Do NSAID's Retard Disc Resorption?
By Mitchell Miglis DC, Melbourne, Florida, USA.

Anti-inflammatory medications are a common medical treatment for discogenic back pain. The best evidence today suggests that the natural history of disc herniation is positive for self-resorption, with more resorption on longer follow up. Autio et al¹ write: “Herniated nucleus pulposus (HNP ) resorption is thought to occur via an inflammatory reaction in the outermost layer of herniation, with macrophages as the predominating cellular population. Recently, the molecular mechanisms of this phagocytotic process have been clarified. Rim enhancement around the herniated disc in contrast-enhanced magnetic resolution imaging (MRI) is thought to represent neovascularized zone with macrophage infiltration, which has an essential role in phagocytosis and herniation regression” pg. 1247

The question follows: Except for short-term acute pain management, do anti-inflammatory medications make sense from a physiologic perspective when an active inflammatory process appears to be the mechanism by which HNP’s are resorbed? This is, of course, a question premised on physiologic theory and, as such, represents a surrogate question. The relevant clinical question is: Do anti-inflammatory medications result in better, same or worse outcomes compared to controls in HNP cases when used beyond the acute phase? Is there evidence that answers this question? In the meantime, the theoretical argument for limiting long-term use, aside from gastric and other toxicity, may be that it could retard disc resorption.

References:

1. Determinants of spontaneous resorption of intervertebral disc herniations. Autio, RA, Karppinen J, Niinima¨ki J, Ojala R, Kurunlahti R, Haapea M, Vanharanta H, and Tervonen O. Spine 2006 May 15; 31(11):1247-52.