Fibromyalgia and Osteoarthritis

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Adam Foster

Director at The Fibro Guy

Adam Foster is the founder of The Fibro Guy and one of the leading voices in hypermobility, EDS, and chronic pain rehabilitation. A former Reconnaissance Soldier, he developed chronic pain after an IED blast in Afghanistan and built his approach from the ground up when the medical system had no answers. Since 2009 he has worked with thousands of people across eight countries, drawing on pain neuroscience, motor learning, and sensorimotor rehabilitation. He co-authored "No Pain, No Pain" with trauma psychologist Dr Mairi Harper, directed the documentary "Invisible Monster," and has been featured in Forbes, BBC Radio 4, ITV News, LiveScience, and The Telegraph.

Latest posts by Adam Foster (see all)

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You can have fibromyalgia and osteoarthritis at the same time, and a great many people do, which seems to come as a genuine surprise to most of the people who get told it. Fibromyalgia turns up in those with knee osteoarthritis a great deal more often than it does in the general population, with estimates running anywhere from about one in twenty to more than one in three, depending on where the counting was done and which criteria were used ^[1][2][3]. Going the other way, osteoarthritis is a well recognised travelling companion of fibromyalgia ^[4]. So a second diagnosis landing on top of the first isn’t a contradiction, and it certainly doesn’t mean somebody got the first one wrong.

The question most people actually arrive with though, is whether one makes the other worse. The honest answer is that fibromyalgia does appear to make osteoarthritis hurt more, and to make sleep, mood and function measurably worse alongside it, but it hasn’t been shown to wear the joint itself out any faster ^[1][5]. That’s a distinction worth holding onto, as those are two very different problems arriving as the same complaint, and what’s useful to do about each of them is different.

And the treatment with the strongest evidence behind it for both conditions is, unfortunately, the same treatment, which is exercise, at a dose you can actually repeat ^[6][7]. That’s an annoying answer and we do know it, particularly when it’s been handed to you by somebody who has never had to do it with your joints. But it’s still the answer.

There’s one thing to clear up first though, as the version of osteoarthritis most people get handed, where a joint simply “wears out” like a tyre and the only question left is when it gets replaced, is out of date, and it’s out of date in both directions at once: the joint is doing rather more than wearing out, and the wearing out explains a good deal less of the pain than you’d expect ^[8][9].

What Osteoarthritis Actually Is

Osteoarthritis is a disease of the whole joint rather than a disease of cartilage. The cartilage does thin and the surface does roughen, that part is real enough, but the bone underneath it changes as well, along with the synovium, the capsule, the ligaments and the menisci, and all of that is part of the condition rather than a side effect of it ^[8][9][10].

The part that’s shifted most in the last decade or so is inflammation. Osteoarthritis has been taught for years as degeneration as opposed to inflammation, with rheumatoid arthritis cast as the inflammatory one, and that nice clean split doesn’t really survive contact with the current evidence. Low grade inflammation, particularly in the synovium, is now treated as central to how the condition progresses and to how much it hurts, rather than as something that occasionally flares up on top of the main event ^[10][11][12].

That’s not the same as saying osteoarthritis is rheumatoid arthritis, because it isn’t, and the mechanisms and the drugs are different. But if you’ve been told there’s no inflammation in osteoarthritis, which is a very common thing to be told (we hear that one constantly), that isn’t what the evidence currently says ^[11].

Why It Happens, and Why Wear and Tear Isn’t the Whole Answer

Age is the single biggest risk factor, so that much of the wear and tear story does hold ^[13][14]. What doesn’t follow from it is the inevitability, as getting older loads the dice, it doesn’t deal the hand, and plenty of people reach eighty with joints that never become symptomatic ^[13][15].

What ageing actually does is shift joint tissue out of maintenance and into slow breakdown. Cells stop dividing and start leaking inflammatory signals and enzymes that chew through the matrix around them, repair gets slower, and oxidative stress climbs ^[13][15][16]. That’s a very different picture from a tyre thinning, as a tyre doesn’t have an immune system and doesn’t spend years trying to repair itself badly.

On top of age, a few things genuinely change your odds, and some of them are things you can actually do something about.

– Weight: The largest modifiable risk factor there is, and it works through two routes rather than one, as extra load through the joint and the metabolic signalling that comes with more fat tissue both push in the same direction ^[14][17]. It gets used as a stick far too often, which is a real shame, as that second route is exactly why the effect turns up in hand joints that carry no body weight at all.

– Previous injury and how the joint is loaded: A joint that has been injured, or one that sits slightly off line so a single compartment takes far more load than it was built for, is a joint at considerably higher risk ^[14][18][19]. That one matters most for those with hypermobility, and we’ll come back to it.

– Sex and hormones: Women have close to twice the prevalence of knee and hip osteoarthritis that men do, and the gap gets wider after the menopause ^[14].

– Genetics: A decent chunk of the risk is inherited, with the estimates varying quite a lot depending on which joint you’re asking about ^[14], so it isn’t destiny, but it isn’t nothing either.

– The modern environment: Metabolic changes and diet appear to have pushed osteoarthritis rates above what turns up in prehistoric skeletons, even after age is accounted for, which is pretty awkward for the pure ageing account ^[20].

Globally, the numbers are climbing steeply, driven by a larger, older and heavier population rather than by anything mysterious ^[21], all of which is fairly depressing in aggregate and pretty much useless at the level of one person and one knee.

Why the Scan and the Pain Often Disagree

Two people can walk in with near identical imaging and completely different lives, one limping and on medication, the other having gone for a run this morning and only finding out about their joints at all because they had a scan for something else. Across the evidence as a whole, the match between how bad a joint looks on plain imaging and how much it hurts is poor to moderate at best ^[8][22][23].

Structural changes that look alarming on a report are also extremely common in people who have no pain at all, and they get more common with every decade, which makes “normal for your age” a genuinely accurate phrase rather than a fob off ^[24]. In professional footballers, degenerative changes turn up in the lumbar spine in the large majority of squads that get scanned, with no symptoms attached at all ^[25]. That’s indirect, to be fair, as it’s spines in athletes rather than knees in the average person, but it does point the same way as everything else.

Now, this gets oversold in the opposite direction too, as saying that structure doesn’t matter at all is its own bit of nonsense, and it’s a line we’ve heard in plenty of waiting rooms over the years. Measure more carefully than a single letter grade on a report, or follow the same joint over time rather than comparing one person to another, and some structural features do track with symptoms: joint space narrowing, synovitis, bone marrow lesions and meniscal damage among them ^{[8][26][27][28]}.

So the accurate version is that structure contributes, it just doesn’t dictate. Your scan is one input into how much this hurts, and it’s nowhere near the whole of it.

Where Osteoarthritis Pain Actually Comes From

Cartilage has no nerve supply and no blood supply ^[29][30], so cartilage loss on its own can’t be what hurts, which is a genuinely useful thing to know and almost nobody ever gets told it.

What does hurt is pretty much everything around the cartilage, as those tissues are richly innervated and they respond to both mechanical stress and inflammatory signalling ^[30][31][32].

– The synovium: Immune cells and fibroblasts in an inflamed joint lining release mediators that lower the threshold of the nociceptors sitting in it, so the same movement produces more nociceptive input than it did a year ago ^[29][33].

– The bone under the cartilage: Bone marrow lesions are well supplied with nerves and new blood vessels, and where they sit alongside bone attrition or cysts they associate with knee pain regardless of what the cartilage is doing ^[34]. Part of that link appears to run through synovitis rather than through the bone directly ^[35].

– Osteophytes, capsule and ligaments: Bone spurs are heavily innervated and can pull on the periosteum, and the capsule and ligaments have been known as major sources of joint pain for more than fifty years now ^[31].

– Nerves growing where they shouldn’t be: Channels open between bone and cartilage and carry nerves and vessels into regions that previously had neither, and the density of those fibres tracks with reported pain ^[32].

Then there’s sensitisation, which is where fibromyalgia walks into the room. Peripheral sensitisation means the nociceptors in and around the joint start firing at lower thresholds, so pain becomes more frequent and less tightly tied to what you were doing at the time ^[29][30]. Central sensitisation means the spinal cord and brain amplify what arrives, and it shows up as tenderness at sites well away from the affected joint, as a slower shutting off of pain once it starts, and as weaker descending inhibition ^[36][37][38].

Almost everyone with a long running painful joint has some degree of this, and it’s particularly marked in those whose pain looks wildly out of proportion to their imaging ^[29][39]. It’s also why joint replacement isn’t the clean full stop it gets sold as: most people do get real relief, which tells you the joint was genuinely driving a lot of it, but around one in five are still in pain afterwards, which tells you the joint wasn’t driving all of it ^[32][39].

How Often They Turn Up Together

Fibromyalgia affects somewhere around two to three in every hundred people in the general population ^[3][40]. In those already diagnosed with osteoarthritis, the figures are several times that, and in early knee osteoarthritis in particular, they climb higher still ^[2][41].

The spread in those estimates is wide, and it’s wide for a reason rather than because somebody has been sloppy, as screening tools, formal criteria and specialist assessment don’t agree with each other, and a specialist referral centre sees a very different population from a GP surgery. In routine rheumatology care, a substantial minority of people attending with osteoarthritis screen positive for anxiety, depression or fibromyalgia on a single questionnaire, at rates broadly similar to those seen in rheumatoid arthritis ^[42][43].

The framing you’ll see most often, which is a neat percentage of those with fibromyalgia who also have osteoarthritis, is the less secure of the two directions. The better supported statement runs the other way round, that fibromyalgia and fibromyalgia like symptom patterns are common among those with osteoarthritis, and that osteoarthritis is a recognised comorbidity within fibromyalgia groups ^[1][4][44].

Does Fibromyalgia Make Osteoarthritis Worse

Symptomatically, yes, and fairly consistently so, as with both conditions together, reported pain is higher, sleep is worse, pain related anxiety is greater, depression scores are higher and quality of life is lower than with osteoarthritis on its own ^[1]. Function follows the same pattern, with worse scores on the measures that actually describe getting up the stairs and walking to the shops ^[1].

In hand osteoarthritis the picture repeats: more disability, more catastrophising, and more of the burning and electrical descriptors that suggest a nervous system contribution rather than a purely mechanical one ^[45]. Among those with fibromyalgia, having osteoarthritis as well is associated with higher pain levels, and it interacts with fatigue rather than simply adding to it ^[46].

The mechanism is the amplification we covered above, and in women with knee osteoarthritis, higher fibromyalgia survey scores go with diffuse pressure tenderness both at the knee itself and at body sites nowhere near it, which is exactly what you’d expect if the gain has been turned up centrally, rather than something new having gone wrong in the joint ^[47].

Now, what hasn’t been shown is that fibromyalgia damages the joint any faster. The same pattern turns up where fibromyalgia sits alongside inflammatory arthritis, where it worsens reported burden and disease activity scores without a matching change in what’s happening to the joint structurally ^[5][48]. So the accurate way to hold all of this is that osteoarthritis plus fibromyalgia is a mixed pain state, part peripheral drive from a genuinely affected joint and part central amplification, and the second part isn’t evidence that the first part is imaginary ^[44][49][50].

That matters practically, as the two halves respond to different things, and a plan aimed only at the joint tends to underperform in those who have both.

Where Hypermobility Sits in This

Joint hypermobility is substantially more common in those with fibromyalgia than in those without it, with the individual estimates ranging from under one in ten to roughly two thirds, depending on how hypermobility was assessed ^[51][52]. In a rheumatology setting, those with hypermobility carried a fibromyalgia diagnosis at several times the rate of those who weren’t hypermobile ^[53], and in a specialist Ehlers-Danlos service, well over half carried both labels ^[54].

What nobody has done is follow those with hypermobility forward and check whether they end up with more osteoarthritis. It hasn’t been tested ^[55]. What we have instead is an indirect argument, which is that hypermobility comes with repeated sprains, subluxations and joints that habitually load off centre, and those mechanical insults are established risk factors for osteoarthritis in their own right ^[18][55]. Which is a reason to suspect it rather than a reason to believe it (in our opinion, anyway).

There’s also a measurement problem sitting underneath the whole question, as Beighton scores fall as people age and joints stiffen, so an older group with osteoarthritis will contain people who were hypermobile earlier in life and no longer score that way ^[55]. Check the bendiness only at the end, and you’ll undercount it.

So, the honest summary is a transitive one: hypermobility is overrepresented in fibromyalgia, fibromyalgia is overrepresented in osteoarthritis, and the direct line from hypermobility to osteoarthritis remains untested ^[55][56].

What Actually Helps Both

Exercise is the only treatment without drugs that carries a strong recommendation for fibromyalgia, and it’s core conservative care for knee and hip osteoarthritis as well, so it’s the one thing on this list that earns its place twice ^[6][7][57].

The detail is worth having though, as “do some exercise” is useless advice, and most people have had it shouted at them already. Repeatedly.

– What type: For fibromyalgia, everything improves pain and mood except pure flexibility work, and aerobic and strengthening work additionally improve sleep ^[57]. Resistance training produces the largest reductions in pain, with mind body approaches close behind it ^[58]. For knee osteoarthritis, aerobic and strengthening work both help pain and strength, and water based programmes perform about as well as land based ones overall, so if a pool is what you can access, use the pool ^[7][59][60].

– How much: For fibromyalgia, aerobic work of at least eight weeks, in sessions of roughly an hour, a couple of times a week, without piling up much beyond three hours across the week, is where the pain relief sits ^[61]. Those who actually hit the recommended dose do better on pain, sleep and fatigue than those whose adherence is patchy, which sounds obvious and is worth knowing anyway ^[62].

– The caveat: Responses vary enormously, and exercise that’s too much or badly matched will make fibromyalgia symptoms worse rather than better ^[61]. So it’s a reason to start lower than feels sensible and to build slower than anyone tells you to, rather than a reason to avoid it altogether.

Beyond exercise, cognitive behavioural therapy improves pain coping, sleep and mood in fibromyalgia at a moderate to large effect, and the internet delivered versions do something fairly similar, including for hand osteoarthritis ^[63][57]. Programmes that combine education, exercise and psychological work reduce mobility problems and improve quality of life, with the benefit still present months later ^[64]. Massage and manual therapy give small, short lived improvements in both conditions, which is a real effect and a modest one, so treat it as something that makes a hard fortnight a bit easier rather than something that changes the trajectory ^[57][65]. Education about the condition itself belongs on the list too, and it’s cheap ^[66].

Two things that get recommended constantly for this pairing have nothing behind them, as drinking more water hasn’t been shown to reduce osteoarthritis or fibromyalgia pain, and neither have cold showers. Cold might well feel good on a hot joint for twenty minutes, and that’s a perfectly reasonable thing to want. It just isn’t treatment, and nobody should be building a plan around it.

Then there’s surgery, which is the one area where the evidence is unusually clear. Arthroscopic washout and debridement for degenerative knee disease doesn’t beat a sham operation, and it doesn’t beat properly delivered physical and medical treatment either ^[67][68][69]. So if it’s been offered to you for osteoarthritis rather than for something else specific, that’s a conversation worth having before you agree to it.

What Nobody Knows Yet

The biggest open question is sorting, as osteoarthritis pain comes in at least three flavours, mechanical, inflammatory and centrally amplified, and most people have a mixture of them. Nobody can yet reliably work out which one dominates in a given person, which means treatment matching is still largely trial and error ^[29][39].

Whether fibromyalgia alters the structural course of osteoarthritis over years, rather than just the experience of it, hasn’t been properly settled either way ^[5]. And the hypermobility question remains open, with a plausible mechanism, a suggestive overlap, and nobody having actually gone and looked (surprise, surprise) ^[55].

If you have both, you’re managing a joint and a nervous system at the same time, and a plan aimed at only one of them tends to disappoint. So load the joint at a level you can actually repeat, and treat the sleep as part of the treatment rather than as something to sort out once the pain has settled.

The Fibro Guy

References

[1] Mahgoub, M.Y., Elnady, B.M., Abdelkader, H.S., Abdelhalem, R.A. and Hassan, W.A. (2020) ‘Comorbidity of Fibromyalgia in Primary Knee Osteoarthritis: Potential Impact on Functional Status and Quality of Life’, Open Access Rheumatology: Research and Reviews. https://doi.org/10.2147/oarrr.s252748

[2] Haliloglu, S., Carlioglu, A., Akdeniz, D., Karaaslan, Y. and Kosar, A. (2014) ‘Fibromyalgia in patients with other rheumatic diseases: prevalence and relationship with disease activity’, Rheumatology International. https://doi.org/10.1007/s00296-014-2972-8

[3] Ponce, Y., Rillo, O., Brigante, A., Leonardi, O., Raad, E. and Lunic, M.C. (2022) ‘POS1486-HPR DETECTION OF ASSOCIATED FIBROMYALGIA IN PATIENTS WITH OSTEOARTHRITIS OF THE KNEE ACCORDING TO THE MULTIDIMENSIONAL HEALTH ASSESSMENT QUESTIONNAIRE/ FIBROMYALGIA ASSESSMENT SCREENING TOOLS (MDHAQ/FAST4).’, Annals of the Rheumatic Diseases. https://doi.org/10.1136/annrheumdis-2022-eular.4217