Analgesic effect of a lidocaine-ropivacaine mixture for extraction of impacted mandibular third molars: a randomized controlled trial.

OBJECTIVES: The painless postoperative period can be significantly prolonged by using long-acting local anesthetics such as ropivacaine, though these local anesthetics are known for their slower onset of action. To compensate for this, a mixture of short-onset (e.g., lidocaine) and long-acting local anesthetics is used. However, the efficacy of such an anesthetic cocktail has not been elucidated in the field of oral and maxillofacial surgery. MATERIALS AND METHODS: To address the research purpose, this prospective randomized controlled trial included 56 patients scheduled for impacted mandibular third molar extraction. All patients received the inferior alveolar nerve block (IANB) using either 2% lidocaine with epinephrine or a 1:1 mixture of 2% lidocaine with epinephrine and 0.75% ropivacaine. RESULTS: Patients anesthetized using the lidocaine-ropivacaine mixture showed significantly prolonged postoperative analgesia and pain control than those anesthetized using lidocaine only. CONCLUSIONS: IANB using a lidocaine-ropivacaine mixture can provide prolonged postoperative anesthesia and pain control with extraction of mandibular third molars. CLINICAL RELEVANCE: This method can be a noteworthy addition to existing methods of local anesthesia for the extraction of mandibular third molars. Trial registration number University Hospital Medical Information Network (No. UMIN000044315).

Sensory Neurons in the Human Geniculate Ganglion.

The geniculate ganglion (GG) contains visceral and somatic sensory neurons of the facial nerve. In this study, the number and cell size of sensory neurons in the human GG were investigated. The estimated number of GG neurons ranged from 1,580 to 2,561 (mean ± SD = 1,960 ± 364.6). The cell size of GG neurons ranged from 393.0 to 2,485.4 µm2 (mean ± SD = 1,067.4 ± 99.5 µm2). Sensory neurons in the GG were significantly smaller in size than those in the dorsal root (range = 326.6-5343.4 µm2, mean ± SD = 1,683.2 ± 203.8 µm2) or trigeminal ganglia (range = 349.6-4,889.28 µm2, mean ± SD = 1,529.0 ± 198.48 µm2). Sensory neurons had similar cell body sizes in the GG and nodose ganglion (range = 357.2-3,488.33 µm2, mean ± SD = 1,160.4 ± 156.61 µm2). These findings suggest that viscerosensory neurons have smaller cell bodies than somatosensory neurons. In addition, immunohistochemistry for several neurochemical substances was performed on the human GG. In the ganglion, sensory neurons were mostly immunoreactive for secreted protein, acidic and rich in cysteine-like 1 (94.3%). One third of GG neurons showed vesicular glutamate transporter 2 immunoreactivity (31.3%). Only 7.3% of GG neurons were immunoreactive for transient receptor potential cation channel subfamily V member 1. Sensory neurons in the human GG may respond to gustatory, nociceptive, and/or mechanoreceptive stimuli from tongues, soft palates, and external auditory canals.

Distribution of CGRP and TRPV2 in Human Paranasal Sinuses.

Immunohistochemistry for protein gene product 9.5 (PGP 9.5), calcitonin gene-related peptide (CGRP) and the transient receptor potential cation channel subfamily V member 2 (TRPV2) was performed on human paranasal sinuses. It was found that in the paranasal sinuses, mucous membranes contain PGP 9.5-immunoreactive (PGP 9.5-IR) nerve fibers. Such nerve fibers terminated around large blood vessels as fine varicosities. Isolated PGP 9.5-IR nerve fibers were scattered beneath the epithelium. Glandular tissues were also innervated by PGP 9.5-IR nerve fibers. These fibers were numerous in the maxillary and ethmoid sinuses, and relatively rare in the frontal and sphenoid sinuses. CGRP-IR nerve fibers were common in the maxillary sinus whereas TRPV2-IR nerve fibers were abundant in the ethmoid sinus. They were located around large blood vessels in the lamina propria. Many subepithelial nerve fibers contained TRPV2 immunoreactivity in the ethmoid sinus. CGRP- and TRPV2-IR nerve fibers were very infrequent in the frontal and sphenoid sinuses. In the human trigeminal ganglion (TG), sensory neurons contained CGRP or TRPV2 immunoreactivity. CGRP-IR TG neurons were more common than TRPV2-IR TG neurons. CGRP-IR TG neurons were of various cell body sizes, whereas TRPV2-IR TG neurons were mostly medium-to-large. In addition, human spinal and principal trigeminal sensory nuclei contained abundant CGRP- and TRPV2-IR varicosities. This study indicates that CGRP- and TRPV2-containing TG neurons probably innervate the paranasal sinus mucosae, and project into spinal and principal trigeminal sensory nuclei.

Factors influencing delayed referral of oral cancer patients from family dentists to the core hospital.

Background/purpose: Most oral cancer (OC) cases are identified by family dentists in Japan. However, a significant number of patients with OC in Japan are referred to core hospitals at advanced stages. Therefore, identifying the factors that contribute to delayed referrals from family dentists to core hospitals is crucial for detecting OC in its earlier stages. The aim of this retrospective study was to identify the risk factors for referral delays from family dentists to core hospitals. Materials and methods: The study included 63 patients with OC who were referred by family dentists to the Yamagata University Hospital between 2010 and 2022. The clinical parameters related to referral delays were retrospectively investigated using letters of reference provided by the family dentists and patient charts. Backward multiple regression analysis was performed to identify the relationships between the length of referral delay and potential risk factors. Additionally, backward multivariate logistic regression analysis was performed to examine the independent association between referral delays of >4 weeks and several clinical parameters. Results: Multiple regression analysis revealed that misdiagnosis of malignant lesions by family dentists (P = 0.047) was significantly associated with longer referral delays. Additionally, misdiagnosis of malignant lesions by family dentists was also an independent risk factor for referral delays of >4 weeks (odds ratio, 10.387; P = 0.006). Conclusion: Misdiagnosis of malignant lesions by family dentists was a significant risk factor for referral delays from family dentists to core hospitals. Our results will motivate family dentists to improve their ability to diagnose OC.

Activation of fibroblasts by plasma cells via PDGF/PDGFR signaling in IgG4-related sialadenitis.

IgG4-related sialadenitis (IgG4-SA) is one of the IgG4-related disease. The histological features of IgG4-SA include dense lymphoplasmacytic infiltrates and fibrosis. This study aimed to reveal the involvement of plasma cells in the development of fibrosis and the mechanism underlying fibrosis in IgG4-SA. Hematoxylin-eosin staining, Azan staining, silver staining, and immunohistochemistry (IHC) were performed on IgG4-SA and chronic sialadenitis specimens, and theses samples were analyzed by image analysis software. Histological spatial analysis was used to analyze the localization of IHC-positive cells and the distances between these cells. In the IgG4-SA group, many secondary lymphoid follicles with germinal centers were found, and many collagen fibers developed around these germinal centers. Collagen fibers composed mainly of type I collagen was abundant at sites away from secondary lymphoid follicles, and reticular fibers composed of type III collagen was abundant near secondary lymphoid follicles. Many FAP+ fibroblasts and MUM1+ plasma cells were localized near secondary lymphoid follicles. Histological spatial analysis demonstrated that 90.4% of MUM1+ plasma cells accumulated within 20 µm of FAP+ fibroblasts. Multiple immunofluorescence assays revealed that MUM1+ plasma cells expressed platelet-derived growth factor (PDGF) ß, and FAP+ fibroblasts expressed PDGF receptor (PDGFR) ß and pSTAT3 in IgG4-SA. We have shown that fibrosis is localized around secondary lymphoid follicles and that fibroblasts are activated by plasma cells via PDGF/PDGFR signaling in IgG4-SA.