Consequences of Trocar Dynamics on Mental Nerve in Transoral Thyroidectomy.

BACKGROUND: Mental nerve (MN) injuries are reported during transoral endoscopic thyroidectomy vestibular approach. Effect of trocar insertion and position on MN are examined in the present study. MATERIALS AND METHODS: Ten millimeter incision was made at the center of the lower lip oral vestibule. Two 5 mm lateral incisions of the lower lip oral vestibule were made at the junction between the incisor and the canine. These 2 lateral incisions were high, just below the edge of lower lip. Nine pigs (18 MN) were randomly divided into 3 groups and MN dissection was performed. The angle between the lateral ports and median line were changed between 15 and 45 degrees among 3 groups and effect on MN was examined. RESULTS: During dissection when insertion and other ports are in neutral position visual inspection of MNs did not reveal any compression bilaterally. The distance between MN and the ports was 18.2±2.1 mm (16.3 to 21.2 mm). In group I and group II, MNs have no compression by the lateral trocars. In group III (45 degrees), left MNs were all compressed. Two MNs (66.7%) were compressed on the right side. The MN was compressed at its ramification. CONCLUSIONS: The results of the present experimental study, endorse the suggested medial and lateral vestibular incisions for transoral endoscopic thyroidectomy vestibular approach. However, during dynamic modification of the lateral port position/angle, MN compression was observed when the angle was >45 degrees.

Involvement of Satellite Cell Activation via Nitric Oxide Signaling in Ectopic Orofacial Hypersensitivity.

: The mechanical head-withdrawal threshold (MHWT) was significantly reduced following inferior alveolar nerve transection (IANX) in rats. Nitrate and nitrite synthesis was dramatically increased in the trigeminal ganglion (TG) at 6 h after the IANX. The relative number of neuronal nitric oxide synthase (nNOS)-immunoreactive (IR) cells was significantly higher in IANX rats compared to sham-operated and N-propyl-L-arginine (NPLA)-treated IANX rats. On day 3 after NPLA administration, the MHWT recovered considerably in IANX rats. Following L-arginine injection into the TG, the MHWT was significantly reduced within 15 min, and the mean number of TG cells encircled by glial fibrillary acidic protein (GFAP)-IR cells was substantially higher. The relative number of nNOS-IR cells encircled by GFAP-IR cells was significantly increased in IANX rats. In contrast, after NPLA injection into the TG, the relative number of GFAP-IR cells was considerably reduced in IANX rats. Fluorocitrate administration into the TG significantly reduced the number of GFAP-IR cells and prevented the MHWT reduction in IANX rats. The present findings suggest that following IANX, satellite glial cells are activated via nitric oxide (NO) signaling from TG neurons. The spreading satellite glial cell activation within the TG results in mechanical hypersensitivity of face regions not directly associated with the trigeminal nerve injury.

Inferior alveolar nerve transection disturbs innate immune responses and bone healing after tooth extraction.

Coordination between the nervous and innate immune systems to maintain bone homeostasis is largely uncharacterized. The present study investigated the sensory-immune interaction in resting alveolar bone and healing socket by surgical sensory denervation. Bone histomorphometry and immunohistochemistry showed that sensory denervation resulted in moderate suppression of bone remodeling, with a proinflammatory milieu manifested by increased neutrophil recruitment and possible alternations in macrophage phenotypes along the resting bone surface. This denervation effect intensified when bone remodeling was triggered by tooth extraction, as revealed by disrupted temporospatial variations in macrophage subpopulations and neutrophil infiltration, which were closely associated with a dramatic decline in socket bone filling and residual ridge height. Antagonism of calcitonin gene-related peptide (CGRP) brought about similar antianabolic and proinflammatory effects as sensory denervation, suggesting that sensory nerves may monitor the bony milieu by CGRP. Depletion of macrophages, rather than neutrophils, ruled out CGRP effects, illustrating that macrophages were the primary immune mechanism that linked sensory innervation, innate immunity, and bone. The data support that sensory innervation is required for control of innate immune responses and maintenance of bone homeostasis. Sensory neuropeptides, such as CGRP, are a possible target for the development of proanabolic treatments in bone disease by modulating innate immune responses.