Objectives: NO is known to be an important inflammatory mediator. It was previously shown that exposure of Porphyromonas gingivalis up-regulates NO and suppresses TNF-a production by cultured macrophages (Frolov et al. Immunology 1998). Recently, we demonstrated the expression of iNOS in gingival tissue (Skaleric et al. J Dent Res 2001) and elevated levels of NO in crevicular fluid of diabetic patients (Skaleric et al. J Dent Res 1997). The aim of this study was to correlate the concentration of NO in crevicular fluid with the number of periodontal pathogens present in the subgingival dental plaque. Methods: In the present study 23 type 1 diabetic patients, 15 males and 8 females were included. Gingival fluid and plaque samples were collected from the deepest pocket of the single-rooted teeth. Gingival fluid was collected by microcapillars (Drummond Co, RA, USA) and subgingival plaque samples by paper points. Concentration of NO in gingival fluid was evaluated by Griess reaction and number of P.g. and P.i. by DNA probes (Omni Gene Co, MA, USA). Data were analyzed by one-way ANOVA followed by LSD test. Results: The results demonstrated the presence of NO in all fluid samples in the range from 9.2 – 86.0µM (26.6mM ± 19.8mM). The concentration of NO was increased in deeper pockets and was correlated with the number of P.g. and P.i. in the pockets less than 6 mm deep. In pockets beyond 6 mm significantly increased concentration of NO (PD<6mm=15.9 ± 4.9mM vs. PD>6mm=34.8 ± 16.5mM, p=0.048) and lower numbers of P.g. (PD<6mm=28478.5±27944.4 vs. PD>6mm=21738.6±19894.2, NS) and P.i. (PD<6mm=11612.5±10670.5 vs. PD>6mm=2028.6±1871.1, p=0.006) were found. Conclusion: We are concluding that NO might be an important co-destructive factor in advanced periodontitis of type 1 diabetic patients.

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