IT’S time GPs threw out the old paradigm of osteoarthritis being a degenerative, “wear and tear” disease of old age – the reality is much more complex and nuanced, says expert Flavia Cicuttini.
Professor Cicuttini, head of the Rheumatology Unit at The Alfred Hospital in Melbourne, and head of Monash University’s Musculoskeletal Unit, has coauthored an editorial published in today’s MJA on the dynamics of osteoarthritis (OA), obesity and inflammation.
“For many years we’ve known that obesity was a risk factor for hand osteoarthritis. Given that we don’t walk on our hands then it really begs the question – can it just be simply loading,” Professor Cicuttini told MJA InSight.
“Many medical students are still taught to think of osteoarthritis as wear and tear. It’s much more complex than [that]. That is partly why we are struggling to come up with treatments.
“OA is the end result of a lot of different pathways.”
While this information was “old hat” to OA specialists and researchers, the message had not been getting through to GPs, she said.
“There are still [some messages] that haven’t seeped down to medical school training and even specialist rheumatology training.
“First of all, OA is not one disease. Even knee OA and hip OA are different diseases driven by different causes – it’s not going to be one size fits all.
“Second, OA is not wear and tear. It’s a heterogeneous group of diseases.
“[Third], obesity does not cause OA simply through loading.
“A person who is 20kg overweight is worse off than someone who you ask to walk around carrying 20kg of concrete for 5 years,” Professor Cicuttini said.
“The concrete just loads [the joints] but the fat is actually metabolically active.”
Better technology, medical resonance imaging for example, has allowed researchers to see that increased weight was associated with early articular cartilage damage, well before symptoms developed.
Body composition was also a vital marker of pre-clinical OA, Professor Cicuttini said.
“Two people can have the same body mass index but one can largely be muscle and one can largely be fat,” she said. “When we started to look at body composition, we found that [the development of OA] was being driven by the amount of fat that person was carrying.
“That raised the question – is it just loading or is it meta-inflammation?”
It was a mistake to think of fat as an inert substance, Professor Cicuttini said.
“It is actually an endocrine organ producing lots of nasty chemicals.
“The whole picture that is emerging is that obesity damages joints, particularly weight-bearing joints, through both loading and metabolically driven inflammation.”
The implications for treatment of OA were profound, Professor Cicuttini said.
“It highlights the importance of targeting obesity early in life. A lot of these changes are occurring very early in people’s lives. In terms of prevention and trying to deal with these diseases, we are going to need to target the prevention of weight gain much earlier.
“Fairly relentlessly as a community, we’re putting on weight – about 0.7kg each a year.”
Related: MJA — Osteoarthritis — the forgotten obesity-related epidemic with worse to come
Related: MJA InSight — Rob Moodie: The fat fight
Professor Cicuttini said the emphasis should be less on massive weight loss – “we’re not very good at that” – and more on the prevention of weight gain.
“It’s certainly more achievable than suddenly trying to lose weight.”
New treatments were also the focus of a lot of research, she said, including different mechanisms for reducing inflammation.
“You could argue that OA is one of the last frontiers of a big disease, with no disease modifications.”
Professor Cicuttini said there were some “very nice” trials being done on treatments for OA, including targeting statins, bisphosphonates and krill oil as disease modifiers.
“Hopefully in the next few years we will do better than we’re doing at the moment.”