What is osteoarthritis?
A joint is made up of two (or more) bones, the ends of which are called subchondral bones. The end of each bone is covered in cartilage, which absorbs mechanical shock and is composed of extracellular matrix (type II collagen and aggrecans: hyaluronic acid + chondroitin). The area where the two bones are closest together is called the joint capsule. This contains the joint cavity, which is filled with synovial fluid. To find out more
Osteoarthritis is a disorder affecting the joints. It most commonly affects the knees, hips, hands and spine. It is estimated that at least 10% of the population and 85% of the elderly population are disabled because of the condition.1 Morning stiffness, joint pain during exercise, and swollen joints are often the first symptoms of this form of joint degeneratiom. To find out more about joint problems
Osteoarthritis involves the gradual and excessive breakdown of cartilage, which can eventually lead to bones rubbing against each other.2 It is a degenerative form of rheumatism. This complex disease also affects the subchondral bones (causing osteophytes and sclerosis, for example), synovial membrane (synovitis), ligaments and muscles.
Many factors can lead to this degeneration, including impact and injury, physical inactivity (undernourishment of immobile joints), malalignment, being overweight, repetitive movements, certain intensive sports, muscle wasting, genetic, metabolic (especially for joints in the hands) and inflammatory factors, or even a vitamin deficiency.
Why is it painful?
In a normal joint, the cartilage enables pain-free movement of the joint by absorbing shock and friction without transmitting them, as it contains no nerve endings. 4 In contrast, the other structures of the joint (bones, ligaments, synovial membrane, etc.) are richly innervated and therefore sensitive to pain. However, the level of pain does not always correlate with the friction caused by cartilage degeneration, as the pain can come from a number of sources: malalignment, metabolic syndrome, bone and cartilage dysfunction, inflammation, or central sensitisation of the nervous system.3 There is therefore a complex interplay between the signals resulting from joint problems, signals from inflammation and the sensitivity of the central nervous system interpreting the signals.4
For example, it is thought that bone marrow lesions may cause microfracture of the subchondral bone, an increase in intraosseous pressure and/or neoinnervation, which could trigger the sensation of pain (nociception) caused by joint problems.4 Moreover, synovial inflammatory molecules may directly activate pain receptors in the joint and increase their sensitivity.4 Lastly, a maladaptation of neural signals to pain, as well as certain psychological and lifestyle factors (e.g. sleep, anxiety) may increase the sensitivity of the central nervous system to pain.4
Diagnosis?
There are various questionnaires to assess joint function (stiffness, capacity for everyday activities) and pain, including the WOMAC index and Lequesne algofunctional index, as well as the visual analogue scale (VAS) for a finer quantification of pain. However, as noted earlier, the perception of pain varies greatly from one person to another and the pain can come from many different sources.
Medical imaging can show the condition of the various parts of a joint, but it remains difficult at present to effectively diagnose the different musculoskeletal disorders.
The structural and clinical signs of osteoarthritis are indeed incredibly varied. It can affect every type of joint tissue (including cartilage, bone, synovial membrane, ligaments, tendons and muscles) and cause varying degrees of inflammation, lesions, bone deterioration, etc.5 For example, some people with osteoarthritis may have substantial cartilage degradation, while others may present primarily with synovial inflammation or severely damaged subchondral bone, or a combination of all of these. These signs may or may not be accompanied by excessively loose tendons, muscle wasting or alignment problems. Other diseases, in particular metabolic or hormonal disorders, may also be present. 5
What are the possible causes?
The causes of osteoarthritis are also incredibly vast and poorly understood.
Ageing shows the strongest correlation with the development of osteoarthritis. Tissue metabolism changes, diminishing the capacity of joint tissue to regenerate.6 This does not, however, imply a causal relationship, as the normal ageing of joints differs from the complex mechanisms related to osteoarthritis.
Normal, everyday use of our joints is not a risk factor for osteoarthritis. As is the case with the brain, using our joints does not mean they wear out. In fact, according to Dr med Erggelet, being sedentary is considered a risk factor for osteoarthritis. Nonetheless, mechanical factors such as excessive loading, repetitive movements or off-axis movements, lack of support or instability of the joint (ligaments), as well as being overweight, can worsen the impact of age-related biochemical changes. Cartilage needs a fine balance in order to withstand strong mechanical forces. Chondrocytes convert these forces into a physiological response and produce fibres of cartilage. An excessive stress (excessive loading) causes chondrocyte death and disturbs the entire biomechanics of cartilage metabolism, resulting in cartilage degradation. This may also cause oxidative stress, which accelerates the degeneration of chondrocytes.6
People who have suffered a traumatic joint injury have an increased risk of developing osteoarthritis a few years later. Genetic predispositions have been shown to distinguish people who will develop osteoarthritis from those who will completely recover from such injuries.6 These predispositions vary greatly between the different manifestations of osteoarthritis (phenotypes) and according to the joint affected. There is no single gene specifically behind this risk, rather it is the combined effect of various genes (related to inflammation, cartilage, bones, etc.) that would produce this genetic predisposition.6
Biochemical and physical changes with osteoarthritis
According to the Osteoarthritis Research Society International (OARSI), the metabolism of joint cells becomes abnormal several decades before symptoms appear. For example, chondrocytes, the cells in cartilage, deteriorate (senescence): their energy-producing organelles (mitochondria) stop functioning optimally, their secretion of molecules changes extensively and the overall microenvironment changes. This produces an imbalance between the synthesis and degradation of molecules in the cartilage and subchondral bone, reducing the regenerative capacity of tissues and promoting the progression of the disease. This metabolic derangement is said to be followed by anatomic and/or physiologic derangements, such as cartilage degradation, bone remodelling, osteophyte formation (bone spurs) and joint inflammation.5 This results in the loss of normal joint function and the appearance of symptoms.5 All parts of the joint can therefore be affected.
Cartilage degradation
It is thought that cartilage degradation is related to remodelling of the extracellular matrix: the fibres (collagen, aggrecans) are cut, chondrocytes are no longer protected and can interact with different molecules, which can alter their development. They will then produce more degradation signals (catabolism) and fewer synthesis signals (anabolism) for organic compounds (e.g. collagen). This leads to degradation, mineralisation and vascularisation of the cartilage (chondropathy).6 The volume of cartilage is reduced, and the cartilage that is left loses its original consistency (elastic, free of blood vessels and nerve endings) and becomes more similar to bone.
Degradation of the adjacent bone part (subchondral bone)
The subchondral bone can also be damaged. Osteophytes (bone proliferation) may appear,6 nerve growth factor levels may increase, possibly in relation to chronic pain,7 and bone metabolism (growth factors) and vascularisation may be disturbed.8 Osteosclerosis of the subchondral bone (decreased mineralisation) often manifests, owing to bone remodelling. This could be due to elevated osteoclast activity (bone resorption) and the presence of certain inflammatory immune cells.9 The interface between cartilage and subchondral bone enables important interactions to take place. In osteoarthritis, the progressive destruction and inflammation of cartilage runs parallel to changes in the underlying bone. However, the precise involvement of these changes in the causation of osteoarthritis remains unclear. 8
Inflammation
Synovial inflammation (synovitis) is not always present, but can often contribute to the pathophysiology and symptoms of osteoarthritis through increased local production of pro-inflammatory cytokines, chemokines and other mediators of joint tissue damage, and immune cell infiltration.5 Inflammation and oxidative stress have been reported to potentially cause the development of osteoarthritis and loss of joint cartilage. Certain inflammatory cytokines, such as TNF‑α and IL-1β, can increase the catabolism (destruction) of the extracellular matrix as well as the cell death of chondrocytes, rendering them unable to produce the fibres to replace the damaged extracellular matrix.10
What can you do about osteoarthritis?
Physical rehabilitation
Rehabilitation is widely recommended as first-line treatment for osteoarthritis, and is often just as effective at reducing the pain as many analgesics, without causing adverse effects. Low impact exercise, such as walking or cycling, resistance training for muscle strengthening or even yoga are often recommended and do not appear to accelerate joint degeneration.4 However, it is generally best to consult a professional to come up with an individualised exercise programme. Physiotherapy and specific exercises adapted to your condition can be particularly effective in overcoming inactivity, teaching you to use the affected joint correctly without overworking it, maintaining its mobility and strengthening the muscles and tendons around it (examples here and here). Certain thermal treatments may also help to alleviate symptoms.
In some advanced cases, doctors may suggest conservative surgery, fitting a prosthesis (partial or total joint replacement), arthroscopic surgery, cartilage transplantation, or osteotomy (bone realignment surgery).
Rethink your lifestyle
The effect of diet, physical activity and lifestyle on osteoarthritis should be taken seriously. It is crucial that patients actively participate and change their behaviour in order to slow the progression of osteoarthritis.2
Psychological and lifestyle factors (e.g. sleep, diet) play an important role in amplifying or attenuating the sensation of pain.4 Meanwhile, the pain and loss of mobility caused by the disease can significantly impact the quality of life and psychological well-being of patients5: nearly 40% of people with osteoarthritis have anxiety or depression, compared to less than 17% in the general population.4
Weight loss is also supported by a number of studies and has been shown to reduce friction, pain, disability of the joint, and inflammation.4 Ideally, weight loss interventions should involve a combination of physical exercise and dietary changes.
In addition, patients with osteoarthritis who make an effort to limit their oxidative stress level (taking vitamin C, vitamin E and omega-3, stopping smoking and drinking alcohol, doing physical activity, losing weight, etc.) have been shown to have an improved quality of life. Free radicals have been linked to chronic inflammation and cartilage destruction.12 Adopting a diet rich in nutrients and including a variety of vegetables is also advised.
Take natural supplements
Certain molecules such as glucosamine, chondroitin, collagen, hyaluronic acid and vitamin D… may help to ease symptoms, limit the progression of joint degeneration and reduce chronic inflammation, pain and oxidative stress.10,11
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- Toulouse, F. de médecine de. L’ARTHROSE.
- Lewis, R. et al. Strategies for optimising musculoskeletal health in the 21 st century. BMC Musculoskeletal Disorders 20, (2019).
- Deveza, L. A., Nelson, A. E. & Loeser, R. F. Phenotypes of osteoarthritis: current state and future implications. Clinical and experimental rheumatology 37, 64–72 (2019).
- Rice, D., McNair, P., Huysmans, E., Letzen, J. & Finan, P. Best Evidence Rehabilitation for Chronic Pain Part 5: Osteoarthritis. Journal of clinical medicine 8, (2019).
- Mobasheri, A. et al. Recent advances in understanding the phenotypes of osteoarthritis. F1000Research 8, 2091 (2019).
- Madry, H., Luyten, F. P. & Facchini, A. Biological aspects of early osteoarthritis. Knee Surgery, Sports Traumatology, Arthroscopy 20, 407–422 (2012).
- Seidel, M. et al. THU0482 HUMAN LUMBAR SPINE FACET JOINT OSTEOARTHRITIS DISPLAYS PREDOMINANT NGF EXPRESSION AND SIGNALING IN CAPSULAR SYNOVIUM AND SUBCHONDRAL BONE MARROW TISSUES INDEPENDENT OF OSTEOARTHRITIS GRADE. in Annals of the Rheumatic Diseases 78, 532.1-532 (BMJ, 2019).
- Findlay, D. M. & Kuliwaba, J. S. Bone-cartilage crosstalk: A conversation for understanding osteoarthritis. Bone Research 4, 1–12 (2016).
- Geurts, J. et al. Elevated marrow inflammatory cells and osteoclasts in subchondral osteosclerosis in human knee osteoarthritis. Journal of Orthopaedic Research 34, 262–269 (2016).
- Kang, Y. H., Lee, H. J., Lee, C. J. & Park, J. S. Natural products as sources of novel drug candidates for the pharmacological management of osteoarthritis: A narrative review. Biomolecules and Therapeutics 27, 503–513 (2019).
- Charlesworth, J., Fitzpatrick, J., Perera, N. K. P. & Orchard, J. Osteoarthritis- a systematic review of long-term safety implications for osteoarthritis of the knee. BMC Musculoskeletal Disorders 20, 151 (2019).
- Lee, J. H. et al. Relationship between oxidative balance score and quality of life in patients with osteoarthritis: Data from the Korea National Health and Nutrition Examination Survey (2014-2015). Medicine (United States) 98, (2019).