Abstract
Tobacco smoking increases the risk of back pain and intervertebral disc degeneration (IDD), but the mechanism of its adverse action on disc metabolism is not well understood [1, 2]. Loss of disc matrix due to dysregulated activities of matrix metalloproteinses (MMPs) is implicated in initiating the IDD cascade [3]. Tobacco smoke condensate (TSC), containing numerous inflammatory and oxidative stress inducing agents [4], has previously been shown to upregulate MMP expression in disc cells [5]. The p38 MAPK pathway is a central mediator of stress-induced MMP expression [6], but it is not known whether tobacco smoking upregulates MMP in disc cells through this pathway.
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