Abstract
Pain symptoms in temporomandibular disorders (TMD) predominantly affect reproductive women, suggesting that estrogen regulates pain perception. However, how estrogen contributes to chronic TMD pain remains largely unclear. In the present study, we performed behavioral tests, electrophysiology, Western blot and immunofluorescence to investigate the role and underlying mechanisms of estrogen in dental experimental occlusal interference (EOI)-induced chronic masseter mechanical hyperalgesia in rats. We found that long-term 17β-estradiol (E2) replacement exacerbated EOI-induced masseter hyperalgesia in a dose-dependent manner in ovariectomized (OVX) rats. Whole-cell patch-clamp recordings demonstrated that E2 (100 nM) treatment enhanced the excitability of isolated trigeminal ganglion (TG) neurons in OVX and OVX EOI rats, and EOI increased the functional expression of transient receptor potential vanilloid-1 (TRPV1). In addition, E2 replacement upregulated the protein expression of TRPV1 in EOI-treated OVX rats. Importantly, intraganglionic administration of the TRPV1 antagonist AMG-9810 strongly attenuated the facilitatory effect of E2 on EOI-induced masseter mechanical sensitivity. These results demonstrate that E2 exacerbated EOI-induced chronic masseter mechanical hyperalgesia by increasing TG neuronal excitability and TRPV1 function. Our study helps to elucidate the E2 actions in chronic myogenic TMD pain and may provide new therapeutic targets for relieving estrogen-sensitive pain.
Highlights
Temporomandibular disorders (TMD) comprise a collection of clinical conditions associated with pain and dysfunction of the masticatory muscles and/or temporomandibular joints (TMJ) [1]
To evaluate whether E2 exacerbated masseter mechanical hyperalgesia caused by experimental occlusal interference (EOI), the head withdrawal thresholds were examined in the sham OVX group and the four OVX groups treated with 0, 20, 80, and 200 μg/d E2, respectively (Figure 1a), and the E2-treated groups have been shown to resemble the physiological E2 levels of rats in menopause, metestrus, proestrus, and pregnancy [9]
EOI-induced mechanical hyperalgesia [20], we examined whether transient receptor potential vanilloid-1 (TRPV1) expression in the
Summary
Temporomandibular disorders (TMD) comprise a collection of clinical conditions associated with pain and dysfunction of the masticatory muscles and/or temporomandibular joints (TMJ) [1]. Administration of exogenous estrogens, such as oral contraceptives or hormone replacement therapy (HRT), increases the incidence of TMD pain [6]. Based on these observations, estrogen has been suggested as an important biological factor in the modulation of TMD pain. The contribution and the underlying mechanism of estrogen in chronic TMD pain remain to be fully understood. We established an animal model of dental experimental occlusal interference (EOI) by bonding a crown onto the right maxillary first molar, which induced sustained mechanical hyperalgesia in bilateral masticatory muscles and simulating chronic myogenic TMD pain [13]. There are no data on whether and how estrogen functions in this model
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
