Liu R, Bal H S, Desta T, Krothapalli N, Alyassi M, Luan Q, Graves D T
Department of Periodontology and Oral Biology, Boston University School of Dental Medicine, 700 Albany Street, Rm. W-202D, Boston, MA 02118, USA.
J Dent Res. 2006 Jun;85(6):510-4. doi: 10.1177/154405910608500606.
Using a ligature-induced model in type-2 Zucker diabetic fatty (ZDF) rat and normoglycemic littermates, we investigated whether diabetes primarily affects periodontitis by enhancing bone loss or by limiting osseous repair. Diabetes increased the intensity and duration of the inflammatory infiltrate (P < 0.05). The formation of osteoclasts and percent eroded bone after 7 days of ligature placement was similar, while four days after removal of ligatures, the type 2 diabetic group had significantly higher osteoclast numbers and activity (P < 0.05). The amount of new bone formation following resorption was 2.4- to 2.9-fold higher in normoglycemic vs. diabetic rats (P < 0.05). Diabetes also increased apoptosis and decreased the number of bone-lining cells, osteoblasts, and periodontal ligament fibroblasts (P < 0.05). Thus, diabetes caused a more persistent inflammatory response, greater loss of attachment and more alveolar bone resorption, and impaired new bone formation. The latter may be affected by increased apoptosis of bone-lining and PDL cells.
利用结扎诱导模型，在2型Zucker糖尿病肥胖（ZDF）大鼠及其血糖正常的同窝仔鼠中，我们研究了糖尿病主要是通过加剧骨质流失还是通过限制骨修复来影响牙周炎。糖尿病增加了炎症浸润的强度和持续时间（P < 0.05）。结扎放置7天后破骨细胞的形成和骨侵蚀百分比相似，而在结扎去除4天后，2型糖尿病组的破骨细胞数量和活性显著更高（P < 0.05）。与糖尿病大鼠相比，血糖正常的大鼠在吸收后新骨形成量高出2.4至2.9倍（P < 0.05）。糖尿病还增加了细胞凋亡，并减少了骨衬细胞、成骨细胞和牙周膜成纤维细胞的数量（P < 0.05）。因此，糖尿病导致了更持久的炎症反应、更大程度的附着丧失和更多的牙槽骨吸收，并损害了新骨形成。后者可能受到骨衬细胞和牙周膜细胞凋亡增加的影响。
