Effect of venlafaxine on bone loss associated with ligature-induced periodontitis in Wistar rats.
BACKGROUND
The present study investigated the effects of venlafaxine, an antidepressant drug with immunoregulatory properties on the inflammatory response and bone loss associated with experimental periodontal disease (EPD).


METHODS
Wistar rats were subjected to a ligature placement around the second upper left molar. The treated groups received orally venlafaxine (10 or 50 mg/kg) one hour before the experimental periodontal disease induction and daily for 10 days. Vehicle-treated experimental periodontal disease and a sham-operated (SO) controls were included. Bone loss was analyzed morphometrically and histopathological analysis was based on cell influx, alveolar bone, and cementum integrity. Lipid peroxidation quantification and immunohistochemistry to TNF-alpha and iNOS were performed.


RESULTS
Experimental periodontal disease rats showed an intense bone loss compared to SO ones (SO = 1.61 +/- 1.36; EPD = 4.47 +/- 1.98 mm, p < 0.001) and evidenced increased cellular infiltration and immunoreactivity for TNF-alpha and iNOS. Venlafaxine treatment while at low dose (10 mg/kg) afforded no significant protection against bone loss (3.25 +/- 1.26 mm), a high dose (50 mg/kg) caused significantly enhanced bone loss (6.81 +/- 3.31 mm, p < 0.05). Venlafaxine effectively decreased the lipid peroxidation but showed no significant change in TNF-alpha or iNOS immunoreactivity.


CONCLUSIONS
The increased bone loss associated with high dose venlafaxine may possibly be a result of synaptic inhibition of serotonin uptake.
Carvalho
Rosimary S
RS
Laboratory of Neurosciences and Behavior, Department of Physiology and Pharmacology, Federal University of Ceará, Rua Coronel Nunes de Melo, 1127, CEP 60430-270, Fortaleza, CE, Brazil. roseperio@yahoo.com.br
de Souza
Carolina M
CM
Neves
Julliana C S
JC
Holanda-Pinto
Sergio A
SA
Pinto
Lívia M S
LM
Brito
Gerly A C
GA
de Andrade
Geanne M
GM
D016301:Alveolar Bone Loss / Q000150:complications* / Q000188:drug therapy* / Q000201:enzymology; D000818:Animals; D003511:Cyclohexanols / Q000494:pharmacology / Q000627:therapeutic use*; D005881:Gingiva / Q000187:drug effects / Q000473:pathology; D007150:Immunohistochemistry; D008026:Ligation; D008315:Malondialdehyde / Q000378:metabolism; D052247:Nitric Oxide Synthase Type II / Q000378:metabolism; D010518:Periodontitis / Q000150:complications* / Q000188:drug therapy* / Q000201:enzymology / Q000473:pathology; D051381:Rats; D017208:Rats, Wistar; D017367:Selective Serotonin Reuptake Inhibitors / Q000494:pharmacology / Q000627:therapeutic use; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D000069470:Venlafaxine Hydrochloride
D003511:Cyclohexanols; D008315:Malondialdehyde; D052247:Nitric Oxide Synthase Type II; D017367:Selective Serotonin Reuptake Inhibitors; D017392:Thiobarbituric Acid Reactive Substances; D014409:Tumor Necrosis Factor-alpha; D000069470:Venlafaxine Hydrochloride