Can Neutrophils Control the Evolution of Pulpitis ?

Objectives: The challenge of improving caries management is based in part on a better understanding of the pulp-dentin complex biology. Among all the actors involved during pulpitis, neutrophils could play a decisive role since they are a pillar of antibacterial immunity but also a major factor in tissue destruction. Both chemokines CXCL1 and CXCL2 have been described as crucial in neutrophils recruitment by binding to the CXCR2 receptor. In this work, we aimed to develop a new in vivo model of pulpitis to better mimic different stages of pulp inflammation, and then to characterize spatial and temporal dimensions of the expression of CXCL1 and CXCL2.
Methods: The model used is a new model of progressive and controlled pulpitis in rat (APAFiS no.19-042). Under operative microscope, the inflammation is induced by mechanically exposing the pulp and bringing it into contact with LPS from Escherichia coli or PBS as a positive control during 30min, 24h, 48h, 72h, 96h or 120h (n=4 per condition). Teeth are then removed for hematoxylin and eosin staining and immunohistological analysis of CXCL1 and CXCL2 expression.
Results: The relevance of the model is validated histologically by the size of the cell degeneration area, which increases with the duration of the inflammatory stimulus, reaching complete necrosis at 120h. CXCL1 and CXCL2 show different expression profiles: CXCL2 is found from 24h in perivascular area and odontoblastic palisade while CXCL1 expression is mostly localized to the area of cell degeneration from 24h.
Conclusions: This model makes it possible to describe tissue changes during inflammation and the results suggest that CXCL1 and CXCL2 could play distinct roles in neutrophils recruitment and in the balance of inflammation. Thereafter it would be interesting to relate those molecular and cellular events with repair capacities of the pulp dentin complex.