Local immunoinflammatory profiles following treatment in primary and permanent dentitions in molar‐incisor pattern periodontitis: One‐year follow‐up

BACKGROUND: The aim of this study is to evaluate the gingival crevicular fluid (GCF) levels of inflammatory markers in both primary and permanent dentitions affected with grade C molar-incisor pattern periodontitis (C-MIP) before and after periodontal therapy. METHODS: Patients from an African American cohort (both sexes; aged 5-21 years) diagnosed with C-MIP in the primary (n = 26) or permanent (n = 44) dentitions were included. After periodontal evaluations, patients received non-surgical periodontal treatment (mechanical debridement with cavitron and hand scaling as needed and 1 week of systemic amoxicillin/metronidazole regimen with dosage modifications for patients weighing under 40 kg). GCF samples were collected from both healthy and diseased sites at baseline, and at 3-, 6-, and 12-months post-therapy, during periodontal maintenance. Levels of 14 cytokines/chemokines were analyzed using multiplex. GCF levels between primary and permanent dentitions and among timepoints were evaluated along with clinical parameters (e.g., probing depth [PD], clinical attachment level, bleeding on probing [BoP], and plaque [PI]). RESULTS: Overall, clinical parameters were improved following treatment in both dentitions up to 12 months. Several cytokines/chemokines were higher in the diseased sites compared with the healthy sites at baseline in both dentitions (p < 0.05). Following treatment, eotaxin reduced in both dentitions in diseased sites (p < 0.05), while other markers were specifically reduced in the permanent (granulocyte-macrophage colony-stimulating factor [GM-CSF], interleukin [IL]-1β, IL-6, IL-8, IL-12p40, tumor necrosis factor-alpha [TNF-α]) dentition. However, some markers, such as eotaxin, IL-1β, IL-2, IL-8, IL-10, IL-12p40, MIP-1α and TNF-α although reduced by 3-, 6-months, showed a tendency of rebound by 6 and 12 months, especially in permanent dentition. Eotaxin and MCP-1 were higher in diseased sites at baseline in the permanent dentition while GM-CSF and interferon-gamma [IFN-γ] in the primary one (p < 0.05). Several cytokines/chemokines were correlated with clinical parameter reductions, and profile analysis showed differences between dentitions up to 6 months. CONCLUSION: Non-surgical therapy combined with systemic antibiotics improved clinical (e.g., PD, CAL, and number of affected sites) outcomes with reductions in pro-inflammatory cytokine/chemokine levels in both primary and permanent dentitions of patients with C-MIP in the long term, with some specific differences observed between the dentitions (NCT01330719).