Effects of epigallocatechin gallate (EGCG) on the biological properties of human dental pulp stem cells and inflammatory pulp tissue.

OBJECTIVE: This study aimed to investigate the effect of epigallocatechin gallate (EGCG) on the proliferation, mineralization, inflammation and hypoxia responses of human dental pulp stem cells (hDPSCs) in vitro and its effect on inflammatory pulp tissue in rats in vivo. DESIGN: The optimum concentration of EGCG was selected by creating a dose response curve. Expression of odontogenic/osteogenic-related genes and inflammatory cytokines after stimulation with Lipopolysaccharide (LPS) was detected by real-time PCR. Under hypoxic conditions, cell proliferation and expression of reactive oxygen species (ROS) and superoxide dismutase (SOD) were detected.In vivo, the maxillary first molars of SD rats were pulpotomized and stimulated with 5 mg/mL LPS for 30 min. Normal saline and EGCG were used to flush the pulp chamber. After 2 months, samples were removed for micro-CT scanning and HE staining. RESULTS: CCK-8 assay revealed that 10 µg/mL EGCG had no significant effect on the proliferation of hDPSCs. EGCG inhibited expression of IL-1ß, IL-6, and TNF-α. Furthermore, EGCG rescued cell proliferation ability, increased SOD activity and reduced ROS expression under hypoxia.In vivo, reduced inflammatory cell accumulation was observed in the coronal pulp in the EGCG group, while in the control group, diffuse inflammatory cells were observed in the radicular pulp. CONCLUSION: EGCG had no obvious effects on calcified nodule formation but significantly inhibited the inflammatory response of hDPSCs and inhibited apoptosis of hDPSCs caused by hypoxia injury. In vivo, EGCG exerts inhibitory effects on pulp tissue inflammation.

Radiographic and Histologic Evaluation of Experimentally Induced Severe Intrusive Luxation of Immature Teeth in Rats.

INTRODUCTION: The aim of this study was to establish an intrusive luxation model in rats and observe the pulpal and periodontal outcomes. METHODS: The intrusion was experimentally induced by an application of 20-N force on the occlusal surface of maxillary right second molar along the tooth axial using a striking instrument in 3-week-old male Sprague-Dawley rats. Thirty rats were divided into 6 groups (n = 5) and were sacrificed after 3, 7, 14, 30, 60, and 90 days of the surgery. The occurrence of pulpal and periodontal complications was observed by micro-computed tomographic scanning and hematoxylin-eosin staining. RESULTS: All experimental teeth were fully intruded into the alveolar bone with their occlusal surface located at the cervical level of the adjacent first molar. Spontaneous re-eruption initiated at 7 days. At 14 days, 4 teeth (80%, 4/5) partially re-erupted, whereas 2 (40%), 3 (75%), and 4 (100%) teeth completely re-erupted at 30, 60, and 90 days, respectively. Pulp degeneration and inflammation mainly occurred in 4 teeth at 3 days, 5 at 7 days, and 2 at 14 days; after 14 days, pulp calcification was observed in 8 teeth. Ankylosis and replacement root resorption mainly occurred in 1 tooth at 30 days, 2 teeth at 60 days, and 3 at 90 days. Marginal bone loss was observed in 3 teeth (60%) at 30 days, 3 (75%) at 60 days, and 2 (50%) at 90 days. CONCLUSIONS: An animal model of intrusive dentoalveolar trauma was successfully established in rats. Pulpal and periodontal complications similar to clinical tooth intrusion were observed, which provided a basis for exploring the mechanisms of complications in the future.