October 2013

The action of the sympathetic nervous system in the control of bone remodeling and immunoinflammatory responses is the basis of the hypothesis that its modulation can influence the progress of periodontal disease. The aim of this study was to analyze the effects of the blockade and of the activation of β-adrenergic receptors in periodontal disease in rats. Thirty-two rats were divided into four groups: 1) animals with induced periodontitis that received propranolol (a non-selective β-adrenergic antagonist) 0.1 mg/kg (PRO); 2) animals with induced periodontitis that received isoproterenol (a non-selective β-adrenergic agonist) 0.75 mg/kg (ISO); 3) animals with induced periodontitis and without drug treatment (L); and 4) animals without induced periodontitis and without drug treatment - control (C). After 14 days of treatment, the rats were euthanized. Right hemi-mandibles were removed and lingual alveolar bone loss measurements were made under a stereomicroscope. Left hemi-mandibles were decalcifi ed and submitted to routine histological preparation for the evaluation of alveolar bone loss in furcation regions, amount of gingival collagen, and immunohistochemistry for receptor activator of nuclear factor-kappa B ligand (RANKL)/osteoprotegerin (OPG) ratio. Animals treated with isoproterenol had significantly more lingual alveolar bone loss than others. The percentage of collagen in gingiva was greater in the propranolol group than in the isoproterenol group. No statistical differences were found among groups with periodontal disease in any other evaluations. The activation of β-adrenergic receptors increased the lingual alveolar bone loss; however, in the model used, the use of β-adrenergic antagonist drugs was not able to modulate the host response significantly. Activation and inhibition of β-receptors have antagonistic actions in collagen degradation in animals with periodontal disease.