Evaluation of peripheral nerve fibers and mast cells in burning mouth syndrome.

Emerging evidence has revealed a cross-talk in the etiopathogenesis of burning mouth syndrome (BMS) related to peripheral nerve fibers (NF) and neuropeptides secreted by mast cells. Here, we investigated the S-100+ density and PGP 9.5+ integrity of peripheral NF and the tryptase+ mast cell density in the oral mucosa of BMS patients and healthy individuals. A total of 23 oral mucosa specimens (12 BMS and 11 controls) were evaluated. The clinical diagnosis of BMS was based on a careful examination, excluding other local and systemic causes. Samples were taken from an incisional biopsy of the tongue mucosa of individuals with symptomatic BMS, while the margins of the non-neoplastic tongue biopsy served as controls of healthy individuals. Immunohistochemistry was performed to determine the density/mm2 of S-100+, PGP 9.5+ peripheral NF, and tryptase+ mast cells. Similar densities of S-100+, PGP 9.5+ peripheral NF, and tryptase+ mast cells were found in cases of BMS, with a median value of 3.70, 0.70, and 29.24/mm2, respectively, and in the control group, with a median value of 2.60, 0.80, and 26.01/mm2, respectively (p > 0.05). Moreover, the relationship between S100+ and PGP 9.5+ peripheral NF was the same in both groups (p = 0.70). This study demonstrated that there were no alterations in the density and integrity of peripheral NF in the tongue of symptomatic BMS patients. However, the sensitization of peripheral NF in this disease may not depend on mast cell density.

Evaluation of peripheral nerve fibers and mast cells in burning mouth syndrome

Abstract Emerging evidence has revealed a cross-talk in the etiopathogenesis of burning mouth syndrome (BMS) related to peripheral nerve fibers (NF) and neuropeptides secreted by mast cells. Here, we investigated the S-100+ density and PGP 9.5+ integrity of peripheral NF and the tryptase+ mast cell density in the oral mucosa of BMS patients and healthy individuals. A total of 23 oral mucosa specimens (12 BMS and 11 controls) were evaluated. The clinical diagnosis of BMS was based on a careful examination, excluding other local and systemic causes. Samples were taken from an incisional biopsy of the tongue mucosa of individuals with symptomatic BMS, while the margins of the non-neoplastic tongue biopsy served as controls of healthy individuals. Immunohistochemistry was performed to determine the density/mm2 of S-100+, PGP 9.5+ peripheral NF, and tryptase+ mast cells. Similar densities of S-100+, PGP 9.5+ peripheral NF, and tryptase+ mast cells were found in cases of BMS, with a median value of 3.70, 0.70, and 29.24/mm2, respectively, and in the control group, with a median value of 2.60, 0.80, and 26.01/mm2, respectively (p > 0.05). Moreover, the relationship between S100+ and PGP 9.5+ peripheral NF was the same in both groups (p = 0.70). This study demonstrated that there were no alterations in the density and integrity of peripheral NF in the tongue of symptomatic BMS patients. However, the sensitization of peripheral NF in this disease may not depend on mast cell density.

Directions of mandibular canal displacement in ameloblastoma: A computed tomography mirrored-method analysis.

PURPOSE: This study was performed to investigate mandibular canal displacement in patients with ameloblastoma using a 3-dimensional mirrored-model analysis. MATERIALS AND METHODS: The sample consisted of computed tomographic scans of patients with ameloblastoma (n=10) and healthy controls (n=20). The amount of mandibular canal asymmetry was recorded as a continuous variable, while the buccolingual (yaw) and supero-inferior (pitch) directions of displacement were classified as categorical variables. The t-test for independent samples and the Fisher exact test were used to compare groups in terms of differences between sides and the presence of asymmetric inclinations, respectively (P<0.05). RESULTS: The length of the mandibular canal was similar on both sides in both groups. The ameloblastoma group presented more lateral (2.40±4.16 mm) and inferior (-1.97±1.92 mm) positions of the mental foramen, and a more buccal (1.09±2.75 mm) position of the middle canal point on the lesion side. Displacement of the mandibular canal tended to be found in the anterior region in patients with ameloblastoma, occurring toward the buccal and inferior directions in 60% and 70% of ameloblastoma patients, respectively. CONCLUSION: Mandibular canal displacement due to ameloblastoma could be detected by this superimposed mirrored method, and displacement was more prevalent toward the inferior and buccal directions. This displacement affected the mental foramen position, but did not lead to a change in the length of the mandibular canal. The control group presented no mandibular canal displacement.