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

<p>Abstract</p> <p>Background</p> <p>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).</p> <p>Materials and Methods</p> <p>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.</p> <p>Results</p> <p>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.</p> <p>Conclusion</p> <p>The increased bone loss associated with high dose venlafaxine may possibly be a result of synaptic inhibition of serotonin uptake.</p

The effect of parenteral iron administration on the development of Staphylococcus aureus-induced experimental pyelonephritis in rats.

The first of the three groups of rats was taken as a control and the other two groups were injected with high (15 mg/kg) and low (5 mg/kg) doses of ferric ammonium citrate given intramuscularly twice daily for 5 days. Pyelonephritis was produced in all groups by intravenous inoculation with Staphylococcus aureus. Serum and urine of each rat was collected periodically and their iron content was determined. The severity of pyelonephritis was evaluated by determination of bacterial growth and pathological lesions in kidneys after 10 days of bacterial inoculation. The results showed that parenteral iron administration markedly aggravated pyelonephritis development in rats. But there was no significant difference in the severity of pyelonephritis between rats treated with high or low iron doses