NOS is classified into three

NOS is classified into three isoforms: endothelial (eNOS), neuronal (nNOS), and inducible (iNOS), iNOS is expressed in macrophages (Eisenstein, Huang, Meissler Jr, & al-Ramadi, 1994) and osteoblast-like cells (Riancho et al., 1995) and is involved in the regulation of inflammatory reactions (Eisenstein et al., 1994). iNOS acts as both an intercellular and intracellular messenger, and its effects are considered to be local (Kendall, Haase, Li, Xiao, & Bartold, 2000). iNOS (which produces NO) has been shown to mediate inflammation-induced bone resorption on the compression side (Baloul, 2016). iNOS production was reported to be increased in the periodontal ligament and connective tissue between the roots of orthodontically positioned teeth (Brennan, Thomas, & Langdon, 2002). Arginine is a semi-essential amino endothelin receptor antagonist involved in various physiologic processes, such as protein and urea synthesis. It is also the precursor of other compounds, including creatinine. NO, polyamines, and proline (Satriano, 2004). Two pathways of arginine metabolism in inflammation are the arginine-NO and arginine-urea-ornithine pathways. NOS and arginase take place in both pathways and they compete for the common substrate L-arginine. Liver arginase uses L-arginine to produce urea and ornithine; however, arginase is also present in extra-hepatic tissues such as the salivary glands (Konarska, Thomaszevski, Colombo, & Terheggen, 1985). Arginase may reduce NO production by depleting the common substrate (Mori, Gotoh, Nagasaki, Takiguchi, & Sonoki, 1998). Thus, increased salivary arginase activities detected in periodontitis patients may cause decreased NO synthesis and lead to a decrease in the antibacterial property of saliva. In turn, periodontal tissues may become more susceptible to existing pathogens (Güllü, Ozmeric, Tokman, Elgün, & Balos, 2005).
Materials and methods
Results The comparison of clinical and biochemical parameters around implants (PISF) and natural teeth (GCF) at baseline are shown in Table 1. For all clinical and biochemical parameters, the differences between teeth and implants were not found to be statistically significant (0.05). Table 2 shows the changes in NO level and arginase enzyme in saliva after loading. Arginase activities in saliva were evaluated at baseline and at months 1, 3, and 6 following loading. Arginase activities increased from baseline to month 6; however, the arginase levels were found similar at each time interval (0.05). Salivary NO levels were not found to be statistically significant at baseline and at months 1, 3, and 6 following loading (0.05). There was no statistically significant difference in GI and PD in the chosen time intervals (0.05) (Table 3). However, the decrease of PI was found to be statistically significant at months 3 and 6 when compared to baseline (0.01). BOP values were found higher in months 3 and 6 when compared to baseline (0.05); however, there were no significant differences in the other time intervals (p<0.05). PISF presented a significant increase in NO levels over time (p<0.001) (Table 3). While the differences of NO levels between baseline and month 1 were not statistically significant (p>0.05), values for months 3 and 6 were significantly higher compared with baseline (0.01, 0.001, respectively). Similar to NO, arginase enzyme increased significantly over time (p<0.001) (Table 3). The difference in arginase enzyme between baseline and month 1 were not statistically significant (p>0.05), whereas values for months 3 and 6 were statistically higher when compared with baseline (p<0.05, p<0.001, respectively). There were also significant differences between months 1 and 6 (p>0.05).
Discussion The maintenance of clinical health at the peri-implant sites and inflammation prevention are critical to the long-term success of dental implants. This is the reason why measures/tools that aim for early detection of the peri-implant inflammatory process are of great importance (Tözüm et al., 2008).