比较具有牙周炎背景的个体（C级，III/IV期——以前的广泛性侵袭性牙周炎）（H-GAP）与牙周健康受试者（H-Health）在伴随实验种植体周围的分子变化（免疫学/微生物学）方面粘膜炎和牙龈炎。招募 H-GAP 和对照 (H-Health) 受试者，并在单个螺钉固位种植体和一颗对侧牙齿周围诱发实验性粘膜炎/牙龈炎。参与者在选定区域 21 天内不进行口腔卫生，然后在 21 天内接受专业预防和卫生指导。在基线、诱导期间（7、14和21天）以及缓解后（42天）收集临床参数、免疫学标志物（多重分析）和微生物数据（16S rRNA基因测序）。临床上，两组之间没有观察到显着差异。组（n = 10/每组）（H-GAP 与 H-Health）（p > .05，Mann-Whitney 检验）和部位类型（牙齿与种植体）（p > .05，Wilcoxon 检验）牙龈/粘膜炎症发生和消退时或严重程度。在基线和诱导粘膜炎期间，H-GAP 显示种植体周围细胞因子白细胞介素 (IL)-1B、IL-4、IL-17、肿瘤坏死因子-α 和干扰素-γ 的浓度低于 H-Health（p < . 05，曼惠特尼测试）。在两组中，与牙齿相比，种植体在基线和所有后续就诊时都显示出明显更高的炎症背景（p<<0.05，Wilcoxon 检验）。 α 和 β 多样性指标显示，在种植体周围粘膜炎和牙龈炎的诱导和消退过程中，微生物组组成和核心物种丰度发生了显着变化（p < .05，分别为 Shannon 和 Bray-Curtis 指数的限制最大似然法） 。当分别比较牙周和种植体周围微生物组时，H-Health 组和 H-GAP 组之间的这些参数差异并不显着；然而，在每个时间点，种植体周围微生物组与牙周微生物组显着不同。在该试点研究的局限性（例如低功率）内，可以得出结论，不同的微生物变化有助于牙周炎症反应的发生和进展。牙齿和种植体以及牙周病史在调节种植体周围和牙周组织对生物膜积累的免疫反应方面发挥着额外的作用。© 2023 作者。约翰·威利出版的《临床牙周病学杂志》

To compare individuals with a periodontitis background (Grade C, stage III/IV-formerly generalized aggressive periodontitis) (H-GAP) with periodontally healthy subjects (H-Health) in terms of molecular changes (immunological/microbiological) accompanying experimental peri-implant mucositis and gingivitis.H-GAP and control (H-Health) subjects were recruited, and experimental mucositis/gingivitis was induced around a single screw-retained implant and one contralateral tooth. Participants refrained from oral hygiene for 21 days in the selected areas, followed by professional prophylaxis and hygiene instructions for 21 days. Clinical parameters, immunological markers (multiplex analysis) and microbial data (16S rRNA gene sequencing) were collected at baseline, during induction (7, 14 and 21 days) and following remission (42 days).Clinically, no significant differences were observed between the groups (n = 10/each group) (H-GAP vs. H-Health) (p > .05, Mann-Whitney test) and the type of site (tooth vs. implant) (p > .05, Wilcoxon test) at the time of onset and resolution, or severity of gingival/mucosal inflammation. H-GAP displayed lower concentrations of the cytokines interleukin (IL)-1B, IL-4, IL-17, tumor necrosis factor-α and interferon-γ around implants than H-Health at baseline and during induction of mucositis (p < .05, Mann-Whitney test). In both groups, implants showed significantly higher inflammatory background at baseline and all subsequent visits when compared with teeth (p < .05, Wilcoxon test). Alpha and β-diversity metrics showed a significant shift in the microbiome composition and abundances of core species during induction and resolution of peri-implant mucositis and gingivitis (p < .05, restricted maximum likelihood method of Shannon and Bray-Curtis indices, respectively). Differences were not significant for these parameters between the H-Health and H-GAP groups when the periodontal and peri-implant microbiomes were compared separately; however, at each time point, the peri-implant microbiome differed significantly from the periodontal microbiome.Within the limitations of this pilot study (e.g. low power), it can be concluded that different microbial shifts contribute to the onset and progression of inflammatory responses around teeth and implants and that history of periodontal disease experience plays an additional role in modulating the immune response of peri-implant and periodontal tissues to biofilm accumulation.© 2023 The Authors. Journal of Clinical Periodontology published by John Wiley & Sons Ltd.