Effect of sodium alendronate on alveolar bone resorption in experimental periodontitis in rats.
BACKGROUND
Bisphosphonates are potent inhibitors of bone resorption and were shown to inhibit bone resorption in experimental periodontitis by unknown mechanisms. We studied the effect of the aminobisphosphonate sodium alendronate (SA) in experimental periodontitis. Wistar rats were subjected to ligature placement around the second upper left molars.


METHODS
Animals were treated with SA 0.01 to 0.25 mg/kg subcutaneously (sc), either 1 hour before (prophylactic) or starting 5 days after (therapeutic) periodontitis induction and daily until the rats were sacrificed (11 days). Controls received saline. Animals were weighed daily. Alveolar bone loss was measured as the difference (in millimeters) between the cusp tip and the alveolar bone. The periodontium and the surrounding gingivae were examined at histopathology, and the neutrophil influx into the gingivae was assayed using myeloperoxidase activity. The local bacterial flora was assessed through culture of the gingival tissue in standard aerobic and anaerobic media.


RESULTS
Alveolar bone loss was significantly and dose dependently inhibited by SA either as a prophylactic or therapeutic treatment compared to the control. SA reduced tissue lesion at histopathology, with partial preservation of the periodontium, coupled to decreased myeloperoxidase activity compared to the control. The reduced neutrophil influx was also shown in carrageenan-induced peritonitis, used as a control experiment for this parameter. SA also significantly inhibited the growth of pigmented bacilli and Fusobacterium nucleatum, which are important in the pathogenesis of periodontal disease. SA also inhibited the in vitro growth of isolated Peptostreptococcus sp.


CONCLUSIONS
Sodium alendronate preserves alveolar bone resorption and has anti-inflammatory and antibacterial activities in experimental periodontitis.
Menezes
Adriana M A
AM
Department of Physiology and Pharmacology, Faculty of Medicine, Federal University of Ceará, Fortaleza, Brazil.
Rocha
Francisco Airton C
FA
Chaves
Hellíada V
HV
Carvalho
Cibele B M
CB
Ribeiro
Ronaldo A
RA
Brito
Gerly Anne C
GA
D019386:Alendronate / Q000627:therapeutic use*; D016301:Alveolar Bone Loss / Q000188:drug therapy / Q000517:prevention & control*; D000818:Animals; D000890:Anti-Infective Agents / Q000627:therapeutic use; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use; D050071:Bone Density Conservation Agents / Q000627:therapeutic use*; D001862:Bone Resorption / Q000188:drug therapy / Q000517:prevention & control*; D004305:Dose-Response Relationship, Drug; D005260:Female; D016967:Fusobacterium nucleatum / Q000187:drug effects; D005881:Gingiva / Q000382:microbiology / Q000473:pathology; D020556:Neutrophil Infiltration / Q000187:drug effects; D009504:Neutrophils / Q000473:pathology; D010462:Peptostreptococcus / Q000187:drug effects; D010518:Periodontitis / Q000188:drug therapy / Q000473:pathology / Q000517:prevention & control*; D010538:Peritonitis / Q000517:prevention & control; D009195:Peroxidase / Q000032:analysis; D011292:Premedication; D051381:Rats; D017208:Rats, Wistar
D000890:Anti-Infective Agents; D000893:Anti-Inflammatory Agents; D050071:Bone Density Conservation Agents; D009195:Peroxidase; D019386:Alendronate