NICOTINE ON THE REVASCULARIZATION OF BONE-GRAFT - AN EXPERIMENTAL-STUDY IN RABBITS

Citation
Tk. Daftari et al., NICOTINE ON THE REVASCULARIZATION OF BONE-GRAFT - AN EXPERIMENTAL-STUDY IN RABBITS, Spine (Philadelphia, Pa. 1976), 19(8), 1994, pp. 904-911
Citations number
NO
Categorie Soggetti
Orthopedics
ISSN journal
03622436
Volume
19
Issue
8
Year of publication
1994
Pages
904 - 911
Database
ISI
SICI code
0362-2436(1994)19:8<904:NOTROB>2.0.ZU;2-8
Abstract
Study Design. In 24 rabbits, the authors transplanted autologous cance llous bones to the anterior chamber of the eye. Half of the rabbits re ceived nicotine and half received placebo (albumin) from mini-osmotic pumps that were implanted subcutaneously. Revascularization of the bon e graft was evaluated postoperatively using ophthalmology slit-lamp an d fluorescein angiography, and after sacrifice using microvascular sil icone injection and histology. Objectives. The hypothesis that nicotin e inhibits the revascularization of bone graft because of its pharmaco logic action on the microvasculature was tested. Summary of Background Data. Pseudoarthrosis after spinal fusion occurs more frequently in s mokers as compared with nonsmokers. Methods. Observations of the graft were made regarding the time after implantation when vessels within t he graft were noted and the pattern of these vessels. Revascularizatio n of the graft was graded based on the observed percent area of fluore scence after injection of fluorescein. Serum levels of nicotine were m easured weakly. Colored silicone was injected at sacrifice to fix the vasculature of the bone graft. Histologic analysis of undecalcified se ctions was performed. Results. Nicotine, as compared with placebo, was associated with delayed revascularization within the graft, a smaller percent area of revascularization, and a larger number of grafts show ing necrosis. Conclusions. Nicotine inhibits, but does not prevent, th e revascularization of cancellous bone grafts. Inhibition of early rev ascularization by nicotine is proposed as the pathophysiologic mechani sm by which smoking may adversely affect the healing of the spinal fus ions.