Rapid pain relief risky in OA

Very rapid relief of osteoarthritis pain may do more harm than good in damaged joints which are unprepared to cope with unaccustomed activity, Melbourne rheumatologists have suggested.

Dr Andrew Teichtahl and Professor Flavia Cicuttini from Monash University said that rapid pain relief with agents such as tanezumab, a monoclonal antibody blocking nerve growth factor, might create a “perfect storm” leading to rapidly-progressing OA.

Increased loading of a healthy joint normally led to appropriate compensatory mechanisms by bone and surrounding muscular support, as well as adequate proprioception, which protected against acute damage.

“In contrast when an osteoarthritic joint is subjected to the same rapid environmental change, poor pre-existing structural integrity such as weak and atrophied muscular supports, impaired proprioception and bone which is susceptible to subchondral insufficiency fractures may initiate a trajectory toward joint failure,” they said.

“It is possible that the acute and significant analgesic effects that results from therapies such as tanezumab may need to be tempered by a graduated increase in activity levels to enable compensatory responses in underlying neuromuscular and bone supports.”

Dr Teichtahl and Professor Cicuttini, in an editorial in Arthritis and Rheumatology, said there was a need to achieve a balance between effective analgesia and protection of the joint against rapid progression of the disease.

They were commenting on an analysis of patients who were thought to have developed osteonecrosis or needed a joint replacement during clinical trials of tanezumab. Concerns about osteonecrosis had temporarily halted further studies of the drug.

In fact, only two of 249 cases were judged by an expert panel as being primary osteonecrosis. A total of 200 cases were classified as due to worsening OA which was rapidly progressive in 68 patients.

Dr Teichtahl and Professor Cicuttini proposed a number of possible mechanisms for rapid progression, including insufficient stabilisation by atrophied muscles. “Improvement in muscle quality and strength requires time,” they said.

Increased activity might also worsen subchondral bone defects.

The drug itself might impair proprioception and increase the risk of structural damage, and perhaps interfere directly with cartilage repair.

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