Methods: BALB/c mice were assigned to 3 groups: RU (n=30), KC (n=30), and control (empty tube, n=30), evaluated at 7, 21, and 63 days. Inflammatory cells and fibroblasts were counted, and fibrous capsule thickness was measured. Fifty-six teeth from 6 dogs, were assigned to 3 groups: RU (n=20), KC (n=20), and control (zinc oxide and eugenol cement, n=16), evaluated at 7 and 70 days. Inflammatory cells, fibroblasts and odontoblasts were counted, and predentin/ tertiary dentin thickness was measured. MMP-2 and MMP-9 expression was investigated by immunohistochemistry. Data were analyzed statistically (alpha=5%).
Results: RU induced low inflammation at 7 and 21 days (p<0.05) which increased at 63 days (p<0.05). KC induced more intense mononuclear inflammatory response at 7 and 21 days (p<0.05), which reduced at 63 days to levels close to the control (p>0.05). Fibrous capsule thickness was thin for RU, KC, and control (p>0.05). Earlier MMP-2 was detected for KC and RU, decreasing afterwards. MMP-9 presented a similar pattern for KC whereas for RU MMP-9 expression was late. In pulp-dentin complex, KC and RU induced low inflammatory response, similar to control (zinc oxide and eugenol) (p>0.05). At 70 days, RU induced tissue response characterized by lower percentage of odontoblasts, higher percentage of mononuclear cells, and tertiary dentin formation (p<0.05) whereas KC induced response similar to the control (p>0.05). In deep cavities, luting agents induced low expression of MMP-2 and MMP-9, similarly to the control.
Conclusions: RU induced inflammatory response and late MMP-9 expression in subcutaneous connective tissue. In pulp tissue, higher percentage of mononuclear inflammatory cells, lower percentage of odontoblasts and tertiary dentin were observed, without MMP modulation. KC response overall was similar to control.