Research

Effect of venlafaxine on bone loss associated with ligature-induced periodontitis in Wistar rats

Rosimary S Carvalho^1,2 , Carolina M de Souza¹ , Julliana CS Neves¹ , Sergio A Holanda-Pinto² , Lívia MS Pinto² , Gerly AC Brito³ and Geanne M de Andrade¹

¹  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

²  Department of Clinical Odontology, Faculty of Pharmacy, Odontology and Nursing, Federal University of Ceará, Rua Monsenhor Furtado, s/n, CEP 60441-750, Fortaleza, CE, Brazil

³  Department of Morphology, Faculty of Medicine, Federal University of Ceará, Rua Delmiro de Farias, s/n, CEP 60416-030, Fortaleza, CE, Brazil

author email corresponding author email

Journal of Negative Results in BioMedicine 2010, 9:3doi:10.1186/1477-5751-9-3

Published:	14 June 2010

Abstract

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).

Materials and 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-α 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-α 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-α or iNOS immunoreactivity.

Conclusion

The increased bone loss associated with high dose venlafaxine may possibly be a result of synaptic inhibition of serotonin uptake.