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Nicotine Increases Osteoblast Activity of Induced Bone Marrow Stromal Cells in a Dose-Dependent Manner: An in vitro Cell Culture Experiment

Previous studies by our group showed that nicotine delivered via a transdermal nicotine patch significantly enhanced posterior spinal fusion rates in rabbits. Nicotine transdermal patches provide a steady serum level; there may be a dose-dependent effect of nicotine on posterior spinal fusion. In an...

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Detalles Bibliográficos
Autores principales: Daffner, Scott D., Waugh, Stacey, Norman, Timothy L., Mukherjee, Nilay, France, John C.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Thieme Medical Publishers 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3864438/
https://www.ncbi.nlm.nih.gov/pubmed/24353962
http://dx.doi.org/10.1055/s-0032-1326946
Descripción
Sumario:Previous studies by our group showed that nicotine delivered via a transdermal nicotine patch significantly enhanced posterior spinal fusion rates in rabbits. Nicotine transdermal patches provide a steady serum level; there may be a dose-dependent effect of nicotine on posterior spinal fusion. In an in vitro cell culture model of rabbit bone marrow–derived osteoblast-like cells, cells were exposed to different concentrations of nicotine (0, 20, 40, 80 ng/mL and 10, 100, 250 μg/mL). Wells were stained with an alkaline phosphatase (ALP) staining kit to determine ALP enzyme activity. Cells were stained with Von Kossa for mineralization. A two-way analysis of variance (ANOVA) using dose and time as variables showed significant differences among groups; post hoc analysis showed that the 100-μg/mL dose of nicotine significantly enhanced ALP activity over controls. A one-way ANOVA using dose as the variable showed that the 100- and 250-μg/mL doses had significantly greater mineralization than controls. Dose-response analysis revealed a statistically significant effect of nicotine dose on ALP activity and Von Kossa activity. The effects of nicotine on spinal fusion may be dose-dependent and due to stimulation of osteoblastic activity. Nicotine may not be responsible for the inhibited bone healing observed in smokers.