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Background and Objectives Neutrophils are emerging as a key player in periodontal pathogenesis. The surface expression of cellular markers enables functional phenotyping of neutrophils which have distinct roles in disease states. This study aimed to evaluate the effect of periodontal management on neutrophil phenotypes in peripheral blood in periodontitis patients over one year. Materials and Methods Peripheral blood and the periodontal parameters, mean probing depth and percentage of sites with bleeding on probing (%BOP), were collected from 40 healthy controls and 54 periodontitis patients at baseline and 3‐, 6‐ and 12‐ months post‐treatment. Flow cytometry was used to identify CD11b+, CD16b+, CD62L− and CD66b+ expression on neutrophils, neutrophil maturation stages as promyelocytes (CD11b−CD16b−), metamyelocytes (CD11b+CD16b−) and mature neutrophils (CD11b+CD16b+), and suppressive neutrophil phenotype as bands (CD16dimCD62Lbright), normal neutrophils (CD16brightCD62Lbright) and suppressive neutrophils (CD16brightCD62Ldim). Results CD62L− expression decreased with treatment. No differences were observed in neutrophil maturation stages in health or disease upon treatment. Suppressive and normal neutrophils showed a reciprocal relationship, where suppressive neutrophils decreased with treatment and normal neutrophils increased with treatment. In addition, %BOP was associated with suppressive neutrophils. Conclusion This study demonstrates that management of periodontitis significantly modifies distinct neutrophil phenotypes in peripheral blood. Suppressive neutrophils may play a role in the pathogenesis of periodontitis. However, their exact role is unclear and requires further investigation.

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AimsT‐cells are known to have a role in periodontitis, however, the effect of periodontal therapy on peripheral memory T‐cells is unclear. This study evaluated variation in peripheral memory T‐cells and red complex bacteria in sub‐gingival plaque in patients undergoing periodontal management.MethodsPeripheral blood mononuclear cells and sub‐gingival plaque were collected from 54 periodontitis patients at baseline, 3‐, 6‐ and 12‐months post‐therapy and 40 healthy controls. Periodontitis patients were divided into treatment outcome (TxO) groups based on prevalence of sites with probing depth ≥5 mm as good (<10% of sites), moderate (10–20%) or poor (>20%) at study conclusion. Naïve (TN—CCR7+CD45RA+), central memory (TCM—CCR7+CD45RA−), effector memory (TEM—CCR7−CD45RA−) and effector memory T‐cells re‐expressing CD45RA (TEMRA—CCR7−CD45RA+) were phenotyped using flow cytometry in CD4+, CD8+, CD4+CD8+ and CD4−CD8− T‐cells and red complex bacteria were quantified using qPCR.ResultsAt baseline, periodontitis subjects had significantly greater mean probing depths and Porphyromonas gingivalis proportions, lower TN but higher CD4+ TCM, CD8+ TCM, CD4+CD8+ TEM and CD4−CD8− TEM cell proportions compared to health. Periodontal therapy decreased mean probing depths, P. gingivalis proportions, TEM and CD4+ and CD8+ TCM cells, but increased TN and CD4+ and CD8+ TEMRA cells. The T‐cell profile in the good TxO group showed therapy‐related changes in CD4+ TEM, and CD8+ TN and TEM cells, whereas, no changes were observed in the poor TxO group.ConclusionManagement and the reduction in red complex bacteria were associated with changes in peripheral memory T‐cells in periodontitis.

Aim: Periodontitis has been associated with other systemic diseases with underlying inflammation responsible for the shared link. This study evaluated longitudinal variation in peripheral T helper cells in periodontitis patients undergoing management over 1 year. Materials and methods: Periodontal parameters and peripheral blood mononuclear cells (PBMCs) were collected from 54 periodontitis patients at baseline, and 3-, 6-and 12-months post-treatment and 40 healthy controls. IFN-γ + , IL-4 + , IL-17 + and Foxp3 + and their double-positive expression were identified in CD4 + and TCRαβ + cells using flow cytometry. PBMCs were incubated with P. gingivalis, and IFN-γ, IL-4, IL-17 and IL-10 in cell supernatant were measured by ELISA. Cells and cytokines were also assessed based on clinical response to treatment where good (<10% of sites), moderate (10-20%) and poor (>20%) treatment outcome (TxO) groups had probing depths of ≥5 mm at study conclusion. Results: IFN-γ + cells were lower at baseline, and 3-and 6-months compared to health, whereas Foxp3 + cells were increased at 12-months compared to all preceding timepoints and health. The good TxO group showed treatment-related variation in IFN-γ + and Foxp3 + cells, whereas the poor TxO group did not. IFN-γ and IL-17 cytokine expression in cell supernatants was significantly lower at baseline compared to health, and IFN-γ and IL-10 showed treatment-related decrease. Conclusion: This study suggests that IFN-γ + and Foxp3 + cells may have a role in the systemic compartment in periodontitis. Periodontal management has local and systemic effects, and thus, assessment and management of periodontitis should form an integral part of overall systemic health.