The role of nitric oxide in oral diseases

Brennan, Peter A.; Thomas, Grunwald; Langdon, John H.

doi:10.1016/s0003-9969(02)00183-8

Cited by 93 publications

(96 citation statements)

References 53 publications

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“…Plaque index (PI) [11], gingival index (GI) [12], probing pocket depth (PPD), and clinical attachment level (CAL) were recorded as clinical parameters. When the CEJ was masked by a restoration or a crown, the relative CAL was recorded.…”

Section: Latha Et Almentioning

confidence: 99%

Effect of Non-Surgical Therapy on Salivary Nitric Oxide and Lipid Peroxidation Levels in Type Ii Diabetic and Non Diabetic Patients With Periodontal Disease

Latha

Uppoor

Nayak

et al. 2018

Asian J Pharm Clin Res

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Objective: Reactive oxygen species have been identified as potential factors causing periodontal tissue destruction. Elevated levels of these in patients with chronic periodontitis and diabetes may aggravate the oxidative stress burden thereby accelerating the tissue damage associated with diabetes. The present study aimed to assess the effect of diabetes and periodontal disease on the oxidative stress markers and the effect of non-surgical therapy on these markers.Methods: A total of 50 participants were divided into four groups based on the selection criteria. In addition to clinical parameters and biochemical parameters (salivary nitric oxide [NO] and malondialdehyde [MDA] levels) were assessed using spectrophotometric method at baseline and 3 months after non-surgical periodontal therapy.Result: There was a statistically significant difference in the clinical parameters as well as NO and MDA levels in patients with type 2 diabetes and chronic periodontitis than other three groups at baseline and at 3 months after non-surgical periodontal therapy. Conclusion:Diabetes mellitus and periodontitis have a compounding effect on the oxidative stress. Periodontal therapy is essential for diabetic patients as it can lower the levels of oxidative damage.

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Section: Latha Et Almentioning

confidence: 99%

Effect of Non-Surgical Therapy on Salivary Nitric Oxide and Lipid Peroxidation Levels in Type Ii Diabetic and Non Diabetic Patients With Periodontal Disease

Latha

Uppoor

Nayak

et al. 2018

Asian J Pharm Clin Res

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“…Nitric oxide (NO) has been intensively studied in the medical field (4). In addition, NO has been linked to the etiopathogenesis of periodontal disease (5,6) and is expressed in salivary glands as well as in their product (7,8).…”

Section: Introductionmentioning

confidence: 99%

Nitric oxide levels in saliva increase with severity of chronic periodontitis

et al. 2007

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The aims of this study were to compare nitric oxide (NO) levels in stimulated whole saliva from individuals with and without generalized chronic periodontitis (GCP), and to evaluate correlations between these levels with a clinical diagnostic parameter. According to specific criteria, 30 individuals were divided into three groups: one comprising individuals without periodontitis (GC), a second comprising individuals with moderate GCP (GM), and a third comprising individuals with advanced GCP (GA). Samples were collected and NO levels measured. NO in the GCP group (GM: 7.78 µM; GA: 15.79 µM) was higher than in the GC group (5.86 µM). NO levels in the GA group were significantly higher (P < 0.0001) than in the GC group, and could also differentiate (P < 0.0001) the moderate and advanced forms of the disease.

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“…However, with activation, these neutrophils have increased secretion of NO with antimicrobial effects. As in other host-pathogen interactions (22), P. gingivalis has been shown to trigger the production of NO in immune and nonimmune host cells by activating the expression of inducible nitric oxide synthases (9,54) and can survive in NO concentrations ranging from 4.9 M to 19.2 M (47). Elevated NO concentrations are reported to cause vasodilatation and a decrease in platelet aggregation, which may contribute to gingival bleeding (18), and to have cytotoxic effects on surrounding host tissue that can lead to alveolar bone loss (7).…”

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confidence: 99%

Nitric Oxide Stress Resistance in Porphyromonas gingivalis Is Mediated by a Putative Hydroxylamine Reductase

et al. 2012

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bPorphyromonas gingivalis, the causative agent of adult periodontitis, must maintain nitric oxide (NO) homeostasis and surmount nitric oxide stress from host immune responses or other oral bacteria to survive in the periodontal pocket. To determine the involvement of a putative hydroxylamine reductase (PG0893) and a putative nitrite reductase-related protein (PG2213) in P. gingivalis W83 NO stress resistance, genes encoding those proteins were inactivated by allelic exchange mutagenesis. The isogenic mutants P. gingivalis FLL455 (PG0893::ermF) and FLL456 (PG2213::ermF) were black pigmented and showed growth rates and gingipain and hemolytic activities similar to those of the wild-type strain. P. gingivalis FLL455 was more sensitive to NO than the wild type. Complementation of P. gingivalis FLL455 with the wild-type gene restored the level of NO sensitivity to a level similar to that of the parent strain. P. gingivalis FLL455 and FLL456 showed sensitivity to oxidative stress similar to that of the wild-type strain. DNA microarray analysis showed that PG0893 and PG2213 were upregulated 1.4-and 2-fold, respectively, in cells exposed to NO. In addition, 178 genes were upregulated and 201 genes downregulated more than 2-fold. The majority of these modulated genes were hypothetical or of unknown function. PG1181, predicted to encode a transcriptional regulator, was upregulated 76-fold. Transcriptome in silico analysis of the microarray data showed major metabolomic variations in key pathways. Collectively, these findings indicate that PG0893 and several other genes may play an important role in P. gingivalis NO stress resistance. Porphyromonas gingivalis is a Gram-negative anaerobic bacterium that is a primary etiologic agent of periodontal disease. This infection-induced disease is characterized by inflammation, which can result in host-mediated destruction of tooth-supporting tissues and structures (18). Nitric oxide (NO) is a key component of the host immune response. Oral neutrophils can constitutively secrete low concentrations of NO via the involvement of multiple NO synthases. However, with activation, these neutrophils have increased secretion of NO with antimicrobial effects. As in other host-pathogen interactions (22), P. gingivalis has been shown to trigger the production of NO in immune and nonimmune host cells by activating the expression of inducible nitric oxide synthases (9, 54) and can survive in NO concentrations ranging from 4.9 M to 19.2 M (47). Elevated NO concentrations are reported to cause vasodilatation and a decrease in platelet aggregation, which may contribute to gingival bleeding (18), and to have cytotoxic effects on surrounding host tissue that can lead to alveolar bone loss (7). NO is present in the saliva and gingival fluid of periodontitis patients (7,18,57). Further, saliva NO concentrations have been shown to increase with the severity of periodontitis (47).P. gingivalis, as an asaccharolytic microorganism, metabolizes nitrogenous compounds as a source of energy and generates a micr...

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The role of nitric oxide in oral diseases

Cited by 93 publications

References 53 publications

Effect of Non-Surgical Therapy on Salivary Nitric Oxide and Lipid Peroxidation Levels in Type Ii Diabetic and Non Diabetic Patients With Periodontal Disease

Effect of Non-Surgical Therapy on Salivary Nitric Oxide and Lipid Peroxidation Levels in Type Ii Diabetic and Non Diabetic Patients With Periodontal Disease

Nitric oxide levels in saliva increase with severity of chronic periodontitis

Nitric Oxide Stress Resistance in Porphyromonas gingivalis Is Mediated by a Putative Hydroxylamine Reductase

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