Peripheral Effects of Periodontitis in Rats: Role of Nitric Oxide

Introduction: High NO production induced by cytokines has a powerful stimulatory effect on osteoclast growth and differentiation. The relation between NO and periodontal disease has not yet been clearly defined, and the available information regarding its production in the mouth cavity is either limited or controversial.

Objective: To investigate the extent of oxidative damage in peripheral organs from rats with periodontitis (P) and under chronic NO synthesis inhibition.

Materials and Methods: P was induced in male Wistar rats by placing a cotton ligature around the first lower molar tooth; sham animals (S) had the ligature immediately removed. Two weeks prior to P induction, and until the end of the experiments, half of the animals received L-NAME (LN; 200mg/L in the drinking water). At days 3 and 7 after the implant procedure, samples of spleen, heart, liver, lung and kidney were collected from all the groups (S, P, S+LN and P+LN) for evaluation of lipid peroxidation (TBARs), protein tyrosine nitration (NT) and granulocyte content (MPO).

Results: Rats with P (day 7) showed significant increases of heart NT and renal MPO, but lower lung MPO activity in comparison to the S group (p<0.05 for all). L-NAME treatment significantly increased liver NT expression in P rats on day 3 (p<0.05), but decreased heart NT on day 7 (p<0.01). In comparison with the P group, P-LN rats showed significantly increased liver, heart and kidney MPO content on day 3 (p<0.05), but lower lung MPO (day 7) and spleen TBARs (day 3) content (p<0.05).

Conclusions: Periodontitis can lead to the oxidative modification of biomolecules in peripheral tissues which, depending on the organ nature and/or the severity of the disease, can be either prevented or exacerbated by inhibiting endogenous NO production. The clinical implications of these findings still remain to be investigated.

Supported by: CNPq/FAPESP