Osteoarthritis – Effective Treatment Without Surgery
Osteoarthritis (OA), also known as degenerative arthritis, is the most common type of arthritis affecting about 20% of people worldwide (Coaccioli et al 2022). It is often considered a “wear and tear” disorder resulting in damage to the articular cartilage of a joint, although as we will see this traditional view is simplistic and outdated, causing many people to assume that it is a normal part of aging. Rest assured age per se is not a cause of pain or worn joints!
To assume that nothing can be done about osteoarthritis is also inaccurate. Around 14% of osteoarthritis is caused by trauma (like a fracture into the joint or a ligament rupture) whilst most other causes are considered “unknown” (termed idiopathic or primary OA). Read on and I will debunk some of the myths surrounding this common condition and what the likely causes are for people who develop atraumatic degenerative joint problems.
Fact: OA is more common as we get older.
Fiction: Age is not the cause! If that were true everyone’s joints would all wear out with advancing age, not just 1 or 2 of their joints, or none at all.
If the process of OA involves “wearing out” of articular cartilage in a joint and this process takes years (usually a decade or longer), then of course it is going to be more prevalent in older age groups. This does not mean that age alone is the cause. Consequently,
the attitude “it’s just age, nothing can be done” is inaccurate. Whilst it is true that we are currently unable to regenerate articular cartilage, we can certainly treat many of the underlying factors resulting in pain and as a result alleviate the pain a damaged joint may exhibit. Since many people do not wear out their joints, it is reasonable to consider why their joints appear more robust and what may be different in those who develop degenerative changes.
Fiction: How bad your Xray or MRI looks matches how severe your pain is.
Fact: The severity of your Xray findings is not related to your pain.
As we age there is an increased incidence of degenerative changes on Xray and advanced imaging. For example, one study reports around 20% of American adults (mean age 63yro) have degeneration present in their hip joints on Xray, but only around 4% have any symptoms (Kim et al 2014). Similar findings have been reported in virtually every region of the body.
Not only is it possible to have your joints wearing out without pain, it’s also common!
This begs the question “what triggers painless degeneration to become painful” and thus be diagnosed as OA? This question is even more pertinent given that the traditional view of OA is a condition involving articular cartilage – except that articular cartilage is not innervated! This means no nerves report sensation from the cartilage that is damaged… Again, why do you have pain if it can’t be coming from the cartilage itself?
One of the explanations for pain in osteoarthritis is that is a condition involving more than just articular cartilage. The modern view of OA it is that of a complex multifactorial condition involving inflammatory and metabolic factors causing damage to the entire joint, which includes not just the articular cartilage, but also the bone, the synovium (the inner capsular lining that secretes lubricating fluid into the joint), the nerves and the associated muscles and tendons (Coaccioli et al 2022). Features of an osteoarthritic joint include:
Chronic low-grade inflammation, which shifts the metabolism of the joint towards catabolism (breakdown of tissues) and may result in pain arising from the soft tissues such as the synovium.
Neurogenic inflammation (a process in which the nerves supplying the joint secrete inflammatory mediators) which, amongst other effects, adds to joint inflammation and pain, activates the immune system and leads to death of cartilage cells.
Inflammation and pain activate the sympathetic nervous system, which can alter pain perception, and alter other autonomic functions such as heart rate, vascular tone (blood flow) and blood pressure (Pongratz and Struab 2014).
As OA progresses an ingrowth of new blood vessels accompanied by nerves occurs in the bone immediately under the cartilage (“subchondral bone”) (Grassel and Muschter 2017), which results in subchondral bone becoming more sensitive and a significant pain generator in OA.
Further bone changes include the formation of spurs which develop at the edges of the joint that over time may cause symptoms including stiffness, and significant damage in the subchondral bone which has a very rich nerve supply.
The blood supply to the bones appears important in OA. Bone is a living and dynamic tissue and adapts according to the loads placed upon it. It requires the nerves and blood vessels that supply the bone to function properly if it is to adapt, for example to cope with increasing load should you start a new sport like running or strength training. If the blood flow to the ends of the bones which form a joint (i.e. subchondral bone) is impaired, there will be a reduced ability for the subchondral bone to adapt to load. This leads to more load being placed on the articular cartilage, resulting in the premature cartilage wear and tear along with the bone changes observed in OA. Chronically reduced blood flow to bone has a significant impact on articular cartilage metabolism since cartilage relies in large part on subchondral bone for its nutrition.
Articular cartilage is both avascular (meaning no blood supply), and as we have already observed it is also aneural – a unique tissue!.
Both impaired venous drainage and arterial inflow have been reported in osteoarthritic bone (Findlay 2007) which suggests that arthritic joints are less capable of repairing damage and adapting to the loads placed upon them.
If impaired blood flow is involved in OA, this will have significant deleterious effects on the joint over a prolonged period. Consequently, it should come as no surprise that by the time a diagnosis of OA is made, there are already considerable degenerative changes and the start of deformity in the joint. In other words, advanced structural findings and joint disease are already present before significant pain begins that causes the person to seek treatment (Felson & Hodgson 2014). The average age of diagnosis is typically around 50yro (MacDonald et al 2014). For those experiencing symptoms before diagnosis the average time of symptoms was almost 8yrs! Part of this delay may be the mistaken assumption that pain is simply part of aging which can lead to an acceptance of symptoms and no treatment. In some studies, the patients’ doctors also viewed OA as part of aging – it’s NOT!
All treatments are more effective if care is sought prior to significant joint deformity – so consider a “wellness consult” with your physio several times per year to check that everything is functioning properly and try to prevent significant joint damage from happening.
How can we manage OA?
I say manage as cure would theoretically involve regeneration of permanently damaged tissues which is not something we can currently do. However, because so many factors contribute to OA, we can address many of these based on what is present in each individual.
At Pain Solutions Queensland, David uses a manual therapy approach known as Fascial Counterstrain which enables the dysfunction in the multiple systems involved in OA to be addressed. This includes sympathetic and sensory nerve dysfunction, dysfunction in the lymphatic – venous drainage of the joint, arterial blood flow to bone and the surrounding tissues including muscles, and muscle and ligamentous dysfunction.
You might be wondering “is my joint too far gone to benefit?”.
The short and only realistic answer is simply to treat it conservatively and see if your symptoms, particularly pain, reduce or resolve. It is a pragmatic and almost universal approach recommended by Physiotherapists and Surgeons alike prior to considering surgery. With excellent treatment, which can also include muscle strengthening and cardiovascular fitness work (Semanik et al 2012), patients frequently no longer require regular pain killers or anti-inflammatories despite joint damage.
Remember that your Xray does not correlate with pain, so the aim of treatment is more about addressing the reasons for your pain and improving your function rather than trying to change an Xray image.
If the dysfunction is removed and symptoms remain unchanged then you might require more aggressive medical or surgical intervention.
It is important to note that medications do nothing to change the underlying risk factors / causes and simply mask symptoms. Around 40% of people manage their pain using medication (MacDonald et al 2014) and only around 20% had consulted a Physiotherapist – the very professional who is most likely to help them! Many do nothing which inevitably leads to further joint deterioration and surgery.
If you have symptoms such as a sore joint, a family history of osteoarthritis, or would like to prevent symptoms from recurring or worsening, consider a consult today.
Coaccioli S et al (2022): Osteoarthritis: New Insight on Its Pathophysiology. J. Clin. Med. 11: 6013.
Felson DT et al (1992): Weight loss reduces the risk for symptomatic knee osteoarthritis in women. The Framingham Study. Ann Intern Med 116(7):535–539.
Felson DT & Hodgson R (2014): Identifying and Treating Pre-Clinical and Early Osteoarthritis. Rheum Dis Clin North Am. 40(4): 699–710.
Findlay DM (2007): Vascular pathology and osteoarthritis. Rheum 46:1763-1768.
Grassel S and Muschter D (2017): Peripheral Nerve Fibers and Their Neurotransmitters in Osteoarthritis Pathology. Int. J. Mol. Sci. 18, 931.
Kim C et al (2014): Prevalence of Radiographic and Symptomatic Hip Osteoarthritis in an urban US Community: the Framingham Osteoarthritis Study. Arthritis Rheumatol. 66: 3013–3017.
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Pongratz C and Struab RH (2014): The sympathetic nervous response in inflammation. Arthritis Research & Therapy 16:504.
Semanik P et al (2012): Aerobic Activity in Prevention & Symptom Control of Osteoarthritis. Phys Med & Rehab 4:S37-44.
Sun Q et al (2022): Peripheral nerves in the tibial subchondral bone. The role of pain and homeostasis in osteoarthritis. Bone J Res 11:439.