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首页> 外文期刊>BMC Oral Health >Porphyromonas gingivalis infection increases osteoclastic bone resorption and osteoblastic bone formation in a periodontitis mouse model
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Porphyromonas gingivalis infection increases osteoclastic bone resorption and osteoblastic bone formation in a periodontitis mouse model

机译:在牙周炎小鼠模型中牙龈卟啉单胞菌感染会增加破骨细胞的骨吸收和成骨细胞的形成

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Background Porphyromonas gingivalis has been shown to invade osteoblasts and inhibit their differentiation and mineralization in vitro. However, it is unclear if P. gingivalis can invade osteoblasts in vivo and how this would affect alveolar osteoblast/osteoclast dynamics. This study aims to answer these questions using a periodontitis mouse model under repetitive P. gingivalis inoculations. Methods For 3-month-old BALB/cByJ female mice, 109?CFU of P. gingivalis were inoculated onto the gingival margin of maxillary molars 4 times at 2-day intervals. After 2?weeks, another 4 inoculations at 2-day intervals were applied. Calcein was injected 7 and 2?days before sacrificing animals to label the newly formed bone. Four weeks after final inoculation, mice were sacrificed and maxilla collected. Immunohistochemistry, micro-CT, and bone histomorphometry were performed on the specimens. Sham infection with only vehicle was the control. Results P. gingivalis was found to invade gingival epithelia, periodontal ligament fibroblasts, and alveolar osteoblasts. Micro-CT showed alveolar bone resorption and significant reduction of bone mineral density and content in the infected mice compared to the controls. Bone histomorphometry showed a decrease in osteoblasts, an increase in osteoclasts and bone resorption, and a surprisingly increased osteoblastic bone formation in the infected mice compared to the controls. Conclusions P. gingivalis invades alveolar osteoblasts in the periodontitis mouse model and cause alveolar bone loss. Although P. gingivalis appears to suppress osteoblast pool and enhance osteoclastic bone resorption, the bone formation capacity is temporarily elevated in the infected mice, possibly via some anti-microbial compensational mechanisms.
机译:背景技术牙龈卟啉单胞菌已显示出侵入成骨细胞并在体外抑制其分化和矿化。但是,尚不清楚牙龈卟啉单胞菌是否可以在体内侵入成骨细胞,以及这将如何影响牙槽成骨细胞/破骨细胞的动力学。本研究旨在使用牙周炎小鼠模型在反复牙龈卟啉单胞菌接种下回答这些问题。方法对3个月大的BALB / cByJ雌性小鼠,每隔2天接种4次10 9 ΔCFU牙龈卟啉单胞菌到上颌磨牙的龈缘。 2周后,每2天间隔再接种4次。在牺牲动物以标记新形成的骨骼之前,第7天和第2天注射了钙黄绿素。最终接种后四周,处死小鼠并收集上颌骨。在标本上进行了免疫组织化学,显微CT和骨组织形态测定。仅用媒介物进行深水感染作为对照。结果发现牙龈卟啉单胞菌侵入牙龈上皮,牙周膜成纤维细胞和肺泡成骨细胞。与对照相比,Micro-CT显示了被感染小鼠的牙槽骨吸收和骨矿物质密度和含量的显着降低。与对照组相比,骨组织形态计量学显示感染的小鼠的成骨细胞减少,破骨细胞增加和骨吸收增加,并且成骨细胞形成惊人地增加。结论牙龈卟啉单胞菌侵入牙周炎小鼠模型的牙槽骨成骨细胞,并导致牙槽骨丢失。尽管牙龈卟啉单胞菌似乎可以抑制成骨细胞集合并增强破骨细胞的骨吸收,但受感染小鼠的骨形成能力可能会通过某些抗微生物补偿机制而暂时升高。

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