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Saliva and Serum Immune Responses in Apical Periodontitis.

ABSTRACT: Apical periodontitis is an inflammatory reaction at the apex of an infected tooth. Its microbiota resembles that of marginal periodontitis and may induce local and systemic antibodies binding to bacteria- and host-derived epitopes. Our aim was to investigate the features of the adaptive immune response in apical periodontitis. The present Parogene cohort (n = 453) comprises patients with cardiac symptoms. Clinical and radiographic oral examination was performed to diagnose apical and marginal periodontitis. A three-category endodontic lesion score was designed. Antibodies binding to the bacteria- and host-derived epitopes were determined from saliva and serum, and bacterial compositions were examined from saliva and subgingival samples. The significant ORs (95% CI) for the highest endodontic scores were observed for saliva IgA and IgG to bacterial antigens (2.90 (1.01-8.33) and 4.91 (2.48-9.71)/log10 unit), saliva cross-reacting IgG (2.10 (1.48-2.97)), serum IgG to bacterial antigens (4.66 (1.22-10.1)), and Gram-negative subgingival species (1.98 (1.16-3.37)). In a subgroup without marginal periodontitis, only saliva IgG against bacterial antigens associated with untreated apical periodontitis (4.77 (1.05-21.7)). Apical periodontitis associates with versatile adaptive immune responses against both bacterial- and host-derived epitopes independently of marginal periodontitis. Saliva immunoglobulins could be useful biomarkers of oral infections including apical periodontitis-a putative risk factor for systemic diseases.

SUBMITTER: Pietiainen M

PROVIDER: S-EPMC6617293 | biostudies-literature | 2019 Jun

REPOSITORIES: biostudies-literature

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Saliva and Serum Immune Responses in Apical Periodontitis.

Pietiäinen Milla M Liljestrand John M JM Akhi Ramin R Buhlin Kåre K Johansson Anders A Johansson Anders A Paju Susanna S Salminen Aino A Mäntylä Päivi P Sinisalo Juha J Tjäderhane Leo L Hörkkö Sohvi S Pussinen Pirkko J PJ

Journal of clinical medicine 20190621 6

Apical periodontitis is an inflammatory reaction at the apex of an infected tooth. Its microbiota resembles that of marginal periodontitis and may induce local and systemic antibodies binding to bacteria- and host-derived epitopes. Our aim was to investigate the features of the adaptive immune response in apical periodontitis. The present Parogene cohort (<i>n</i> = 453) comprises patients with cardiac symptoms. Clinical and radiographic oral examination was performed to diagnose apical and marg ...[more]

PMID: 31234349

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Project description:Apical periodontitis (AP) is an inflammatory disease occurring following tooth infection with distinct osteolytic activity. Despite increasing evidence that sensory neurons participate in regulation of non-neuronal cells, their role in the development of AP is largely unknown. We hypothesized that Nav1.8+ nociceptors regulate bone metabolism changes in response to AP. Methods: A selective ablation of nociceptive neurons in Nav1.8Cre/ DTALox mouse line was used to evaluate the development and progression of AP using murine model of infection-induced AP. Micro-computed tomography examination was applied to quantify osteolytic lesions following induction of AP. Additionally, RT-PCR, RNAscope, and immunohistochemical (IHC) analysis were used to investigate the expression of immune cells, osteoblasts, and osteoclasts. Co-culture of trigeminal ganglia (TG) neurons from DTALox (control) and Nav1.8Cre/ DTALox mice with either IDG-SW3 or MC3T3-E1 osteoblast precursor cell lines or RAW264.7 murine macrophages were used to assess osteoblast and osteoclast function, by RNA sequencing, mineralization, and osteoclastic assays. Results: Ablation of Nav1.8+ nociceptors had earlier progression of AP with larger osteolytic lesions compared to the controls. IHC and RNAscope analysis demonstrated greater number of macrophages, T-cells, osteoclast and osteoblast precursors as well as an increased RANKL:OPG ratio at earlier time points among Nav1.8Cre/ DTALox mice. There was an increased expression of IL-1a and IL-6 within lesions of nociceptor-ablated mice. Further, co-culture experiments demonstrated that TG neurons promoted osteoblast mineralization and inhibited osteoclastic function. Conclusion: The findings suggest that TG Nav1.8+ neurons contribute to modulation of the AP development by delaying the influx of immune cells, promoting osteoblastic differentiation, and decreasing osteoclastic activities. This newly uncovered mechanism could become a therapeutic strategy for the treatment of AP and minimize the persistence of osteolytic lesions in refractory cases.

Project description:AimThe aim of the study was to measure serum levels of molecular markers of inflammation in patients undergoing non-surgical root canal retreatment (Re-RCT) and periapical surgery (PS) for the treatment of apical periodontitis and to establish if such levels are influenced by the size of apical radiolucencies at baseline and by the treatment outcome.MethodologyA total of 115 participants were recruited (n = 50 Controls, n = 35 Re-RCT, n = 30 PS). Preoperative periapical radiographs and cone beam CT (CBCT) scans of teeth were taken. Blood was collected from treatment groups at baseline, 3-, 6-, and 12-month post-treatment and from controls at baseline and 12 months. Serum levels of IL-1β, IL-6, IL-8, TNF-α, Pentraxin 3, ICAM-1, VCAM-1, hs-CRP, FGF-23, MMP-2, MMP-8, MMP-9, C3 and ADMA were analysed using multiplex immunoassay and enzyme-linked immunosorbent assay. Different time points within the same group were compared using Wilcoxon signed-rank test, and differences between groups were analysed using the Mann-Whitney test. Non-linear association between different factors was assessed using Spearman's correlation.ResultsPreoperative serum levels of FGF-23, IL-1β, hs-CRP and ADMA were significantly higher in the diseased groups compared with controls (p < .001; p = .008; p < .001; p = .013, respectively). The preoperative size of the radiolucency was associated with increased levels of FGF-23, IL-1β and IL-6. At 3-months following treatment, IL-1β, IL-8, hs-CRP, C3, MMP-2 and MMP-9 levels increased compared with baseline in treatment groups. IL-1β and IL-8 further increased at 6 months, whereas FGF-23, hs-CRP, C3, MMP2 and MMP-9 decreased. One-year post-treatment, FGF-23, pentraxin-3 and ADMA were significantly reduced below baseline levels. At the 1-year review, CBCT revealed that 25.9% of treated cases completely healed, while 63% were healing, and 11.1% failed. Treatment outcome was found to be influenced by preoperative levels of ADMA and IL-8 levels at 6 months.ConclusionsBoth symptomatic and asymptomatic apical periodontitis (AP) can contribute to increased levels of molecular markers of inflammation. A further transient inflammatory markers rise after root canal retreatment and apical surgery were demonstrated. Successful endodontic treatment and periapical surgery result in a long-term reduction in inflammatory marker levels.

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Saliva and Serum Immune Responses in Apical Periodontitis.

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Saliva and Serum Immune Responses in Apical Periodontitis.

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