Contribution of Endocannabinoid Gene Expression and Genotype on Low Back Pain Susceptibility and Chronicity

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Abstract

Background:

A major research emphasis has been focused on defining the molecular changes that occur from acute to chronic pain to identify potential therapeutic targets for chronic pain. As the endocannabinoid system is dynamically involved in pain signaling, a plausible mechanism that may contribute to chronic pain vulnerability involves alterations in the amount of circulating endocannabinoids. Therefore, this study sought to examine cannabinoid type 1 (CNR1), type 2 (CNR2) receptors, fatty acid amide hydrolase (FAAH), and the vanilloid receptor (transient receptor potential cation channel subfamily V member 1 [TRPV1]) gene expression profiles among individuals with acute and chronic low back pain (cLBP) at their baseline visit. We also assessed associations among selected single nucleotide polymorphisms (SNPs) of FAAH and CNR2 and measures of somatosensory function and self-report pain measures.

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