#381 Does Medication Routinely Used for Discography Influence Intervertebral Disc Biology?

General Session: What's New in Biologics and Biomechanics

Presented by: M. Ogon

Author(s):

C. Eder (1)
A. Pinsger (1)
S. Schildböck (1)
M. Ogon (1)

(1) Orthopädisches Spital Speising, Vienna, Austria

Abstract

Introduction: Eugene Carragee1 was the first to prove that provocative discography may contribute to intervertebral disc degeneration. Disc degeneration can be induced either by mechanical trauma caused by the puncturing needle or as a pharmacological effect of the drugs instilled into the disc.

Materials and Methods: Nucleus pulposus cell cultures were incubated in standard medium or medium supplemented with either 93.75µl/ml Iopamidol, 31,25 µl/ml Lidocaine or 31,25 µl/ml Triamcinolonacetonid, representing a clinical dosage of 3 ml Iopamidol, 1 ml Lidocaine and 1 ml Cortisone per nucleus pulposus. Cell count, viability, proliferation and differentiation features were analysed.

Results: After 24 hours, a significant decrease in cell counts was observed in all three test groups. Population doubling time was 16 hours in the control group and increased to 25 hours (Iopamidol), 21 hours (Triamcinolonacetonid) and 38 hours (Lidoocaine) after incubation in discography medication (p< 0,001). Cell viability was slightly, but not significantly decreased in all medication groups. Cells incubated in Lidoocaine were significantly smaller (p< 0,01) and showed clearly reduced pseudopode formation. Incubation in Prilocaine and Iopamidol also significantly reduced glycosaminoglycan synthesis.

Discussion: Although only a small decrease in cell viability was observed, cell count and proliferation decreased significantly. Incubation in Lidocaine inhibited pseusopode formation and might therefore interfere with intercellular signalling and cell migration. Glycosaminoglycan syntheses was significantly decreased after contact with Lidocaine as well as Iopamidol. These observations suggest that all 3 medications tested might interfere with biological repair mechanisms of the intervertebral disc and contribute to a further degeneration of the intervertebral disc.

References: 1 Carragee EJ et al. Spine (Phila Pa 1976). 2009 Oct 1;34(21):2338-45.