Genistein reverses the effect of 17β-estradiol on exacerbating experimental occlusal interference-induced chronic masseter hyperalgesia in ovariectomised rats.

Abstract

Oro-facial pain is more prevalent in women than in men, and oestrogen may underlie this sex difference. Genistein reversed the potentiation of 17β-estradiol (E2) on glutamate-induced acute masseter nociceptive behaviour, but its role in dental experimental occlusal interference (EOI)-induced chronic masseter hyperalgesia remains unclear. This study aimed to investigate sex differences, and to explore the role and underlying mechanisms of genistein in E2-potentiated EOI-induced chronic masseter hyperalgesia in rats. Female and male rats were prepared to compare the sex differences of masseter hyperalgesia induced by EOI using a 0.4-mm-thick metal crown. Female rats were ovariectomised (OVX) and treated with E2 and genistein, followed by EOI. The head withdrawal threshold (HWT) was examined to assess masseter sensitivity. The protein expression of transient receptor potential vanilloid-1 (TRPV1) in the trigeminal ganglion (TG) was detected using western blotting. Immunofluorescence staining was used to reveal the colocalisation of oestrogen receptors (ERs) with TRPV1 and the percentage of TRPV1-positive neurons in the TG. To some extent, female rats displayed enhanced sensitivity to EOI-induced chronic masseter hyperalgesia compared with males. Female rats showed the lowest HWT in the pro-oestrus phase. Pre-treatment with genistein antagonised E2 potentiation in EOI-induced masseter hyperalgesia and blocked the effect of E2 by downregulating TRPV1 protein expression and the percentage of TRPV1-positive neurons in the TG. Female rats showed greater masseter hyperalgesia than males under EOI. Genistein antagonised the facilitation of EOI-induced chronic masseter hyperalgesia by E2 probably through inhibiting TRPV1 in the TG.