After decades of viscosupplementation use for treating Osteoarthritis (mostly injected into knees), the jury is still out on its efficacy. A metaanalysis is difficult to do, mainly due to the fact that most of the clinical trials were sponsored by the manufacturers of such products (with obvious vested interest), and non-standardisation of trial design and outcome measures.
But it seems that the high molecular weight or cross-linked hyaluronic acid preparations may yield better results on pain relief and improved function.
Other than Viscosupplementation, Platelet-Rich Plasma (PRP) is the other Osteoarthritis treatment that is gaining popularity. This is in no small part due to glowing endorsements by several sports celebrities, like Kobe Bryant.
However, while its use in tendinosis and other soft tissue injuries may have some evidence, this is sorely lacking in treating degenerative OA. That is, until now.
This is a very significant study. While it may be industry-sponsored, it is sanctioned by the US FDA. The study design yields level 1 evidence (the best): randomised double-blind placebo-controlled trial. The 2 arms were well-matched for potential confounders at baseline. The results across the spectrum of clinical outcomes (pain, stiffness, function) at the end of 1 year were consistently superior in the PRP arm, by a factor of 10! The stats were significant, especially notable given its small sample size (33 in each arm) as mandated by FDA on ethical grounds.
Bottomline: it works (very well), it’s safe, it lasts (1 year at least)!
A point to note: this is not the classical PRP used in treating tendinopathies and enthesopathies. It is leukocyte-poor (to reduce risk of inflammation), and it is combined with Autologous Conditioned Plasma (ACP).
While the PRP component is believed to aid healing and repair by the production of growth factors, ACP is enriched in IL1RA (IL1 receptor antagonist) through incubation with glass beads, thereby reducing cartilage inflammation through antagonism of IL1, the key cytokine in OA pathogenesis.