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Introduction We investigated the use of oral antibiotics (OA) and surgical site infection (SSI) related to extractions of ordinary teeth and mandibular wisdom teeth in a dental outpatient clinic from January 2015 to December 2019. Methods The following information were surveyed: (1) presence/absence of OA, (2) timing, (3) type, (4) administration period, and (5) SSI rates. Results The use of OA during ordinary tooth extraction decreased from 68.3% to 41.3%, but SSI rate did not change during this period of time. Total SSI rate was 0.8% (122/14,832) on average. For mandibular wisdom tooth extraction, preoperative administration of third-generation cephalosporins decreased from 70.4% to 0.3% while that of penicillin (AMPC) increased from 0% to 98%. SSI rate was not changed after these improvements. Total SSI rate was 3.5% (180/5106) on average. The duration of OA was slightly decreased to two days in 2018 and 2019, and it was found that there was no significant difference in SSI rates between 2- and 3-day durations. Preoperative administration had 0.37 odds ratio (OR) (95% confidence interval (95%CI): 0.22–0.63) of SSI compared with postoperative administration. AMPC had 0.76 OR (95% CI: 0.55–1.04) of SSI compared with Third-generation cephalosporins and others. Timing of OA was P Conclusions SSI rates did not change over time, administration period of OA decreased and the use of AMPC increased. Therefore, it seems necessary to continue to investigate the effects of SSI risk factors proactively in the future and to make efforts in the advocacy of appropriate antimicrobial use.

Cleft palate is one of the most common congenital diseases. Therefore, elucidating the molecular mechanisms of palate development is crucial for basic science and the clinical field. Cleft palate in mouse with targeted gene mutation is an excellent experimental model for clarifying the mechanisms driving palate development. Cleft palate occurs in two forms: a cleft between the primary and secondary palates (primary cleft palate) and a cleft between the secondary palates (secondary cleft palate). It remains unclear whether primary palate development is under similar molecular control as secondary palate formation, since most of studies have focused on secondary palate development using mutant mice. CL/Fraser (CL/Fr) is a mouse strain that often exhibits spontaneous primary cleft palate; however, the molecular changes in primary cleft palate in CL/Fr mice are not fully understood. Several signaling pathways, including Shh, Fgf, Bmp, and Wnt signaling, have been shown to play key roles in secondary palate development. In the present study, we found that Shh and Wnt signaling pathways were downregulated in the primary cleft palate region in CL/Fr mice.

Objective To assess the postoperative speech and pharyngeal space changes after surgical maxillary advancement, we sought to objectively evaluate these parameters in patients with velopharyngeal insufficiency following palatoplasty due to cleft palate. Subjects and methods The subjects were 10 cleft palate patients (Group C: 4 males and 6 females, with a mean age of 18 years and 1 month at the time of operation) who had undergone Le-Fort I osteotomies with a mean maxillary advancement of 3.85 mm (range 3.0–5.0 mm). A nasometer test was performed using a nasometer. Articulation during speech was evaluated by a speech therapist. These evaluations were performed immediately before surgery and several weeks, 3 months, and 6 months after the surgery, respectively. Lateral cephalograms of the skull were used for morphological evaluation at 3 months before the surgery and at several weeks and 6 months after the surgery. We examined several parameters using the cephalograms. These data were compared with those of 10 patients without cleft palate who had undergone surgical maxillary advancement for jaw deformities. Results The nasalance scores ( p = 0.001) and the lengths of the soft palate ( p Discussion and conclusions Surgical maxillary advancement may be a useful strategy for patients with velopharyngeal insufficiency following palatoplasty due to cleft palate.

Rodent incisors maintain the ability to grow continuously and their labial dentin is covered with enamel. Bcl11b zinc-finger transcription factor is expressed in ameloblast progenitors in mouse incisors and its absence in Bcl11bKO/KO mice results in a defect in embryonic tooth development. However, the role of Bcl11b in incisor maintenance in adult tissue was not studied because of death at birth in Bcl11bKO/KO mice. Here, we examined compound heterozygous Bcl11bS826G/KO mice, one allele of which has an amino acid substitution of serine at position 826 for glycine, that exhibited hypoplastic maxillary incisors with lower concentrations of minerals at the enamel and the dentin, accompanying the maxillary bone hypoplasia. Histological examinations revealed hypoplasia of the labial cervical loop in incisors, shortening of the ameloblast progenitor region, and impairment in differentiation and proliferation of ameloblast-lineage cells. Interestingly, however, juvenile mice at 5 days after birth did not show marked change in these phenotypes. These results suggest that attenuated Bcl11b activity impairs ameloblast progenitors and incisor maintenance. The number of BrdU label-retaining cells, putative stem cells, was lower in Bcl11bS826G/KO incisors, which suggests the incisor hypoplasia may be in part a result of the decreased number of stem cells. Interestingly, the level of Shh and FGF3 expressions, which are assumed to play key roles in the development and maintenance of ameloblasts and odontoblasts, was not decreased, though the expressed areas were more restricted in ameloblast progenitor and mesenchyme regions of Bcl11bS826G/KO incisors, respectively. Those data suggest that the incisor maintenance by Bcl11b is not directly related to the FGF epithelial–mesenchymal signaling loop including Shh but is intrinsic to ameloblast progenitors and possibly stem cells.

Ghost cell odontogenic carcinoma (GCOC) is a rare malignant variant of odontogenic tumor with ghost cells; only 29 cases are documented. Our patient was a 68-year-old man with a painless, well-defined, radiolucent swelling of the mandibular gingiva in the right incisor-to-molar region. It was diagnosed as a benign calcifying cystic odontogenic tumor (CCOT) on fenestration biopsy. Eighteen years later, he returned with swelling in the same area. The lesion was excised, diagnosed as GCOC, and considered a secondary malignant manifestation of the benign CCOT. No adjuvant chemotherapy or radiotherapy was administered, and his postoperative course was uneventful for 48 months, with no recurrence or distant metastasis. Among the 30 reported cases of GCOC, the mean age at diagnosis was 40.3 years, 22 (73%) involved the maxilla. Twelve (40%) were secondary malignant manifestations of benign CCOTs or dentinogenic ghost cell tumors. Five patients died of recurrence or distant metastasis.

The diagnosis of orofacial pain associated with temporomandibular disorders after repeated temporomandibular joint (TMJ) surgeries can be quite difficult. This case report describes a 52-year-old woman who had previously undergone five TMJ surgeries and developed divergent pain caused by a trigger point in the left preauricular area. Computed tomography and magnetic resonance imaging could not be used to identify a lesion because of metallic artifacts from a TMJ prosthesis. However, sonography indicated the location of the suspected lesion. Moreover, a neurological examination performed with local anesthesia was clinically effective in ruling out other diagnoses of orofacial pain. Ultimately, a histopathological examination of a biopsy specimen from the painful site confirmed the lesion to be a traumatic neuroma. This case report suggests the value of including traumatic neuroma in the differential diagnosis of patients with a history of previous TMJ surgery who present with orofacial pain in the region of the TMJ.

A case is presented of extensive alveolar bone grafting in a patient with bilateral cleft lip and palate and polyostotic fibrous dysplasia. The patient previously underwent bisphosphonate therapy. Because of an abnormal and often decreased bone turnover caused by the fibrous dysplasia and the bisphosphonate therapy, bone grafting in such a patient poses several potential difficulties. In addition, the histomorphometric analysis of the bone grafts showed markedly decreased bone turnover. However, alveolar bone grafting using the iliac crest was performed successfully. Sufficient occlusion was achieved by postoperative low-loading orthodontic treatment.

Operations to the face and skull can obscure the landmarks that are required to locate the position of the foramen ovale. We describe the use of three-dimensional computed tomography (3D-CT) to guide the approach to the foramen ovale to block the mandibular nerve in a patient with a mandibular deformity that had been caused by segmental mandiblectomy. Successful blockage of the mandibular nerve controlled the pain, contributed to the relief of physical and mental stress, and avoided the side effects of analgesics and pain from inserting the blocking needle.