Masseter corticomotor excitability is decreased after intramuscular administration of nerve growth factor

Abstract

Background Quantification of motor‐evoked potentials (MEPs) can contribute to better elucidate the central modulation of motor pathways in response to nociceptive inputs. The primary aim of this study was to assess the modulatory effects of nerve growth factor (NGF) injection on masseter corticomotor excitability. Methods The healthy participants of this randomized, double blind placebo‐controlled experiment were assigned to have injected into the right masseter muscle either NGF (n = 25) or isotonic saline (IS, n = 17). The following variables were assessed at baseline and 48 hr after the injection: right masseter MEP amplitude and corticomotor mapping and clinical assessment of jaw pain intensity and function. Repeated Measures ANOVA was applied to the data. Results NGF caused jaw pain and increased jaw functional disability after the injection (p < 0.050). Also, the participants in the NGF group decreased the MEP amplitude (p < 0.001) but the IS group did not present any significant modulation after the injection (p > 0.050). Likewise, the participants in the NGF group reduced corticomotor map area and volume (p < 0.001), but the IS group did not show any significant corticomotor mapping changes after the injection (p > 0.050). Finally, there was a significant correlation between the magnitude of decreased corticomotor excitability and jaw pain intensity on chewing 48 hr after the NGF injection (r = −0.51, p = 0.009). Conclusion NGF‐induced masseter muscle soreness can significantly reduce jaw muscle corticomotor excitability, which in turn is associated with lower jaw pain intensity and substantiates the occurrence of central changes that most likely aim to protect the musculoskeletal orofacial structures. Significance Intramuscular administration of nerve growth factor into masseter muscle causes inhibitory corticomotor plasticity, which likely occurs to prevent further damage and seems associated with lower pain intensity on function.

Retrograde nerve growth factor signaling modulates tooth mechanical hyperalgesia induced by orthodontic tooth movement via acid-sensing ion channel 3

“… 7 , 17 In-depth investigations revealed that NGF played an important role in pain modulation. 18 Local administration of NGF could elicit pain and neutralizing antibody against NGF could significantly alleviate pain, 8 rendering neutralizing antibody treatment against NGF a good pain-relief option in clinical practice. 19 Released by local injured tissues, NGF elicits profound inflammatory reactions that ultimately cause painful sensations.…”

Mapping research trends of temporomandibular disorders from 2010 to 2019: A bibliometric analysis

“…Furthermore, Hodges highlighted that the nuances of the motor system adaptation to pain were affected by individual variations and motor task differentiation 20,21 . And now, surface electromyography (EMG), 22 motor‐evoked potentials (MEPs) and transcranial magnetic stimulation (TMS) have been used to evaluate the relationship among oro‐facial pain, muscle function state and the activity and function of specific brain circuits 23,24 …”

A novel cortical biomarker signature for predicting pain sensitivity: protocol for the PREDICT longitudinal analytical validation study

“…After cleaning the skin with alcohol, a sterile solution of recombinant human NGF (dose of 5 μg [0.2 mL]) will be given as a bolus injection into the right masseter on days 0 and 2 using a 1-mL syringe with a disposable needle (27 G). Following the procedure of Costa et al, 4 the needle will be inserted perpendicular to the masseter body until bony contact. The needle will then be retracted ∼2 mm, aspiration performed, and NGF injected.…”