Electroacupuncture Promotes Functional Recovery after Facial Nerve Injury in Rats by Regulating Autophagy via GDNF and PI3K/mTOR Signaling Pathway / 中国结合医学杂志

OBJECTIVE@#To explore the mechanism of electroacupuncture (EA) in promoting recovery of the facial function with the involvement of autophagy, glial cell line-derived neurotrophic factor (GDNF), and phosphatidylinositol-3-kinase (PI3K)/mammalian target of rapamycin (mTOR) signaling pathway.@*METHODS@#Seventy-two male Sprague-Dawley rats were randomly allocated into the control, sham-operated, facial nerve injury (FNI), EA, EA+3-methyladenine (3-MA), and EA+GDNF antagonist groups using a random number table, with 12 rats in each group. An FNI rat model was established with facial nerve crushing method. EA intervention was conducted at Dicang (ST 4), Jiache (ST 6), Yifeng (SJ 17), and Hegu (LI 4) acupoints for 2 weeks. The Simone's 10-Point Scale was utilized to monitor the recovery of facial function. The histopathological evaluation of facial nerves was performed using hematoxylin-eosin (HE) staining. The levels of Beclin-1, light chain 3 (LC3), and P62 were detected by immunohistochemistry (IHC), immunofluorescence, and reverse transcription-polymerase chain reaction, respectively. Additionally, IHC was also used to detect the levels of GDNF, Rai, PI3K, and mTOR.@*RESULTS@#The facial functional scores were significantly increased in the EA group than the FNI group (P<0.05 or P<0.01). HE staining showed nerve axons and myelin sheaths, which were destroyed immediately after the injury, were recovered with EA treatment. The expressions of Beclin-1 and LC3 were significantly elevated and the expression of P62 was markedly reduced in FNI rats (P<0.01); however, EA treatment reversed these abnormal changes (P<0.01). Meanwhile, EA stimulation significantly increased the levels of GDNF, Rai, PI3K, and mTOR (P<0.01). After exogenous administration with autophagy inhibitor 3-MA or GDNF antagonist, the repair effect of EA on facial function was attenuated (P<0.05 or P<0.01).@*CONCLUSIONS@#EA could promote the recovery of facial function and repair the facial nerve damages in a rat model of FNI. EA may exert this neuroreparative effect through mediating the release of GDNF, activating the PI3K/mTOR signaling pathway, and further regulating the autophagy of facial nerves.

Neuropatia pós-implante / Post-implant neuropathy

Atualmente, a utilização de implantes dentários tem sido considerada o padrão-ouro para reabilitação de arcos parcial ou totalmente edêntulos. Devido aos recursos avançados de exame por imagem, principalmente da tomografia computadorizada de feixe cônico, esses procedimentos apresentam altas taxas de sucesso; no entanto, algumas complicações trans- e pós-cirúrgicas ainda são passíveis de ocorrer, sendo uma delas a neuropatia pós-implante. A neuropatia pós-implante se trata de uma neuropatia traumática orofacial secundária a traumas diretos ou indiretos aos nervos da face, sendo os nervos alveolar inferior e lingual os mais acometidos. Essa condição pode apresentar diferentes formas clínicas, sendo elas a anestesia, parestesia, hipoestesia, hiperestesia e/ou disestesia. Por se tratar de uma complicação pouco frequente, porém de alto impacto social para o paciente e de difícil diagnóstico e tratamento, o presente artigo tem como objetivo, por meio de uma revisão de literatura dos estudos mais relevantes na área, esclarecer o que é a neuropatia pós-implante, como ela pode ser desencadeada, bem como as melhores formas de diagnóstico e tratamento.

Nowadays, the use of dental implants in partial or total edentulous arch is considered the gold standard in oral rehabilitation. This procedure has high success rates mainly due to the advanced features of radiograph exams like the cone beam computerized tomography (CBCT). However, some intra- and post-operative complication may occur. One of the possible complications is post implant neuropathy (PIN). PIN is a traumatic trigeminal neuropathy that can be due to direct or indirect nerve trauma. The most affected nerves are inferior alveolar nerve and lingual nerve. This condition can be clinically reported as anesthesia, paresthesia, hypoesthesia, hyperesthesia and/or dysesthesia. PIN is not a frequent condition but has a major impact on everyday social life and it is a very difficult pathology to diagnose and to treat. Based on that, the aim of this article is to review the most relevant studies in the field and to clarify what is PIN and what are the possible causes of it. As well as identify the best diagnostic and treatment approach.

Development of an intraoral device for facial muscle retraining and its clinical application

El objetivo de este trabajo fue desarrollar una técnica de reeducación de la musculatura facial lesionada en cuadros de parálisis facial, por medio de una aparatología intraoral de sencilla manipulación para el paciente, que permita corregir patrones neuromusculares incorrectos y mejore la estética. La parálisis facial es una alteración motora de múltiple etiología que resulta en una simetría facial. Sus tratamientos actuales en constante discusión incluyen cirugías de anastomosis, descompresivas y estéticas, terapia con corticoesteroides, toxina botulínica y otros medicamentos. Además se aplican terapias físicas con electroestimulación y feedback para reentrenar la musculatura facial. Se diseñó y confeccionó un aparato intraoral removible de acrílico de termopolimerización y retenedores de alambre forjado según técnica de laboratorio convencional. Se aplicó a un caso clínico de parálisis facial instalando el sistema e indicando el uso diario, 4 veces al día, realizando ejercicios al espejo durante 20 minutos cada ez, tratando de coordinar la acción del aparato con la sonrisa del lado sano. Se tomaron fotografías digitales de la paciente en reposo y sonrisa con el sistema puesto y sin el sistema y se compararon los movimientos comisurales con software. Se observó que el índice de movimiento anatómico para la porción inferior de la cara fue de 1,77 y el índice de movimiento no anatómico para la porción inferior de la cara fue de 0 (con el sistema instalado). El dispositivo utilizado mejoró la asimetría facial en reposo oponiéndose a la tracción de los músculos contralaterales, logrando una mejor ubicación del filtrum en reposo, permitiendo que el paciente practique en su casa movimientos simulatorios de una sonrisa.

The aim of this work was to develop a facial neuromuscular retraining technique for cases of facial palsy, involving an easyto use intraoral device that allows correcting abnormal neuromuscular patterns and improving esthetics. Facial palsy is a motor alteration of multiple origin that results in facial asymmetry. Treatment remains controversial to date and includes, surgical anastomosis and decompressive and plastic surgery, corticosteroids therapy, injection of botulinum toxin, and administration of other medicinal drugs. Physical therapy involving electrical stimulation and feedback are also used to retrain facial muscles. A removable thermopolymerized acrylic intraoral device with wrought wire clasps was developed and constructed. The device was used on a patient with facial palsy who was instructed to wear it 4 times a day during 20 minutes and perform exercises in front of the mirror, trying to coordinate the action of the device with the smile movement on the unaffected side of the face. Digital photographs of the patient were taken during smile movement and at rest with and without the device, and movements of the oral commissures were compared using specific software. Results showed anatomic and nonanatomic indices of facial motion for the lower part of the face with the device to be 1.77 and 0 respectively. The device improved facial symmetry during rest by opposing traction forces of the contralateral muscles, resulting in a better position of the filtrum during rest, and allowed the patient to exercise smile movements at home.

Traumatic facial paralysis

The cosmetic deformity caused by facial nerve paralysis is very annoying both for the patient and the surgeon. Traumatic injury of the facial nerve, together with Bell's palsy, remain as the two major causes of facial nerve paralysis. Traumatic facial nerve injury may be operative, post-operative or in a casuality, as it may be involved in fracture base of the skull. With the progress of ear surgery, more cases of operative and post-operative facial nerve paralysis are met with. It is the variations in opinion concerning the management of such cases that make the difference in the prognosis. Fisch and Schwartzenberg [4] stated that, under conservative treatment, 90% of late and 75% of early facial paralysis recover satisfactorily. The problem is still with the remaining 10-25% of cases