Nicotine stimulates osteoclast resorption in a porcine marrow cell model.
BACKGROUND
Combustible tobacco use is generally linked with accelerated periodontal bone loss and diminished post-surgical wound healing; however, the pathogenesis of this process at the cellular level remains unclear. Nicotine is known to affect human gingival fibroblast orientation, attachment, and beta1 integrin expression, yet little is known about its effects on osteoclasts, the cells most responsible for bone resorption. The purpose of this study was to determine the effects of physiologically relevant nicotine levels on porcine osteoclast function as measured by resorption of calcium phosphate.


METHODS
Pure nicotine was diluted in medium to the following concentrations: 0.03 microM, 0.15 microM, 0.30 microM, 0.60 microM, and 1.50 microM. Porcine osteoclasts were seeded onto calcium phosphate multi-test slides and incubated at 37 degrees C with half media changes every 24 hours. Cells received 0, 0.15, 0.30, 0.60, and 1.50 microM nicotine, or 25 nM parathyroid hormone (PTH). Osteoclast resorption was quantified by measuring the resorbed surface area of the calcium phosphate substrate.


RESULTS
Osteoclast cultures resorbed bone slices and calcium phosphate substrate. All nicotine concentrations and PTH resulted in statistically significantly greater mean percent resorptions than the control group (P < 0.05). However, no statistical difference was found between the various nicotine doses or PTH. The number of osteoclasts increased in a linear relationship to the increasing nicotine concentrations; however, no correlation was found between osteoclast number and the amount of resorption.


CONCLUSIONS
Nicotine is non-toxic to osteoclasts at the clinically relevant levels tested. Nicotine appears to stimulate osteoclast differentiation and resorption of calcium phosphate, the major component of bone. Nicotine-modulated osteoclast stimulation may, in part, explain the increased rapidity of periodontal bone loss and refractory disease incidence in smokers.
Henemyre
Claudia L
CL
Department of Clinical Investigation, Dwight D. Eisenhower Army Medical Center, Fort Gordon, GA 30905, USA.
Scales
Donald K
DK
Hokett
Steven D
SD
Cuenin
Michael F
MF
Peacock
Mark E
ME
Parker
M Harry
MH
Brewer
Phyllis D
PD
Chuang
Augustine H
AH
D000704:Analysis of Variance; D000818:Animals; D001854:Bone Marrow Cells; D001862:Bone Resorption / Q000139:chemically induced*; D002130:Calcium Phosphates / Q000378:metabolism; D002478:Cells, Cultured; D004195:Disease Models, Animal; D005260:Female; D008855:Microscopy, Electron, Scanning; D009538:Nicotine / Q000633:toxicity*; D018722:Nicotinic Agonists / Q000633:toxicity*; D010010:Osteoclasts / Q000187:drug effects* / Q000378:metabolism; D018709:Statistics, Nonparametric; D013552:Swine
D002130:Calcium Phosphates; D018722:Nicotinic Agonists; C485828:alpha-tricalcium phosphate; C485830:tetracalcium phosphate; D009538:Nicotine; C485838:calcium phosphate, monobasic, anhydrous; C020243:calcium phosphate; C485829:calcium phosphate, dibasic, anhydrous