A limited number of experimental animal studies and in vitro data confirm t
hat nicotine impairs bone healing, diminishes osteoblast function, causes a
utogenous bone graft morbidity, and decreases graft biomechanical propertie
s. Therefore, our long-term goal is to develop an effective therapy to reve
rse the adverse impact of nicotine from tobacco products. However, before a
ccomplishing this goal, we had to develop an animal model: Our hypotheses w
ere nicotine administration preceding:and following autoenous bone grafting
adversely affected autograft incorporation and:depressed donor site healin
g in a characterized animal wound model. Hypothesis testing was accomplishe
d in bilateral, 4-mm diameter parietal bone defects prepared in 60 Long-Eva
ns rats (male, 35-day-old). A 4-mm diameter disk of donor bone was removed
from the left parietal bone and placed in the contralateral defect. The don
or site served as a spontaneously healing bone wound. The rats were partiti
oned equally among three doses of nicotine administered orally in the drink
ing water (12.5, 25, and 50 mg/L). For each dose, the duration and sequence
of nicotine treatment followed four courses, including no nicotine and des
ignated combinations of nicotine administration and abatement prior to and-
following osseous surgery. Experimental sites were recovered on 14 and 28 d
ays postsurgery, responses quantitated, and data analyzed by analysis of va
riance and post hoc statistics (p less than or equal to 0.05). We developed
a convenient and effective osseous model, and the results validated our hy
pothesis that nicotine negatively impacts on bone healing. (C) 1999 John Wi
ley & Sons, Inc.