Effect of serum nicotine level on posterior spinal fusion in an in vivo rabbit model

Daffner, Scott D.; Waugh, Stacey; Norman, Timothy L.; Mukherjee, N.

doi:10.1016/j.spinee.2015.02.041

Cited by 18 publications

(14 citation statements)

References 42 publications

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“…38 However, in contrast Daffner et al showed in an animal model that a small (5.25 mg) dose of nicotine actually improved fusion rates compared to the control. 43 These findings suggest that effects of nicotine on fusion may be dose-dependent and that the negative of effects of smoking on nonunion may be attributable to other components of cigarette smoke. Lee et al used a rabbit model to show that acute cigarette inhalation may delay but not prevent the spinal fusion process.…”

Section: In Vivo Animal Studies and Lumbar Fusionmentioning

confidence: 93%

“…They determined that the effects of nicotine on spinal fusion are complex, may be dosedependent, and may not always be detrimental, concluding that the effects of smoking on spinal fusion may be due to other components of cigarette smoke. 63 Another study by Daffner claimed to show that nicotine increased osteoblast activity of induced bone marrow stromal cells in a dose dependent manner. 64 These studies should be scrutinize further because of the long-held consensus about the negative effects of nicotine on both bone health and bone healing, but they potentially open the door to the idea that other components of cigarette smoke may be even more harmful to the fusion healing process than nicotine alone.…”

Section: Is There Anything That Can Be Done To Overcome the Effects Omentioning

confidence: 99%

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The Effect of Smoking on Spinal Fusion

et al. 2017

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It has been clearly demonstrated from both a biochemical and clinical perspective that smoking increases the rate of perioperative complications for patients undergoing spinal fusion surgery, particularly pseudoarthosis. It has also been shown that there are certain approaches that can reduce the risk of morbidity. The most important recommendation is smoking cessation for four weeks after surgery. In addition, patients may be treated with certain surgical techniques, including the use of BMPs, to reduce the risk of pseudoarthrosis. Lastly, nicotine replacement therapy is an area of continued interest in relation to spinal fusion outcomes and more research needs to be done to determine its efficacy moving forward.

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Section: In Vivo Animal Studies and Lumbar Fusionmentioning

confidence: 93%

Section: Is There Anything That Can Be Done To Overcome the Effects Omentioning

confidence: 99%

The Effect of Smoking on Spinal Fusion

et al. 2017

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“…We also measured blood nicotine levels in our previous study: 36.5 to 124.8 ng/ml (mean: 72.1 ng/ml) [25]. This concentration range corresponds to 10 to 70 ng/ml (mean: 33 ng/ml) reported for 330 human smokers who smoked 20.7 cigarettes/day on average [25, 31]. Therefore, this model is comparable to humans who are smoking 20 to 40 cigarettes/day.…”

Section: Discussionmentioning

confidence: 98%

Detection of apoptosis and matrical degeneration within the intervertebral discs of rats due to passive cigarette smoking

Nakahashi

Esumi

Tokuhashi

2019

Preprint

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Although low-back pain is considered to be associated with cigarette smoking, the influence of cigarette smoking on the intervertebral discs (IVD) has not been confirmed. We established a rat model of passive cigarette smoking-induced IVD degeneration, and investigated the cytohistological changes in the IVD and the accompanying changes in gene expression. IVD from rats exposed to 8 weeks of passive cigarette smoking were stained with Elastica van Gieson, and exhibited marked destruction of the supportive structure of the reticular matrix in the nucleus pulposus (NP). Positive signals on safranin O, alcian blue, type II collagen and aggrecan staining were decreased in the destroyed structure. Safranin O and type II collagen signals were also decreased in the cartilage end-plate (CEP) after 4- and 8-weeks of cigarette smoking. In the CEP, the potential for apoptosis was increased significantly, as demonstrated by staining for single-strand DNA. However, there were no signs of apoptosis in the NP or annulus fibrosus cells. Based on these findings, we concluded that passive cigarette smoking-induced stress stimuli first affect the CEP through blood flow due to the histological proximity, thereby stimulating chondrocyte apoptosis and reduction of the extracellular matrix (ECM). This leads to reduction of the ECM in the NP, destroying the NP matrix, which can then progress to IVD degeneration.

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“…4). Previous work has shown that the effects of nicotine on osteoblasts are nuanced and may be concentration- and time-dependent (Rothem et al, 2009, Daffner et al, 2015, Marinucci et al, 2014). In this work, we utilized a moderate-to-low dose (Rothem et al, 2009) of nicotine (50 μM) and found that its effect on ALP activity, BMSC migration, and matrix mineralization were minor compared to those of dioxin.…”

Section: Discussionmentioning

confidence: 99%

“…Nicotine is a potent anti-inflammatory and immunosuppressive, and has been shown to have deleterious effects on fibroblasts, red blood cells, and macrophages (Zevin et al, 1998, Jorgensen et al, 1998, Leow and Maibach, 1998), in addition to diminishing blood flow to tissues by promoting vasoconstriction (Leow and Maibach, 1998, Bornmyr and Svensson, 1991). Interestingly, the overall impact of nicotine on bone formation is still uncertain, and may be concentration-dependent; high concentrations of nicotine have been shown to inhibit osteoblast proliferation, whereas low concentrations actually have a proliferative effect (Rothem et al, 2009, Daffner et al, 2015, Gotfredsen et al, 2009, Syversen et al, 1999). Numerous studies have proposed that reactive oxygen species and other pro-inflammatory constituents and metabolites are responsible for dysregulation of bone homeostasis, reduction in bone mineral density, and inhibition of fracture healing (Rothem et al, 2009, Syversen et al, 1999, Holzer et al, 2012).…”

Section: Introductionmentioning

confidence: 99%

Mechanistic insight into the effects of Aryl Hydrocarbon Receptor activation on osteogenic differentiation

et al. 2017

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While inhibition of bone healing and increased rates of pseudarthrosis are known adverse outcomes associated with cigarette smoking, the underlying mechanisms by which this occurs are not well understood. Recent work has implicated the Aryl Hydrocarbon Receptor (Ahr) as one mediator of the anti-osteogenic effects of cigarette smoke (CS), which contains numerous toxic ligands for the Ahr. 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD, dioxin) is a high-affinity Ahr ligand frequently used to evaluate Ahr pathway activation. The purpose of this study was to elucidate the downstream mechanisms of dioxin action on bone regeneration and investigate Ahr antagonism as a potential therapeutic approach to mitigate the effects of dioxin on bone. Markers of osteogenic activity and differentiation were assessed in primary rat bone marrow stromal cells (BMSC) after exposure to dioxin, Ahr antagonists, or antagonist + dioxin. Four Ahr antagonists were evaluated: α-Naphthoflavone (ANF), resveratrol (Res), 3,3′-Diindolylmethane (DIM), and luteolin (Lut). Our results demonstrate that dioxin inhibited ALP activity, migratory capacity, and matrix mineralization, whereas co-treatment with each of the antagonists mitigated these effects. Dioxin also inhibited BMSC chemotaxis, while co-treatment with several antagonists partially rescued this effect. RNA and protein expression studies found that dioxin down-regulated numerous pro-osteogenic targets, whereas co-treatment with Ahr antagonists prevented these dioxin-induced expression changes to varying degrees. Our results suggest that dioxin adversely affects bone regeneration in a myriad of ways, many of which appear to be mediated by the Ahr. Our work suggests that the Ahr should be investigated as a therapeutic target to combat the adverse effects of CS on bone healing.

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Effect of serum nicotine level on posterior spinal fusion in an in vivo rabbit model

Cited by 18 publications

References 42 publications

The Effect of Smoking on Spinal Fusion

The Effect of Smoking on Spinal Fusion

Detection of apoptosis and matrical degeneration within the intervertebral discs of rats due to passive cigarette smoking

Mechanistic insight into the effects of Aryl Hydrocarbon Receptor activation on osteogenic differentiation

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