Abstract
Matrix metalloproteinases (MMPs) are involved in extracellular matrix degradation and the modulation of cell behavior. These proteinases have also been implicated in tissue repair and regeneration. Our previous studies have demonstrated that MMP-3 elicits stimulatory effects on the proliferation and the migration of endothelial cells as well as anti-apoptotic effects on these cells in vitro. In addition, we found that MMP-3 enhanced the regeneration of lost pulp tissue in a rat incisor pulp injury model. However, continuously erupting rodent incisors exhibit significantly different pulp organization compared with mature erupted teeth. Therefore, we have further extended these studies using a canine irreversible pulpitis model to investigate the effects of MMP-3. In this study, the crowns of the canine mature premolars were removed and the pulp tissues were amputated. The amputated pulp tissues remained exposed for 24 or 72 hours to induce mild or severe irreversible pulpitis, respectively, followed by sealing of the cavities. In both models, the whole pulp tissues became necrotic by day 14. In this mild pulpitis model, the regeneration of pulp tissue with vasculature and nerves was observed until 14 days after sealing with MMP-3, followed by extracellular matrix formation in the regenerated pulp tissues until day 28. The treatment with MMP-3 resulted in a decrease in the number of macrophage and antigen-presenting cells and a significant inhibition of IL-6 expression on day 3. The inhibition of MMP-3 activity abolished these anti-inflammatory effects. Immunofluorescence staining demonstrated that MMP-3 was involved in the modification of serum-derived hyaluronan-associated proteins and hyaluronan (SHAP-HA) complexes possibly through the degradation of versican. These results demonstrate that MMP-3 can act as an anti-inflammatory agent and suggest that MMP-3 might represent a useful therapy for the treatment of mild irreversible pulpitis.
Highlights
Inflammation of the dental pulp is caused by dental caries, which result from bacterial infection
If pulp exposure injuries are not treated for infection and re-sealed, the introduction of bacteria into the pulp tissues can readily cause irreversible pulpitis that does not allow for their spontaneous healing, resulting in the necrosis and death of the pulp tissue [4]
The entire pulp tissue was necrotic by day 14 in both of the teeth that were sealed after exposure for 24 or 72 hours (Figure 1B, C right panel), indicating that these teeth could be used as models of irreversible pulpitis
Summary
Inflammation of the dental pulp is caused by dental caries, which result from bacterial infection. Long-term studies have shown that the rate of tooth loss is higher for endodontically treated teeth compared to nontreated teeth, due to fracture, secondary caries and complex restoration-associated problems [5,6,7,8]. This has been one of the central challenges in dentistry, and the improvement of antimicrobial agents and restorative materials and the diagnosis of pulp vitality to facilitate the control of infection are great interest [9]. This restoration requires the recruitment of stem/progenitor cells and the differentiation of these cells into tissue-specific somatic cells as the result of intrinsic factors and extrinsic microenvironmental cues
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