Aims

The aim of this study was to verify the impact of periodontitis in the course of chronic obstructive pulmonary disease (COPD) in C57Bl/6J mice.

Main methods

The animals were randomly divided into four groups (n = 8): Basal, Periodontitis (P), COPD and COPD+P. COPD was induced by orotracheal instillation of 30 μl of cigarette extract 3 times/week for 7 weeks. Periodontitis was induced by ligation technique for 22 days. Euthanasia was performed on 51st day. The analyzes were total/differential cells and cytokines recovered from bronchoalveolar lavage (BAL), total/differential blood cell count, platelets, total marrow cell count, airway collagen deposition, alveolar enlargement analyzed by mean linear intercept (Lm), mucus and bone crest reabsorption. One-way ANOVA followed by the Student-Newman-Keuls was used.

Key findings

The association COPD+P decreased macrophages (p = 0,0351), TNF-α (p = 0,0071) and INF-γ (p = 0,0004) in BAL, when compared to the COPD group maintaining emphysema levels by alveolar enlargement (p < .05) reorganization of collagen fibers (p = .001) and also mean linear intercept (lm) (p = .001) and mucus (p = .0001). The periodontitis group caused TNF-α increase (p = 0, 0001) in BAL.

Significance

Periodontitis, per se, does not alter any of the parameters analyzed, except for increased TNF-α in BAL. However, its association with COPD caused macrophages TNF-α and INF-γ alterations, when compared to the COPD group maintaining emphysema levels by alveolar enlargement and reorganization of collagen fibers. It seems that periodontitis is influencing the course of Th1 profile cell, and cytokines and pulmonary alterations. Further studies are needed to clarify the regulatory process underlying these two diseases.

中文翻译：

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牙周炎在慢性阻塞性肺疾病过程中的影响：肺和全身作用。

目的

这项研究的目的是验证在C57Bl / 6J小鼠的慢性阻塞性肺疾病（COPD）过程中牙周炎的影响。

主要方法

将动物随机分为四组（n  = 8）：基础，牙周炎（P），COPD和COPD + P。经口气管滴注30μl香烟提取物3次/周，持续7周，可诱发COPD。结扎技术诱导牙周炎22天。安乐死在第51天进行。分析包括从支气管肺泡灌洗（BAL）中回收的总/差异细胞和细胞因子，总/差异血细胞计数，血小板，总骨髓细胞计数，气道胶原蛋白沉积，通过平均线性截距（Lm），黏液和骨c分析的肺泡肿大重吸收。使用单向方差分析，然后使用Student-Newman-Keuls。

主要发现

与 通过肺泡维持肺气肿水平的COPD组相比，COPD + P降低了 BAL中的巨噬细胞（p = 0,0351），TNF-α（p = 0,0071）和INF-γ（p = 0,0004）。 胶原纤维的增大（p <.05）重组（p  = .001），平均截距（lm）（p  = .001）和粘液（p  = .0001）。牙周炎组引起 BAL中TNF-α升高（p = 0，0001）。

意义

牙周炎本身并不会改变任何分析的参数，除了BAL中TNF-α升高。然而，与COPD组相比，其与COPD的结合会导致巨噬细胞TNF-α和INF-γ的改变，而COPD组则通过肺泡增大和胶原纤维的重组来维持肺气肿水平。牙周炎似乎正在影响Th1轮廓细胞，细胞因子和肺部改变的进程。需要进一步研究来阐明这两种疾病的调控过程。