IADR Abstract Archives
A New Model of Pulpal Inflammation to Characterize Pulp Healing
Objectives: Vital pulp therapy is an alternative to endodontic treatment to maintain pulp vitality in case of pulpitis. However, so far, the indication of these therapeutics in case of irreversible pulpitis is not settled.
Our study aims firstly to develop a new model of pulpitis (reversible and irreversible) in rats’ molars and secondly to evaluate in vivo the pulp repair process. More specifically, the main purpose is to identify the critical level of inflammation biomarkers allowing pulp repair after pulpotomy.
Methods: The work presented here is a pilot study with 24 Sprague Dawley rats. Dental pulp inflammation was induced on the upper first molar after pulpal effraction with tungsten bur followed by injection of Lipopolysaccharides (LPS) of E.Coli at 10mg/ml or phosphate buffered saline (PBS) (T0). This induction was repeated at 6h (n=16), 24h (n=8). Animals were sacrificed after 6, 24 or 48 hours and teeth were processed for histological, immunohistological (IHC) analyses. Furthermore, quantitative polymerase chain reaction and enzyme linked immunosorbent assay were performed in order to quantify the level of pulpal inflammation markers
Results: From T0 to 48 hours, hematoxylin/eosin staining showed that the induced inflammation with LPS gradually increased throughout the pulp chamber to the root canal. This histological result was confirmed by IHC using anti-CD-68 which marks among other macrophages. IL6, CXCL1, MMP3, CCL2 were significantly upregulated after 6 h of LPS stimulation as compared with PBS. IL1-β, CXCL2 and iNOS were upregulated throughout the experiment. The immunoregulatory cytokine IL10 was also upregulated after 6 h and 48h, suggesting that LPS stimulates also immunoregulation.
Conclusions: This new model permits to correlate inflammation markers to the status of pulpitis, in order to identify molecules improving precision diagnosis and allowing development of new materials involved in regulation of inflammation, stimulation of cellular repair and healing process.
Our study aims firstly to develop a new model of pulpitis (reversible and irreversible) in rats’ molars and secondly to evaluate in vivo the pulp repair process. More specifically, the main purpose is to identify the critical level of inflammation biomarkers allowing pulp repair after pulpotomy.
Methods: The work presented here is a pilot study with 24 Sprague Dawley rats. Dental pulp inflammation was induced on the upper first molar after pulpal effraction with tungsten bur followed by injection of Lipopolysaccharides (LPS) of E.Coli at 10mg/ml or phosphate buffered saline (PBS) (T0). This induction was repeated at 6h (n=16), 24h (n=8). Animals were sacrificed after 6, 24 or 48 hours and teeth were processed for histological, immunohistological (IHC) analyses. Furthermore, quantitative polymerase chain reaction and enzyme linked immunosorbent assay were performed in order to quantify the level of pulpal inflammation markers
Results: From T0 to 48 hours, hematoxylin/eosin staining showed that the induced inflammation with LPS gradually increased throughout the pulp chamber to the root canal. This histological result was confirmed by IHC using anti-CD-68 which marks among other macrophages. IL6, CXCL1, MMP3, CCL2 were significantly upregulated after 6 h of LPS stimulation as compared with PBS. IL1-β, CXCL2 and iNOS were upregulated throughout the experiment. The immunoregulatory cytokine IL10 was also upregulated after 6 h and 48h, suggesting that LPS stimulates also immunoregulation.
Conclusions: This new model permits to correlate inflammation markers to the status of pulpitis, in order to identify molecules improving precision diagnosis and allowing development of new materials involved in regulation of inflammation, stimulation of cellular repair and healing process.