The role of inflammation in lumbar pain

Abstract

The clinical features of many cases of low back pain is inadequately explained by anatomic abnormalities alone. A pathophysiologic mechanism that includes a combination of mechanical and biochemical factors is an alternative explanation that is accompanied by less paradox than a purely structural paradigm. A potential unifying feature includes inflammation of neural elements caused by the chemical components of the intervertebral disc. There is a historical basis to the concept of an immunologic potential of the lumbar disc. No discrete in situ evidence or discrete mechanism has been previously identified. The recent demonstration of immunohistopathologic evidence of an immunocompetent cellular response at the epidural interface of lumbar HNPs supports the concept of the immunogenic capacity of nucleus pulposus. The identification of high levels of an inflammatory enzyme, phospholipase A2, in lumbar herniated and degenerative discs presents the basis for a direct inflammogenic capability of lumbar discs, separate from a immunologic mechanism. Subsequent experimental findings of conduction block and perineural inflammation as a consequence of extrathecal application of autologous nucleus pulposus and axonal injury after animal nerve injection of the human disc phospholipase A2 further validates this concept. There is a strong theoretic basis to support the concept that the clinical features of many lumbar disc patients may be explained by inflammation caused by biochemical factors alone or combined with mechanical deformation of lumbar tissues, rather than mechanical factors alone.