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New insights in Osteoarthritis

by Roberto Russo

As you know the Holy Grail of cure or even disease modifying therapy continues to elude us, despite an ever-increasing knowledge in the pathophysiology of the disease. However, there have been recent publications that have added to the body of knowledge around risk factors for pain, the relevance of inflammation, and in that context the value of certain treatments.

Source: http://www.morguefile.com/

Source: http://www.morguefile.com/

In terms of risk factors for pain severity in Osteoarthritis, smoking appears to be another contributing factor. Evaluation of data from the MOST study (Multicenter Osteoarthritis Study) showed that smokers had scored significantly higher on the WOMAC pain scale in a dose dependant manner. The authors though accept that they could not determine if the relationship to pain severity was causal or whether smoking was simply a surrogate measure for the culprit factor, such as socioeconomic status.

Source: http://www.morguefile.com/

Source: http://www.morguefile.com/

Proposed mechanisms include a down regulation of the hypothalamic-pituatary-adrenal axis resulting in reduced cortisol secretion and/or triggering of nicotine-sensitive acetylcholine receptors in the dorsal root ganglion. Interestingly though, pain sensitization was not increased in smokers. However, it was increased in those with poor sleep habits and in those who catastrophise their pain (Arthritis Care Res 2015).

These results prompt us to consider counseling our patients to stop smoking and undertake efforts to improve their sleep and change their approach to pain. In fact, a study evaluating the effect of cognitive behavioural therapy for insomnia in patients with Osteoarthritis is now underway.

Source: http://www.morguefile.com/

Source: http://www.morguefile.com/

Further research has also recently emerged again highlighting the inflammatory aspect of steoarthritis. C-Reactive Protein (CRP), a protein released by the liver in response to an inflammatory signal, has been associated with the presence and progression of bone marrow oedema in the joints of patients with Osteoarthritis, which has previously been shown to be a marker of severity and a predictor of pain in OA. This low-grade systemic inflammation is thought to be a risk factor towards cardiovascular disease, which has been supported by the finding of increase in ischaemic cardiac events in a cohort of patients with hand OA (ARD 2013). Obesity, through the release of inflammatory mediators from adipose cells, is most often the pivotal factor, highlighting the importance of weight loss in this disease.

Pharmacological attempts to reduce this inflammation with 400mg/day of Hydroxychloroquine (Plaquenil), used in RA and SLE for joint symptoms, did not result in any meaningful improvements in pain, disability, or physical, emotional, or social well-being. Statins (Atorvastatin 40mg/day – TRACE-RA study), used to reduce cholesterol levels, did significantly reduce the incidence of cardiac events, which many believe actually arises from the anti-inflammatory effects of these medications.

Finally, a further nail is hammered into the Arthroscopic knee surgery coffin with a recent meta-analysis published in the June edition of BMJ finding that arthroscopic surgery, including partial meniscectomy, debridement, or both performed in a middle aged population with OA resulted in modest early benefits similar to that achieved with Panadol that were no longer present at 12 months and no improvement in function was noted.

I hope you have found these points of relevance to your practice as I have.