4.4 Article

Effects of Caffeine on Intervertebral Disc Cell Viability in a Whole Organ Culture Model

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GLOBAL SPINE JOURNAL
卷 12, 期 1, 页码 61-69

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SAGE PUBLICATIONS LTD
DOI: 10.1177/2192568220948031

关键词

intervertebral disc; caffeine; nicotine; disc degeneration; degenerative disc; cell viability; whole organ culture

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This controlled laboratory study investigated the impact of caffeine concentrations on intervertebral disc cell viability and extracellular matrix composition. The results suggest that caffeine intake may be a risk factor for intervertebral disc degeneration, especially in conjunction with disc injury. Further studies are needed to elucidate mechanistic pathways and potential benefits for caffeine restriction.
Study Design: Controlled laboratory study. Objective: To investigate the impact of exposure to physiologically relevant caffeine concentrations on intervertebral disc (IVD) cell viability and extracellular matrix composition (ECM) in a whole organ culture model as potential contributing mechanisms in development and progression of IVD disorders in humans. Primary outcome measures were IVD viable cell density (VCD) and ECM composition. Methods: A total of 190 IVD whole organ explants from tails of 16 skeletally mature rats-consisting of cranial body half, endplate, IVD, endplate, and caudal body half-were harvested. IVD explants were randomly assigned to 1 of 2 groups: uninjured (n = 90) or injured (20G needle disc puncture/aspiration method, n = 100). Explants from each group were randomly assigned to 1 of 3 treatment groups: low caffeine (LCAF: 5 mg/L), moderate caffeine (MCAF: 10 mg/L), and high caffeine (HCAF: 15 mg/L) concentrations. Results: Cell viability was significantly higher in the low-caffeine group compared with the high-caffeine group at day 7 (P= .037) and in the low-caffeine group compared with the medium- and high-caffeine groups at day 21 (P <= .004). Analysis of ECM showed that all uninjured and control groups had significantly higher (P< .05) glycosaminoglycan concentrations compared with all injured groups. Furthermore, we observed a temporal, downward trend in proteoglycan to collagen ratio for the caffeine groups. Conclusions: Caffeine intake may be a risk factor for IVD degeneration, especially in conjunction with disc injury. Mechanisms for caffeine associated disc degeneration may involve cell and ECM, and further studies should elucidate mechanistic pathways and potential benefits for caffeine restriction.

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