77 ± 1.66 leucocytes × 103 mm−3) (Fig. 3(a)), when compared to its baseline data (11.56 ± 0.31). This leucocytosis

was marked (p < 0.05) by neutrophilia (5.20 ± 0.28 neutrophil × 103 mm−3), when p38 MAPK inhibitor compared to its baseline (1.37 ± 0.08) ( Fig. 3(b)). Following, on the 2nd day, there was a decrease in total leucocyte count; however, the basal cell counts were not achieved. New leucocytosis was observed on the 7th (21.73 ± 0.87 leucocytes × 103 mm−3) and 11th (25.84 ± 1.23) days, with predomination of mononuclear cells (7th day = 18.24 ± 1.05; 11th day = 23.21 ± 1.48 mononuclear cells × 103 mm−3) when compared to its baseline (10.19 ± 0.25) ( Fig. 3(c)). All doses of ALD prevented neutrophilia at the 6th hour (ALD 0.01 = 4.00 ± 0.42; ALD 0.05 = 2.98 ± 0.21; ALD 0.25 = 2.50 ± 0.22), when compared buy SB431542 to saline (5.20 ± 0.28) (p < 0.05) ( Fig. 3(b)). However, only ALD (0.25 mg kg−1) prevented mononuclear cell peaks on the 7th (12.29 ± 0.66) and 11th (15.74 ± 0.52) days ( Fig. 3(c)). Periodontitis caused body weight loss noted on the 3rd day after ligature placement when compared to normal animals. After that, animals showed gain of weight and a tendency to follow the normal animal corporal mass curve. Animals treated with ALD showed a similar corporal mass pattern

to saline. ALD did not alter initial loss of weight, when compared to saline. After the 3rd day, gain of mass was observed accompanying animals from the saline group (Fig. 4). In the present study, it was seen that ligature-induced periodontitis caused intense alveolar bone resorption and periodontal inflammation, as demonstrated by macroscopic and histological analyses. In addition, a significant decrease Dapagliflozin in BALP and TALP serum levels was observed, and no change in AST and ALT serum levels. Periodontitis caused leucocytosis marked by neutrophilia at the 6th h and marked by lymphomonocytosis on the 7th and 11th days. In addition, an initial weight loss followed by tendency to accompany normal rat corporal mass curve was observed. Treatment with ALD prevented alveolar bone resorption of animals submitted to ligature-induced periodontitis, confirmed in macroscopic and

histological analyses, when compared to saline. ALD, at the higher dose, prevented the reduction of BALP serum levels when compared to saline, and did not alter transaminases’ serum levels. Besides, ALD prevented 6th-h neutrophilia, as well as lymphomonocytosis observed on the 7th and 11th days. ALD did not prevent the initial weight loss, although the animals had shown gain of corporal mass similar to saline corporal mass curve. It has been described that ALD is rapidly eliminated from plasma, and mainly distributed to the bone, where about 60% of the dose is localised in bone tissue of rats.11 Accordingly, Azuma et. al.12 observed the concentration of [14C]-alendronate in several bone tissues at various times after the 0.05 mg kg−1 IV dose.