Disturbance of Periodontal Tissue Caused by Mechanical Compression into the Gingival Col of Streptozotocin-induced Diabetic Rats

Abstract

FThe purpose of this study is to clarify the destructive processes of periodontal tissue, especially of alveolar bone, induced by food impaction. Streptozotocin-induced diabetic rat was used, gutter percha point (GP) was inserted into interdental gingival col space between upper M1 and M2, and the change of body weight, histopathological findings and 3D SEM structure of alveolar bone were compared between diabetic (Group DM) and control (Group N) animals (Experiment 1). Large amounts of bacterial deposits and sequester were observed at the alveolar crest, and subsequently experiment 2 was carried out to explore the relationship between bacterial infection and sequester formation. The combination of mechanical compression and daily twice cleaning with 3% oxydol and Periocline were carried out. As a result of experiment 1, ulceration with partial exposure of alveolar crest, inflammatory infiltrates and hyaline degeneration occurred in the col, and bone resorption was scarcely observed at 1d in Group N. Bone resorption of alveolar bone progressed at 3d and 5d, decreasing the height of alveolar crest and the width of alveolar bone. Reepithelization of ulcer surface was observed at 7d and 14d, and concurrently bone resorption regressed and new bone formation suggested reparative changes. SEM observation confirmed these changes of alveolar bone. On the contrary, massive bacterial deposits were observed, and bone resorption was scanty in the upper region and slight in the middle to lower region of alveolar bone at 1 day of Group DM. Massive bacterial deposits with partial exposure of alveolar bone were observed at 3d and 5d, and sequester was isolated owing to intense undermining bone resorption. Regeneration of epithelium was seen beneath the sequester at 14d, showing the phenomenon of foreign body exclusion. The light microscopic changes of Group DM were consistent with SEM findings. The total number of osteoclasts was fewer at 1d and larger at 3d and 5d in Group DM. Osteoclasts at the upper region of alveolar bone increased from 1d to 5d in Group N, although the number of osteoclasts did not show a significant change in Group DM. At the middle to lower portion of alveolar bone, the number of osteoclast was significantly fewer at 1d, larger at 3d and 5d in Group DM. In experiment 2, the col with ulceration and necrosis did not show bacterial deposits or sequester, suggesting the intimate relation between bacterial infection and sequestration. The present study suggests that food impaction and subsequent mechanical compression to the col could induce various damages of periodontal tissue, including sequester formation, and elaborate plaque control at the initial stage of food impaction could prevent sequester formation and protect the height of alveolar bone.

The Effect of Insulin Administration and Antibacterial Irrigation with Chlorhexidine Gluconate on the Disturbance of Periodontal Tissue Caused by Food Impaction in Streptozotocin-Induced Diabetic Rats

“…Study results showed that the disturbance of the periodontal tissue, including the alveolar bone resorption that was induced by the mechanical compression of the col by GP was similar and significantly different from the findings reported by Matsuura et al 8) . Based on these results, we designed our present experiment to further investigate the mechanical compression procedure by using GP and then compare our findings to those reported by Tokunaga, et al 47) , who also examined periodontal tissue disturbances in STZ-induced diabetic rats. Diabetic rats were prepared by using alloxan and STZ, which are known to induce a diabetic state.…”

“…Intraperitoneal injection of 125 mg/kg was also performed in the present study in order to be able to compare our results with those in the previous studies 44,47) . In our study, we confirmed the diabetic status to be >+2 (which is comparable to a value of 500 mg/dl of urine sugar) by examining the animals with…”

“…Concerning the reparative phenomenon at this time point, the transition from destructive to reparative changes appeared to be induced by the rapid resorption of the alveolar bone that directly resulted from the food impaction, along with the weakening of the mechanical compression at the col. In contrast, Tokunaga et al 47) examined the disturbance in the changes of the periodontal tissue after col compression in diabetic model rats and reported findings: (1) The adhesion of numerous bacterial masses, in addition to the appearance of hyaline necrosis, ulceration, and inflammatory cell infiltrates on the superficial layer after col compression beginning from an early stage; (2) Sequestrum formation due to the invasion of numerous bacterial masses on the alveolar crest at 3 and 5 days after the col compression; (3)…”

“…STZ injury is specific and directed at the beta cells of islets of Langerhans, thereby inducing hyperglycemia without ketosis. STZ can be used to maintain a diabetic state for a long period, with the metabolic mechanism similar to that found in human type I diabetic mellitus [45][46][47] .…”

“…In addition, they determined that the resistance of the periodontal tissue was poor in the diabetic state. Tokunaga et al 47) examined the gingival col of streptozotocin (STZ) -induced diabetic rats and found that mechanical compression induced hyalinization, necrosis, inflammatory cell infiltrates and ulcer formation at the col during the early stages. They also described finding characteristic and massive bacterial deposits, delays in bone resorption at the alveolar crest, and sequester separation.…”