:

  1. Arthritis Foundation. “Osteoarthritis”. Accessed online 01/08/2017:
    https://www.arthritis.org/about-arthritis/types/osteoarthritis
  2. MOVE muscle, bone & joint health (Arthritis Victoria). “Osteoarthritis”. Accessed online 01/08/2017: https://www.move.org.au/Conditions-and-Symptoms/Osteoarthritis
  3. National Institute of Arthritis and Musculoskeletal and Skin Diseases. “Handout on Health: Osteoarthritis”. May 2015; Accessed online 01/08/2017:
    https://www.niams.nih.gov/Health_Info/Osteoarthritis
  4. PubMed Health. “Osteoarthritis: Overview”. Last updated July 2016; Accessed online 01/08/2017: https://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0072773
  5. Bartels EM, et al. “Aquatic exercise for the treatment of knee and hip osteoarthritis”. Cochrane Database of Systematic Reviews 2016; 23 March.
    https://www.ncbi.nlm.nih.gov/pubmed/27007113
  6. Garne MR, et al. “Osteoarthritis: genes, nature–nurture interaction and the role of leptin”. International Orthopaedics 2013; 37:2499-2505. 
    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3843192/
  7. Goodwin JL, et al. “The use of opioids in the treatment of osteoarthritis: when, why, and how?” Current Rheumatology Reports 2009; 11:5-14.
    https://www.ncbi.nlm.nih.gov/pubmed/19171106
  8. Papathanasiou I et al. “Molecular changes indicative of cartilage degeneration and osteoarthritis development in patients with anterior cruciate ligament injury”. BMC Musculoskeletal Disorders 2016; 17:21.
    https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/26762166/
  9. Rutjes AWS, et al. “Therapeutic ultrasound for osteoarthritis of the knee or hip”. Cochrane Database of Systematic Reviews 2010; 20 January.
    https://www.ncbi.nlm.nih.gov/pubmed/20091539
  10. Singh JA, et al. “Chondroitin for osteoarthritis”. Cochrane Database of Systematic Reviews 2015; 28 January.
    https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/25629804/
  11. Thijssen E, et al. “Obesity and osteoarthritis, more than just wear and tear: pivotal roles for inflamed adipose tissue and dyslipidaemia in obesity-induced osteoarthritis”. Rheumatology 2015; 4:588-600.
    https://www.ncbi.nlm.nih.gov/pubmed/25504962
  12. Image by BruceBlaus (Own work) [CC BY-SA 4.0 (https://creativecommons.org/licenses/by-sa/4.0)], via Wikimedia Commons. https://commons.wikimedia.org/wiki/File:Osteoarthritis.png