Abstract：
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.
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.
摘要：
目的：比较有牙周炎背景的个体（C级，III/IV期-以前是全身性侵袭性牙周炎）（H-GAP）与牙周健康受试者（H-Health）在分子变化（免疫学/微生物学）方面伴随实验性种植体周围粘膜炎和牙龈炎。
方法：招募H-GAP和对照（H-Health）受试者，实验性粘膜炎/牙龈炎是在单个螺钉保留的植入物和一个对侧牙齿周围引起的。参与者在选定地区保持21天的口腔卫生，随后是21天的专业预防和卫生指导。临床参数,在基线时收集免疫学标记（多重分析）和微生物数据（16SrRNA基因测序），在诱导期间（7、14和21天）和缓解后（42天）。
结果：临床，组间无显著差异（每组10例）（H-GAPvs.H-健康）（p>.05，Mann-Whitney检验）和部位类型（牙齿与植入)(p>.05，Wilcoxon检验)在发病和消退时，或牙龈/粘膜炎症的严重程度。H-GAP显示较低浓度的细胞因子白细胞介素（IL）-1B，在基线和诱导粘膜炎期间，植入物周围的IL-4，IL-17，肿瘤坏死因子-α和干扰素-γ比H-Health（p<0.05，Mann-Whitney检验）。在这两组中,与牙齿相比，植入物在基线和所有后续就诊时显示出显着更高的炎症背景（p<.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解决过程中，微生物组组成和核心物种的丰度发生了显着变化（p<.05，Shannon和Bray-Curtis指数的有限最大似然方法，分别)。当分别比较牙周和种植体周围微生物组时，H-Health和H-GAP组之间的这些参数差异不显著；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著不同.
结论：在本初步研究的限制范围内（例如低功率），可以得出结论，不同的微生物转移有助于牙齿和种植体周围炎症反应的发生和发展，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中起着额外的作用。
方法：招募H-GAP和对照（H-Health）受试者，实验性粘膜炎/牙龈炎是在单个螺钉保留的植入物和一个对侧牙齿周围引起的。参与者在选定地区保持21天的口腔卫生，随后是21天的专业预防和卫生指导。临床参数,在基线时收集免疫学标记（多重分析）和微生物数据（16SrRNA基因测序），在诱导期间（7、14和21天）和缓解后（42天）。
结果：临床，组间无显著差异（每组10例）（H-GAPvs.H-健康）（p>.05，Mann-Whitney检验）和部位类型（牙齿与植入)(p>.05，Wilcoxon检验)在发病和消退时，或牙龈/粘膜炎症的严重程度。H-GAP显示较低浓度的细胞因子白细胞介素（IL）-1B，在基线和诱导粘膜炎期间，植入物周围的IL-4，IL-17，肿瘤坏死因子-α和干扰素-γ比H-Health（p<0.05，Mann-Whitney检验）。在这两组中,与牙齿相比，植入物在基线和所有后续就诊时显示出显着更高的炎症背景（p<.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解决过程中，微生物组组成和核心物种的丰度发生了显着变化（p<.05，Shannon和Bray-Curtis指数的有限最大似然方法，分别)。当分别比较牙周和种植体周围微生物组时，H-Health和H-GAP组之间的这些参数差异不显著；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著不同.
结论：在本初步研究的限制范围内（例如低功率），可以得出结论，不同的微生物转移有助于牙齿和种植体周围炎症反应的发生和发展，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中起着额外的作用。
