RESUMO
BACKGROUND: Trigeminal nerve injury following endodontic treatment, leading to unpleasant sensations or partial sensory loss in the face or oral mucosa, is uncommon but significant when it occurs. OBJECTIVE: This study analysed the pharmacological management of trigeminal nerve injuries (TNI) in a university-based hospital. METHODS: We conducted a retrospective analysis of 47 patients who visited the Department of Orofacial Pain and Oral Medicine at Yonsei University Dental Hospital, Seoul, Korea, after TNI following endodontic procedures in primary clinics. Both objective tests and subjective evaluations, assessed the extent and duration of sensory injury during the initial visit. The patient's initial symptoms, presumed cause of TNI, referral delay (time interval between TNI and the first visit to our clinic), and medications were analysed to determine whether these factors affected the outcomes. RESULTS: Most patients with TNI experienced dysesthesia with hypoesthesia (70.2%). The mandibular molars were predominantly affected (72.3%), with the inferior alveolar nerve (IAN), lingual nerve (LN), both IAN and LN, and maxillary nerve compromised in 83.0, 12.8, 2.1, and 2.1% of cases, respectively. Causes of TNI included local anaesthesia (29.8%), overfilling/over-instrumentation (25.5%), endodontic surgery (17.0%), and unknown factors (27.7%). A shorter referral delay was associated with better outcomes, with an average delay of 8.6 weeks for symptom improvement compared with 44.1 weeks for no change. The medication regimens included steroids, NSAIDs, topical lidocaine, vitamin B complex, Adenosine Triphosphate (ATP), antiepileptics, antidepressants, and opioids administered alone or in combination, with a mean duration of 20.7 weeks. 53.2% of the patients reported improvement in their symptoms, 27.7% experienced no significant change, and 19.1% had unknown outcomes. CONCLUSIONS: Swift referral to an orofacial pain specialist is recommended for effective recovery in cases of TNI arising from endodontic treatment.
RESUMO
The purpose of this study is to evaluate the effects of botulinum toxin type A (BoNT-A) for managing sleep bruxism (SB) in a randomized, placebo-controlled trial. Thirty SB subjects were randomly assigned into two groups evenly. The placebo group received saline injections into each masseter muscle, and the treatment group received BoNT-A injections into each masseter muscle. Audio-video-polysomnographic recordings in the sleep laboratory were made before, at four weeks after, and at 12 weeks after injection. Sleep and SB parameters were scored according to the diagnostic and coding manual of American Academy of Sleep Medicine. The change of sleep and SB parameters were investigated using repeated measures analysis of variance (RM-ANOVA). Twenty-three subjects completed the study (placebo group 10, treatment group 13). None of the SB episode variables showed a significant time and group interaction (p > 0.05) except for electromyography (EMG) variables. The peak amplitude of EMG bursts during SB showed a significant time and group interaction (p = 0.001). The injection decreased the peak amplitude of EMG bursts during SB only in the treatment group for 12 weeks (p < 0.0001). A single BoNT-A injection cannot reduce the genesis of SB. However, it can be an effective management option for SB by reducing the intensity of the masseter muscle.
