ORAL INFECTION WITH PORPHYROMONAS-GINGIVALIS AND INDUCED ALVEOLAR BONE LOSS IN IMMUNOCOMPETENT AND SEVERE COMBINED IMMUNODEFICIENT MICE
ORAL INFECTION WITH PORPHYROMONAS-GINGIVALIS AND INDUCED ALVEOLAR BONE LOSS IN IMMUNOCOMPETENT AND SEVERE COMBINED IMMUNODEFICIENT MICE
复制标题
DOI：
10.1016/0003-9969(94)90055-8
复制
发表时间：
1994-12-01
影响因子：
3
通讯作者：
ROOPENIAN, DC
中科院分区：
文献类型：
--
作者：
BAKER, PJ;EVANS, RT;ROOPENIAN, DC
探讨了牙龈卟啉单胞菌诱导牙槽骨丢失的宿主反应小鼠模型的适用性。免疫正常小鼠和重度联合免疫缺陷（SCID）小鼠口腔分别感染牙龈卟啉卟啉ATCC 53977。感染前未从这些小鼠的口腔中分离出牙龈卟啉卟啉菌，但在感染后至少42天存在。在实验结束（42天）时，感染的免疫正常小鼠的血清中存在牙龈假单胞菌特异性IgG。特异性IgG不存在于假感染或未感染的免疫正常小鼠中，也不存在于任何免疫缺陷小鼠中。在42天的任何血清中都不存在特异性IgM。与假感染或未感染的免疫能力小鼠相比，感染两种菌株的免疫能力小鼠的骨质流失显著（p < 0.05）。感染SCID的小鼠遗传上缺乏B淋巴细胞和T淋巴细胞，与假感染或未感染SCID的小鼠相比，也表现出明显的骨质流失（p < 0.05）。然而，免疫正常小鼠的骨丢失程度比免疫缺陷小鼠更大：感染小鼠的相对骨量是假感染免疫正常小鼠的77%，是假感染SCID小鼠的86% （p = 0.025）。因此，小鼠口腔感染是研究宿主反应对牙龈假单胞菌诱导的牙槽骨丢失影响的可行模型。由于在免疫正常小鼠和SCID小鼠中均可诱导骨质流失，但在免疫正常小鼠中骨质流失更严重，因此似乎B细胞和T细胞对于牙龈假单胞菌感染的骨吸收都不是绝对必要的，但它们可能会显著调节骨吸收的程度。
The suitability of a mouse model for host response in the induction of alveolar bone loss by Porphyromonas gingivalis was explored. The mouths of immunocompetent and severe combined immunodeficient (SCID) mice were infected with P. gingivalis ATCC 53977. P. gingivalis was not isolated from the mouths of these mice before infection, but was present at least 42 days after infection. P. gingivalis-specific IgG was present in sera from the infected, immunocompetent mice at the end of these experiments (42 days). Specific IgG was not present in sham-infected or uninfected immunocompetent mice, nor in any immunodeficient mice. Specific IgM was not present in any sera at 42 days. Infected, immunocompetent mice of two strains showed significant bone loss in comparison to sham-infected or uninfected immunocompetent mice (p < 0.05). Infected SCID mice, which are genetically lacking both B and T lymphocytes, also showed significant bone loss compared with sham-infected or uninfected SCID mice (p < 0.05). However, the degree of bone loss was greater in immunocompetent than immunodeficient mice: the relative amount of bone in infected mice was 77% of that in sham-infected immunocompetent mice, and 86% of sham values in SCID mice (p = 0.025). Thus oral infection of mice is a feasible model for studying the effects of host response on P. gingivalis-induced alveolar bone loss. Because bone loss was induced both in immunocompetent and SCID mice but was greater in immunocompetent mice, it appears that neither B nor T cells are absolutely necessary for bone resorption in response to P. gingivalis infection but they may significantly modulate the degree of resorption.