种植体周围炎与牙周炎部位的微生物复杂性对比

William Bane DMD
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引用次数: 0

摘要

方法从诊断为种植体周围炎、III/IV 期牙周炎或临床牙龈健康(对照组)的人体供体中各收集七份龈下菌斑标本。提取细菌 DNA 并扩增 16s rRNA 基因的 V4 区域。对 PCR 产生的扩增子进行测序,并使用 Silva 数据库对操作分类单元(OTU)进行分类。估算香农多样性指数(SDI),并使用方差分析检验α多样性差异。计算布雷-柯蒂斯指数以估计各组的贝塔多样性,并完成主坐标分析(PCoA)排序。使用 PERMANOVA 评估各组微生物组结构的显著差异。结果根据样本来源将微生物群分为三个不同的组。PCoA 结果显示,临床健康与种植体周围炎之间(P 调整后为 0.05)、临床健康与牙周炎之间(P 调整后为 0.05)以及种植体周围炎与牙周炎之间(P 调整后为 0.05)的差异具有统计学意义。临床健康病例的生物膜平均 SDI 为 2.46。相比之下,种植体周围炎组和牙周炎组的平均 SDI 分别为 3.023(Padjusted <0.05)和 3.061(P-adjusted <0.05)。在种植体周围炎组和牙周炎组之间,有 8 个 OTU 的丰度差异具有统计学意义。结论病变环境之间的微生物差异不能归因于特定细菌的明确存在或缺乏。启示牙周病学和牙科种植学中一个新出现的假说认为,组织的炎症性破坏不是由一种或几种关键细菌造成的。相反,疾病是由真正的多微生物活动引起的,其特点是生物膜中特定基因的积累,因此也具有特定的功能。此外,已知种植体周围炎的发病机制与影响炎症反应的钛微粒有关。本研究观察到的生物膜多样性和组成的差异可能反映了钛颗粒、宿主免疫细胞和种植体周围炎部位生物膜之间复杂的相互作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Microbial complexity at peri-implantitis versus periodontitis sites

OBJECTIVES

The purpose of this investigation was to compare the diversity of microbial communities at peri-implantitisversus stage III/IV periodontitis-affected sites using next-generation sequencing.

METHODS

Seven subgingival plaque specimens from each group of human donors diagnosed with peri-implantitis, stage III/IV periodontitis, or clinical gingival health (control group) were collected. Bacterial DNA was extracted, and the V4 region of the 16s rRNA gene was amplified. PCR-generated amplicons were sequenced, and operational taxonomic units (OTUs) were classified using the Silva database. Shannon Diversity Indices (SDIs) were estimated, and alpha diversity differences were tested using ANOVA. Bray-Curtis indices were computed to estimate beta diversity across groups, and Principal Coordinate Analysis (PCoA) ordination was completed. Significant variations in microbiome structure across groups was assessed using PERMANOVA. Genera that were differentially abundant across groups (absolute log2 fold change > 2) were identified.

RESULTS

OTUs clustered into three distinct groups based on sample source. PCoA results demonstrated statistically significant differences between clinical health and peri-implantitis (P-adjusted < 0.05), between clinical health and periodontitis (P-adjusted < 0.05), and between peri-implantitis and periodontitis (P-adjusted < 0.05). Biofilms derived from cases of clinical health exhibited a mean SDI of 2.46. By comparison, mean SDIs in the peri-implantitis and periodontitis groups amounted to 3.023 (Padjusted < 0.05) and 3.061 (P-adjusted < 0.05), respectively. Between the peri-implantitis and periodontitis groups, 8 OTUs exhibited statistically significant differential abundance. The genera Streptobacillus and Psychrobacter were dominant in the peri-implantitis group.

CONCLUSIONS

Microbial differences between the diseased environments could not be attributed to the unequivocal presence or absence of specific bacteria. Nonetheless, statistically significant differences in biofilm composition and complexity could be identified between peri-implantitis and stage III/IV periodontitis specimens.

IMPLICATIONS

An emerging hypothesis in periodontology and dental implantology posits that inflammatory destruction of tissue results not from the presence of one or a few key bacterial species. Rather, disease results from true polymicrobial activity characterized by accumulation of specific genes, and thus functions, within the biofilm. Moreover, the pathogenesis of peri-implantitis is known to involve the presence of titanium particles that influence the inflammatory response. The observed differences in biofilm diversity and composition in this investigation may reflect complex interactions involving titanium particles, host immune cells, and the biofilm at peri-implantitis sites.

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