Determination of levels of nitric oxide in smoker and nonsmoker patients with chronic periodontitis

Abstract

PurposeCigarette smoking is a major risk factor in periodontal diseases. The pathogenesis of periodontal diseases may be affected by alterations of the inflammatory response by smoke. Nitric oxide (NO) is a gaseous, colorless, highly reactive, short-lived free radical with a pivotal role in the regulation of various physiological and pathological mechanisms in the body. It is important in host defense and homeostasis, on the one hand, whereas, on the other hand, it modulates the inflammatory response in periodontitis, leading to harmful effects. The aim of this study was to assess the levels of NO in both the serum and saliva of smokers and nonsmokers having chronic periodontitis and to compare them with periodontally healthy controls.MethodsSixty subjects participated in the study and were divided into three groups: group I, healthy nonsmoking subjects; group II, nonsmoking patients with chronic periodontitis; group III, smoking patients with chronic periodontitis. Each group consisted of twenty subjects. The biochemical estimation of NO in the collected serum and in the saliva was performed using the Griess colorimetric reaction.ResultsThe results showed that the mean value of the salivary and serum NO was greater in group II than in group I, and also greater in group III than in group II.ConclusionsNO appears to play an important and rather complex role in the immuno-inflammatory process and in the remodeling and maintenance of osseous structures. It is therefore logical that modulation of this mediator has potential for the treatment of a number of inflammatory conditions including periodontal disease.

Nitrosative Stress Biomarkers in the Non-Stimulated and Stimulated Saliva, as well as Gingival Crevicular Fluid of Patients with Periodontitis: Review and Clinical Study

“…↑ NO p = 0.000 Positive correlation with PD Despite the fact that the Griess reaction was the most frequently used method in the methodology for determining the nitric oxide, these test results are very heterogeneous. Significantly higher salivary NO levels in the course of periodontitis, as in our assessment, were obtained in five other studies [6,25,26,28,29], and significantly decreased in two others [7,27]. These differences resulted from many reasons.…”

“…Table 2 shows the test results on nitric oxide levels in GCF, saliva, and blood serum in periodontitis (the previous classification of periodontitis was used in tests. [6,7,[24][25][26][27][28][29][30].…”

“…Currently, biochemical methods, compatible with a new classification, are being sought. Table 2 shows the test results on nitric oxide levels in GCF, saliva, and blood serum in periodontitis (the previous classification of periodontitis was used in tests) [6,7,[24][25][26][27][28][29][30]. ↑ NO p = 0.000 Positive correlation with PD Despite the fact that the Griess reaction was the most frequently used method in the methodology for determining the nitric oxide, these test results are very heterogeneous.…”

Enterosalivary nitrate metabolism and the microbiome: Intersection of microbial metabolism, nitric oxide and diet in cardiac and pulmonary vascular health

“…A long-described, yet puzzling and hitherto unproven, association between periodontal disease and CVD[280–282] has been variably attributed to direct vascular entry of these largely nitrate-reducing oral pathogens[283–286], generalized immune activation, systemic inflammation, and endothelial dysfunction, all processes that are improved with periodontal treatment (typically bactericidal chlorhexidine rinses with or without quadrant scaling)[193,287–290]. Interestingly, both salivary nitrate and nitrite concentrations and gingival expression of NO-forming NOS have been found to be increased in periodontal disease, which also tend to increase with disease severity and improve with periodontal treatment[99,193,291,292]. However, it remains uncertain whether increased nitrite derives from oxidation of gingival NOS-derived NO or bacterial reduction of salivary nitrate.…”

Protective effect of catalpol on nicotine-induced injury of alveolar bone and associated underlying mechanisms

“…It may affect the synthesis of osteoblasts during maturation, and is an important marker for bone mineralization and activity of osteoblasts (23). Osteocalcin is secreted by osteoblasts during the matrix mineralization stage, and primarily facilitates bone mineralization (24). The present study demonstrated that nicotine inhibited AP and osteocalcin expression, thereby leading to injury to alveolar bone.…”