Increase in serum and salivary neutrophil gelatinase-associated lipocalin levels with increased periodontal inflammation

Abstract

Increase in serum and salivary neutrophil gelatinase-associated lipocalin levels with increased periodontal inflammation Objective: This study aimed to determine serum and salivary levels of neutrophil gelatinase-associated lipocalin (NGAL) and evaluate NGAL correlation with key anti-interleukin 10 (IL-10) and pro-inflammatory (IL-1β) cytokines in different severities of periodontal diseases. We also calculated the systemic inflammation using the periodontal inflamed surface area (PISA) to evaluate its correlation with NGAL in the study groups. Methodology: Eighty systemically healthy and non-smoking individuals were separated into four groups of 20: clinically healthy (Group 1), gingivitis (Group 2), stage I generalized periodontitis (Group 3, Grade A), and stage III generalized periodontitis (Group 4, Grade A). Sociodemographic characteristics and periodontal parameters were recorded, and PISA was calculated. The serum and salivary levels of interleukin (IL)-1β, IL-10, and NGAL were determined using the enzyme-linked immunosorbent assay (ELISA). Results: We observed a significant increase in serum and salivary NGAL levels from healthy to periodontitis groups (p=0.000). Group 2 presented significantly higher serum and salivary IL-10 levels and salivary IL-1β levels than Group 3 (p=0.000). Serum and salivary parameters (IL-1β, IL-10, and NGAL levels) were strongly positively correlated to periodontal parameters and PISA values (p=0.000). Groups 2 and 3 showed overlapping PISA values. Conclusion: The overlapping PISA values found in Groups 2 and 3 suggest that gingivitis might progress to a systemic inflammatory burden somewhat comparable to stage I periodontitis. This finding is supported by the higher serum and salivary cytokines/mediators levels in the gingivitis group than in stage I periodontitis group. Serum and salivary NGAL levels increased proportionally to disease severity and PISA. NGAL seems to play a role in the pathogenesis of periodontal disease, within the limitation of our study.

Periodontal Inflammation and Systemic Diseases: An Overview

“…Tan and collaborators recently reported that an increase in serum and salivary neutrophil gelatinase-associated lipocalin is positively correlated with periodontal inflammation (Tan et al, 2020 ) though further independent validation trials are currently being carried out. Levels of MMP-12 and of the damage-associated molecular pattern (DAMP) molecule S100s in saliva have been found to be effective markers of PD progression (Holmström et al, 2019 ).…”

Gingival crevicular fluid lipocalin‐2 and semaphorin3A in stage III periodontitis: Non‐surgical periodontal treatment effects

“…Lipopolysaccharide (LPS), interleukin‐1β (IL‐1β), and tumor necrosis factor‐α (TNF‐α) are the strongest inducers of LCN2 11 . LCN2 has been identified in gingival crevicular fluid (GCF), gingival tissues, and saliva, 12 with increased levels in periodontitis patients compared with healthy controls 13,14 …”

Gene expression of inflammatory immune factors and clinical parameters in diabetes and nondiabetes patients with periodontal disease

“…These results are according to Cutler et al (Cutler et al, 1999), Garcia-Hernández et al (Garcia-Hernandez et al, 2012 and Mesia et al (Mesia et al, 2016) that found similar increase in the IL1-β expression in diabetic patients with periodontitis. The higher levels of IL-1β are associated with the severity of periodontitis (Salvi et al, 1997;Tan et al, 2020). Tan et al (Tan et al, 2006), Bastos et al (Bastos et al, 2012), Negrato et al (Negrato et al, 2013), Gomes et al (Gomes et al, 2016) also related high levels of TNF-α in diabetics.…”