目的： 比较丝线结扎和涂抹牙龈卟啉单胞菌诱导小鼠牙周炎模型的牙槽骨骨吸收程度、激活破骨细胞及去除诱因后成骨的过程。方法： 48只C57BL6小鼠随机分配，采用分口设计，根据涂抹2%（质量分数）羧甲基纤维素（carboxymethylcellulose, CMC）或109个菌落形成单位（colony-forming units, CFU）的牙龈卟啉单胞菌以及是否丝线结扎分为4组（n= 24），分别为对照组（右上第二磨牙单纯涂抹CMC）、丝线结扎组（围绕左上第二磨牙结扎9-0丝线）、涂菌组（右上第二磨牙单纯涂抹牙龈卟啉单胞菌）和丝线结扎+涂菌组（结扎左上第二磨牙并涂抹牙龈卟啉单胞菌），测量釉牙骨质界至牙槽骨嵴顶（cementoenamel junction to the alveolar bone crest，CEJ-ABC）的距离，监测牙槽骨的吸收。48只C57BL6小鼠设计和分组同上，牙槽骨骨面的破骨细胞采用抗酒石酸酸性磷酸酶（tartrate-resistant acid phosphatase，TRAP）染色并计数。36只C57BL6小鼠随机分配，其中30只小鼠在左侧上颌第二磨牙结扎9-0丝线，观察3周，有12只小鼠在丝线结扎1周后拆除丝线，继续观察2周，分别在丝线结扎1、2、3周以及丝线拆除1周和2周共5个时间点（n=6）各处死6只小鼠，检测CEJ-ABC距离；未行丝线结扎的小鼠CEJ-ABC距离（n=6）为基线水平。采用单因素方差分析（ANOVA）法对所有数据进行统计学分析。结果： 丝线结扎组的小鼠牙周炎，在3、6、9和12周后的CEJ-ABC距离分别为（0.16±0.04） mm、（0.16±0.02） mm、（0.18±0.03） mm、（0.17±0.02） mm，与对照组［（0.09±0.03） mm、（0.10±0.01） mm、（0.12±0.04） mm、（0.12±0.01） mm］和涂菌组［（0.09±0.03） mm、（0.12±0.01） mm、（0.12±0.02） mm、（0.10±0.01） mm］相比差异有统计学意义（P<0.05）。与对照组［（0.09±0.03） mm］相比，丝线结扎组第3周的CEJABC距离为（0.16±0.04） mm，比涂菌组［（0.09±0.03） mm］诱导的牙槽骨骨吸收更迅速，丝线结扎和涂抹牙龈卟啉单胞菌结合并未进一步增加牙槽骨的吸收破坏。在丝线结扎1 d后，牙槽骨表面的破骨细胞即被激活，与对照组［（2±2）个］相比在第3天达到高峰［（12±4）个，P<0.01］。丝线结扎诱导的小鼠牙周炎，在丝线去除2周后CEJ-ABC距离为（0.07±0.02） mm，与去除丝线前［（0.13±0.01） mm］相比显著降低，提示有显著的牙槽骨再生（P<0.01）。结论： 丝线结扎术是一种迅速且有效的诱导小鼠牙周炎牙槽骨骨吸收的方式，其诱导的破骨细胞活化在丝线结扎后24 h内发生，3 d达到高峰，去除实验性牙周炎的诱导因素即去除结扎的丝线有助于牙槽骨骨再生。

Objective： To compare the extent and time course of alveolar bone loss and osteoclast activation in two murine models of periodontal disease: molar ligation and Porphyromonas gingivalis (P. gingivalis) oral inoculation. Methods: A splitmouth design was applied to two groups of mice (C57BL6, 6-8 weeks old, n=24 in both groups), resulting in four treatment groups: (1) Control group: unliga-ted upper right 2nd molars receiving CMC only, (2)Ligature group: ligation of a 9-0 suture around the upper left 2nd molar, (3) P. gingivalis group: unligated upper right 2nd molar receiving P. gingivalis challenge only, (4)Ligature + P.gingivalis group: ligation of the upper left 2nd molar in combination with oral inoculation with 109 colony-forming units(CFU) P. gingivalis. Alveolar bone loss was measured as the cementoenamel junction and alveolar bone crest (CEJ-ABC) distance. In the study, 48 C57BL6 mice were designed and treated as described above, and osteoclasts were counted on histological sections following tartrate-resistant acid phosphatase (TRAP) staining and counts were normalized to alveolar bone surface distance. Then 36 C57BL6 mice were investigated, of which 30 were ligated a 9-0 silk ligature around the 2nd molar in the left maxillary quadrant and 6 were not ligated. After ligation for 1 week, the ligatures in 12 mice were taken off for either 1 week or 2 weeks. The CEJ-ABC distance of the 6 mice without ligation was baseline. The CEJ-ABC distances were measured and analyzed. The data were analyzed with one-way ANOVA. Results: Molar ligation induced marked alveolar bone loss after 3, 6, 9 and 12 weeks ［(0.16±0.04) mm, (0.16±0.02) mm, (0.18±0.03) mm, (0.17±0.02) mm］, vs. corresponding controls ［（0.09±0.03）mm，（0.10±0.01）mm，（0.12±0.04）mm，（0.12±0.01）mm］ and P. gingivalis group ［（0.09±0.03）mm、（0.12±0.01）mm，（0.12±0.02）mm，（0.10±0.01）mm］， P<0.05.  Combined treatment with molar ligation and P. gingivalis did not further increase the CEJ-ABC distance. Evidence for osteoclast activation was found one day after molar ligation, and TRAP-positive cell numbers peaked on day 3 (12±4 vs. control 2±2, P<0.01). After taking off ligature following ligation for 2 weeks, it showed significantly regrowth of alveolar bone compared with that before removal of the ligature on day 7 ［（0.07±0.02）mm vs. （0.13±0.01）mm, P<0.01］. Conclusion: Molar ligation is a rapid and effective way to induce periodontal bone loss in mice. Osteoclast activation occurs within 24 hours of ligature placement, and the extent of bone loss well exceeds that of the P.gingivalis-induced bone loss. Removing ligature after periodontal disease might help bone regeneration by regrowth of the alveolar bone.