Nakajima K, Hamada N, Takahashi Y, Sasaguri K, Tsukinoki K, Umemoto T, Sato S
Department of Craniofacial Growth and Development Dentistry, Division of Orthodontics, Kanagawa Dental College, Yokosuka, Japan.
J Periodontal Res. 2006 Dec;41(6):527-34. doi: 10.1111/j.1600-0765.2006.00901.x.
The purpose of the present study was to examine the effects of restraint stress on periodontal breakdown resulting from Porphyromonas gingivalis-challenged periodontitis in rats.
To examine the influence of restraint stress on periodontal breakdown, rats were orally challenged with the periodontal pathogen P. gingivalis. Twenty male, specific pathogen-free (SPF) 3-wk-old, Sprague-Dawley rats were divided into four groups: group A (controls), group B (exposed to restraint stress for 12 h/d for 22 d), group C (orally challenged with P. gingivalis), and group D (exposed to restraint stress for 12 h/d for 22 d and orally challenged with P. gingivalis). After 22 d, all animals were killed. The distance from the alveolar bone crest to the cemento-enamel junction was determined, concentrations of adrenocorticotropic hormone were measured as stress markers, and atrophy of the thymus and spleen were assessed. In addition, the furcation area of the maxillary molars was examined histologically, while gingival cytokine gene expression was assessed by mRNA using reverse transcription-polymerase chain reaction (RT-PCR).
In the restrained group, all stress markers were elevated, and the thymus and spleen were atrophied. Combined restraint stress and oral challenge with P. gingivalis resulted in significantly higher bone loss, and osteoclasts were observed. RT-PCR analysis revealed low cytokine gene expression in the restrained groups.
These results suggest that the presence of restraint stress significantly enhances the progression of P. gingivalis-challenged periodontitis in rats.
本研究旨在探讨束缚应激对牙龈卟啉单胞菌诱导的大鼠牙周炎所致牙周组织破坏的影响。
为研究束缚应激对牙周组织破坏的影响,将牙周病原体牙龈卟啉单胞菌经口感染大鼠。20只3周龄雄性无特定病原体(SPF)斯普拉格-道利大鼠分为四组:A组(对照组)、B组(每天束缚应激12小时,持续22天)、C组(经口感染牙龈卟啉单胞菌)和D组(每天束缚应激12小时,持续22天并经口感染牙龈卟啉单胞菌)。22天后,处死所有动物。测定牙槽嵴顶至牙骨质釉质界的距离,检测促肾上腺皮质激素浓度作为应激指标,并评估胸腺和脾脏萎缩情况。此外,对上颌磨牙的根分叉区进行组织学检查,同时采用逆转录聚合酶链反应(RT-PCR)通过mRNA评估牙龈细胞因子基因表达。
在束缚应激组中,所有应激指标均升高,胸腺和脾脏萎缩。束缚应激与牙龈卟啉单胞菌经口感染共同作用导致骨吸收显著增加,并观察到破骨细胞。RT-PCR分析显示束缚应激组细胞因子基因表达水平较低。
这些结果表明,束缚应激显著促进了牙龈卟啉单胞菌诱导的大鼠牙周炎的进展。