Treatment of localized aggressive periodontitis alters local host immunoinflammatory profiles: A long-term evaluation

Abstract

Aim: To evaluate the local immunoinflammatory profiles in localized aggressive periodontitis patients (LAP) before and after periodontal treatment and maintenance.

Methods: Sixty-six African-Americans with LAP (7-21 years old) were included. After periodontal examination, all patients received periodontal treatment with mechanical debridement plus systemic amoxicillin/metronidazole for 7 days. Gingival crevicular fluid was collected from diseased and healthy sites at baseline and 3, 6, 12, and 24 months following treatment. Levels of 16 inflammatory/bone resorption markers were determined using Milliplex® . Univariate and correlation analyses were performed among all parameters/biomarkers. Discriminant analyses (DA) evaluated profile differences between LAP diseased and healthy sites at each time point as compared to the baseline.

Results: Reductions in the clinical parameters (except for visible plaque) were observed at all time points compared to the baseline. Levels of IL-12p70, IL-2, IL-6, MIP-1α, RANKL, and OPG were reduced after treatment, and several cytokines/chemokines were correlated with clinical parameters reductions. DA showed that differences in the immunoinflammatory profiles between LAP diseased and healthy sites decreased after periodontal treatment compared to the baseline.

Conclusions: Periodontal treatment modified the local immunoinflammatory profile of LAP sites in the long term, as suggested by changes in biomarkers from baseline, along with clinical stability of the disease. (Clinicaltrials.gov number, NCT01330719).

Keywords: aggressive periodontitis; gingival crevicular fluid; inflammation; long-term effects; therapy.

Conflict of interest statement

Conflict of Interest Statement:

The authors declare that there are no conflicts of interest in this study.

© 2020 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.

Figures

Figure 1.

Clinical periodontal parameters of localized aggressive periodontitis (LAP) patients in response to treatment with mechanical debridement plus 1-week administration of systemic amoxicillin and metronidazole. Parameters were recorded at baseline (BL) and 3, 6, 12 and 24 months (M) post periodontal treatment/maintenance. (A) Mean probing depth of full mouth (PD All). (B) Mean probing depth for diseased sites sampled for GCF (PD Site). (C) Mean clinical attachment levels of all affected sites (CAL All). (D) Mean clinical attachment levels for diseased sites sampled for GCF (CAL Site). (E) Percentage of bleeding on probing (BOP). (F) Percentage of visible plaque (Plaque). ****p

Figure 2.

Gingival crevicular fluid biomarker levels of eotaxin, GM-CSF, IFN-γ, IL-10, IL-12p 40, IL-12p70, IL-1β, and IL-12 in diseased sites and healthy sites of localized aggressive periodontitis (LAP) patients in response to periodontal treatment/maintenance. Biomarkers were evaluated at baseline (BL) and 3, 6, 12 and 24 months (M) after treatment. ##P<0.01 and #P<0.05, significant difference between baseline diseased and healthy sites; + P>0.05, but less than 0.1 between baselines (Wilcoxon signed-rank test). ***P

Figure 3.

Gingival crevicular fluid biomarker levels of IL-6, IL-8, IP-10, MCP-1, MIP-1α, TNF-α, RANKL, and OPG in diseased sites and healthy sites of localized aggressive periodontitis (LAP) patients in response to periodontal treatment/maintenance. Biomarkers were evaluated at baseline (BL) and 3, 6, 12 and 24 months (M) after treatment. ##P<0.01 and #P<0.05, significant difference between baseline diseased and healthy sites; + P>0.05, but less than 0.1 between baselines (Wilcoxon signed-rank test). ***P

Figure 4.

Discriminatory potential of gingival crevicular fluid biomarkers in localized aggressive periodontitis diseased sites (LAP-D) and localized aggressive periodontitis healthy sites (LAP-H) in response to periodontal treatment/maintenance. Biomarkers were evaluated at baseline (BL) and 3, 6, 12 and 24 months (M) after periodontal treatment/maintenance. Figure 3 (A–E) represent plots of significant separation in DA according to biomarkers among groups: A: comparison between BL and 3M (Wilks’ lambda = 0.002 in canonical function 1); B: comparison between BL and 6M (Wilks’ lambda = 0.113 in canonical function 1); C: comparison between BL and 12M (Wilks’ lambda = 0.001 in canonical function 1); D: comparison between BL and 24M (Wilks’ lambda = 0.000 in canonical function 1); E - comparison between diseased sites at BL, 3M, 6M, 12M, 24M (Wilks’ lambda = 0.003 in canonical function 1).