The influence of type I diabetes mellitus on the expression and activity of gelatinases (matrix metalloproteinases-2 and -9) in induced periodontal disease.

BACKGROUND AND OBJECTIVE

Periodontal disease corresponds to a group of lesions that affect the tooth-supporting tissues present in the dental follicle. Although bacterial plaque is important, the immune response also contributes to the destruction of periodontal tissues. Diabetes mellitus is closely associated with the development, progression and severity of periodontal disease because it not only affects extracellular matrix organization but also the tissue response to inflammation. The objective of the present investigation was to study the influence of diabetes on experimental periodontal disease by evaluating the degradation of extracellular matrix through the analysis of matrix metalloproteinase (MMP)-2 and MMP-9 expression and activity, using immunofluorescence, zymography and real-time reverse transcription-polymerase chain reaction.

MATERIAL AND METHODS

Wistar rats were divided into normal and diabetic groups and evaluated 0, 15 and 30 d after the induction of periodontal disease by ligature.

RESULTS

MMP-2 and -9 were detected in epithelial cells, in the blood vessel endothelium and in connective tissue cells. The same profile of enzymatic expression of MMP-2 and -9 was observed in normal and diabetic animals, with a peak in activity at day 15 of inflammation. However, in diabetic animals, MMP-2 gelatinolytic activity was reduced after the inflammatory stimulus, whereas that of MMP-9 was increased. MMP-2 gene expression decreased with inflammation in both normal groups and groups with diabetes. In contrast, MMP-9 expression increased in normal animals and decreased in diabetic animals after inflammation.

CONCLUSION

The results suggest the involvement of MMP-2 and -9 in the dynamics of periodontal disease and that variation in their expression levels results in differences in tissue organization and wound healing in normal and diabetic animals.