Abstract

Although diabetes mellitus is known to aggravate periodontal disease, the precise relationship between these two entities is far from being completely understood. Further study of this relationship was therefore undertaken in the form of observation of both naturally occurring gingivitis in rats (ODUS/Odu) and effects produced by induction of experimental diabetes mellitus by injection of streptozotocin (STZ: 65 mg/kg, i.v.). At one and 3 mon after STZ injection, liquid paraffin was injected intraperitoneally. Four days thereafter, pocket probing depths of rats were measured and blood samples as well as peritoneal macrophages were collected from both experimental animals and non diabetic controls. Both chemotaxis and phagocytosis of macrophages were studied. At one and 3 mon after STZ injection, pocket probing depths of diabetic animals were significantly deeper than those of controls (p < 0.001). Pocket probing depths were deeper at 3 mon after STZ injection than after 1 mon in diabetic animals. At three months after STZ injection, there was a high degree of positive correlation between pocket probing depths, blood glucose levels, triglyceride, and hemoglobin A1c levels (p < 0.01). Also, macrophage chemotaxis was more suppressed in diabetic rats than it was in controls. Additionally, both phagocytosis ratios and phagocytosis indices of macrophages in the diabetes group were significantly more suppressed than those in controls in both experimental periods (p < 0.001). Findings suggest that both chemotaxis and phagocytosis are compromised in macrophages from rats rendered diabetic by STZ injection. Thus as host defense mechanisms become weakened, there is a corresponding progression of periodontal disease.

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