Role of macrophages in trigeminal ganglia in ectopic orofacial pain associated with pulpitis.

OBJECTIVES

This study aimed to elucidate the role of macrophages in the trigeminal ganglia (TG) in developing pulpitis-associated ectopic orofacial pain.

METHODS

Rats underwent maxillary pulp exposure, and Fluoro-Gold (FG) was administered in the ipsilateral whisker pad (WP). Head withdrawal threshold (HWT) upon mechanical stimulation of the WP was recorded, and liposomal clodronate clophosome-A (LCCA; macrophage depletion agent) was administered to the TG at three and four days after pulp exposure. Immunohistochemically, TG sections were stained with anti-Iba1 (a macrophage marker) and anti-Nav1.7 antibodies.

RESULTS

Pulp exposure decreased HWT and increased the number of Iba1-IR cells near FG-labelled TG neurons. LCCA inhibited the decrease in HWT and stopped the increase of FG-labelled Nav1.7-IR TG neurons in the pulpitis group.

CONCLUSIONS

Activation of macrophages by pulpitis induces the overexpression of Nav1.7 in TG neurons receiving inputs from WP, resulting in pulpitis-induced ectopic facial mechanical allodynia.