Effect of Nicotine on the Rate and Strength of Long Bone Fracture Healing

Raikin, Steven M.; Landsman, Jonathan C.; Alexander, Vladimir A.; Froimson, Mark I.; Plaxton, Nicholas

doi:10.1097/00003086-199808000-00027

Cited by 120 publications

(91 citation statements)

References 23 publications

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“…Nicotine seems to affect the early revascularization of the fractured bone, probably through down-regulated gene transcription of fibroblast growth factor, vascular endothelial growth factor, and bone morphogenetic protein cytokines known to be important to angiogenesis and osteoblast function [1]. In experimental animals, exposure to nicotine decreases union rate and increases complications [2]. The influence of nicotine on bone healing in animals remains controversial; nicotine exposure enhances angiogenesis but cannot compensate for the adverse effect of vasoconstriction [3].…”

Section: Introductionmentioning

confidence: 99%

Smoking as a predictor of negative outcome in diaphyseal fracture healing

Hernigou

Schuind

2013

International Orthopaedics (SICOT)

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Purpose The purpose of this study was to evaluate the impact of tobacco abuse in the consolidation of fractures. Methods We retrospectively identified all patients with a diaphyseal fracture (femur, tibia, or humerus), between January 1999 and December 2010, in our orthopaedic trauma registry (Erasme hospital, Brussels, Belgium). Thirty-eight diaphyseal nonunions (ten femurs, 16 tibias and 12 humerus) were identified. Each nonunion was paired (on age, sex and location) with two control-healed fractures (76 control patients). The chi-squared test and a binary logistic regression were used for statistical analysis. Results In multivariate analysis, smoking (tobacco use) was significantly associated with nonunion, whether the fracture was open or closed (p<0.01). In univariate analysis, open fracture was associated with a higher risk of nonunion (p<0.05), while external fixation was associated with better bone healing (p<0.05). Conclusion Tobacco is confirmed as a deleterious factor for diaphyseal bone healing.

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Section: Introductionmentioning

confidence: 99%

Smoking as a predictor of negative outcome in diaphyseal fracture healing

Hernigou

Schuind

2013

International Orthopaedics (SICOT)

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“…1 Previous studies have shown a relationship between smoking and a variety of orthopedic conditions, including delayed healing and nonunion of fractures in human and animal models. [2][3][4][5] An inadequate or delayed fracture healing response results in a significant cost to society in terms of lost work productivity and recreational ability. Currently, the molecular mechanism by which smoking causes deleterious effects on fracture healing is poorly understood.…”

Section: Introductionmentioning

confidence: 99%

Smoking delays chondrogenesis in a mouse model of closed tibial fracture healing

et al. 2006

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Smoking delays the healing process and increases morbidity associated with many common musculoskeletal disorders, including long bone fracture. In the current study, a murine model of tibial fracture healing was used to test the hypothesis that smoking delays chondrogenesis after fracture. Mice were divided into two groups, a nonsmoking control group and a group exposed to cigarette smoke for 1 month prior to surgical tibial fracture. Mice were euthanized at 7, 14, and 28 days after surgery. The outcomes measured were immunohistochemical staining for type II collagen protein expression as a marker of cartilage matrix and proliferating cell nuclear antigen (PCNA) staining to measure proliferation at the site of injury. Toluidine blue staining and histomorphometry were used to quantify areas of cartilaginous and noncartilaginous fracture callus. Radiographs were analyzed for evidence of remodeling after injury. At day 7 after injury, mice exposed to cigarette smoke had a smaller fracture callus with less cartilage matrix compared to controls. Proliferation was present at high levels in both groups at this time point, but proliferating cells had a more immature morphology in the smoking group. At day 14, chondrogenesis was more active in smokers compared to controls, while a higher percentage of bone was present in the control animals. At day 28, X-ray analysis revealed a larger fracture callus remaining in the smoking animals. Together, these findings show that the chondrogenic phase of tibial fracture healing is delayed by smoking. This study represents, to our knowledge, the first analysis of molecular and cellular mechanisms of healing in a smoking mouse fracture model. ß

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“…Sigara kullanımının kırık iyileşmesinde yavaşla-maya ya da kaynamamaya neden olduğu, yapılan çalışmalarda gözlemlenmiştir. [66] Sigaranın içinde bulunan nikotinin vazokonstrüktif etkisi, karbonmonoksitin oksijen taşınması mekanizmasını bozması ve hidrojen siyanidin enzimleri olumsuz etkilemesiyle, iyileşmeyi geciktirici ya da önleyici etki yarattığı düşünülmektedir. [67] xiii.…”

Section: Elektriksel Uyarı Ve Kırık İyileşmesiunclassified

Kırık iyileşmesi

Tanrıkulu¹,

Gönen²

2017

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patolojik kemik yapılarında görülür ve lamellar kemiğe göre daha fazla sayıda osteosit içeren, daha dayanıksız ve daha esnek bir yapıdadır.Kortikal kemik yapısının; Haversian kanallarla birbirine bağlanan osteonlardan oluştuğu görülür. Bu kanallar arteriol, venül, kapiller damarlar, sinirler ve lenfatik kanallar içerir. Osteonlar arasında birbirine fibriller ile bağlanan interstisiyel lameller vardır. Fibriller osteonun dış sınırın oluşturan sement çizgisine kadar uzanır. Kemiğin beslenmesi intraosseöz kan dolaşımı ile olur. Kortikal kemiğin yavaş bir döngüsü vardır, torsiyon ve bükülme kuvvetlerine karşı direnci kansellöz kemikten daha fazladır.

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Effect of Nicotine on the Rate and Strength of Long Bone Fracture Healing

Cited by 120 publications

References 23 publications

Smoking as a predictor of negative outcome in diaphyseal fracture healing

Smoking as a predictor of negative outcome in diaphyseal fracture healing

Smoking delays chondrogenesis in a mouse model of closed tibial fracture healing

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