Impact of the Oral Commensal Flora on Alveolar Bone Homeostasis
Impact of the Oral Commensal Flora on Alveolar Bone Homeostasis
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DOI：
10.1177/0022034514540173
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发表时间：
2014-08-01
影响因子：
7.6
通讯作者：
Darveau, R. P.
中科院分区：
文献类型：
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作者：
Irie, K.;Novince, C. M.;Darveau, R. P.
健康牙周组织的内稳态受到响应于正常口腔植物群的先天性和适应性免疫监视机制的影响。最近的比较无菌（GF）和正常的特定病原体（SPF）的小鼠揭示了宿主免疫监视机制的影响，在正常的口腔植物群的牙槽骨高度。先前的报道表明，正常SPF小鼠的牙槽骨高度明显低于年龄和应变匹配的GF小鼠，这表明自然发生的牙槽骨丢失是健康牙周组织稳态的正常组成部分。在这份报告中，组织形态计量学分析证实，与GF小鼠相比，SPF小鼠的牙槽骨丢失增加，并显示牙槽骨表面排列的TRAP+骨细胞数量增加。与GF小鼠相比，SPF小鼠牙周组织中RANKL+细胞和IL 17+细胞数量的增加证明了介导破骨细胞生成上调和牙槽骨丢失的可能分子机制。与GF小鼠相比，SPF小鼠结合上皮中T淋巴细胞和T辅助细胞的数量增加表明适应性免疫应答有助于健康牙周组织中的生理性牙槽骨丢失。该GF动物模型研究开始阐明宿主免疫监视机制对正常口腔植物群的响应的影响，介导健康牙周组织中分解代谢的牙槽骨稳态。
Homeostasis of healthy periodontal tissues is affected by innate and adaptive immunosurveillance mechanisms in response to the normal oral flora. Recent comparisons of germ-free (GF) and normal specific-pathogen-free (SPF) mice have revealed the impact of host immunosurveillance mechanisms in response to the normal oral flora on alveolar bone height. Prior reports that alveolar bone height is significantly less in normal SPF mice compared with their age-and strain-matched GF counterparts suggest that naturally occurring alveolar bone loss is a normal component of healthy periodontal tissue homeostasis. In this report, histomorphometric analyses confirmed increased alveolar bone loss and revealed increased numbers of TRAP+ osteoclastic cells lining the alveolar bone surface in SPF compared with GF mice. Increased numbers of RANKL+ cells and IL17+ cells in the periodontium of SPF mice demonstrate possible molecular mechanisms mediating the up-regulated osteoclastogenesis and alveolar bone loss in SPF mice compared with GF mice. Increased numbers of T-lymphocytic cells and T-helper cells in the junctional epithelium of SPF mice compared with GF mice suggest that the adaptive immune response contributes to physiologic alveolar bone loss in the healthy periodontium. This GF animal model study notably begins to elucidate the impact of host immunosurveillance mechanisms in response to the normal oral flora, mediating catabolic alveolar bone homeostasis in the healthy periodontium.