Oral submucous fibrosis (OSF) is an oral precancerous disorder associated with the habit of areca nut chewing. MiR-10b has been shown to be upregulated in the oral cancer cells and induced by Twist. Our previous work has revealed that Twist participated in the pathogenesis of OSF and therefore we aimed to investigate whether Twist/miR-10b axis was involved in the activation of myofibroblast in the oral cavity. The expression levels of miR-10b in OSF tissues and fibrotic buccal mucosal fibroblasts (fBMFs) were examined. Besides, the expression of miR-10b was determined in fBMFs following knockdown of Twist or in BMFs after arecoline stimulation. Myofibroblast activities, including collagen gel contraction, migration and wound healing abilities, as well as the expression of α-SMA were measured in fBMFs treated with miR-10b inhibitor. Last, we investigated whether the effect of Twist overexpression could be reversed by suppression of miR-10b. MiR-10b expression was overexpressed in both OSF tissues and fBMFs. The silence of Twist resulted in the downregulation of miR-10b in fBMFs and arecoline treatment led to an increase of miR-10b in a dose-dependent manner. Inhibition of miR-10b ameliorated the activation of myofibroblasts and the expression of α-SMA. Moreover, we demonstrated that suppression of miR-10b hindered the increased collagen gel contraction caused by Twist overexpression. MiR-10b upregulation in OSF may be due to the stimulation of areca nut, leading to elevated myofibroblast activation. Our findings showed that the areca nut-induced expression of miR-10b was under the regulation of Twist and inhibition of miR-10b may provide a direction for treatment of OSF.

This study evaluated short-term and long-term changes in bone height after mandibular reconstruction using an osteotomized fibula graft, with the aim of identifying factors associated with atrophy of the graft in an elderly population. This retrospective study involved patients who underwent mandibular reconstruction using a free vascularized fibula graft from 2005 through 2015 and had at least 12 months of follow-up. Postoperative panoramic radiographs were used to measure bone height at standardized locations on each segment of the graft at 1 year postoperatively and at later follow-up. The sample was composed of 30 patients (15 men, 15 women; mean age, 62.6 years; age range, 50 to 80 years). According to the HCL classification (H, hemimandibular segment including the condyle; C, central segment including both mandibular canine teeth; L, lateral segment without the condyle), mandibular defect types were L (n = 19), LC (n = 7), LCL (n = 3), and H (n = 1). There were 0 to 3 segmental osteotomies with the fibula graft. None of the patients received an osseointegrated dental implant during a mean follow-up of 4.0 years (range, 1.5 to 9.7 yr). All patients underwent reconstruction of the mandibular body, 10 of whom also underwent reconstruction of the mandibular ramus. Atrophy of the fibula graft was observed in 9.9 and 15.0% of the body segment and 5.9 and 6.6% of the ramal segment at 1 year postoperatively and at later follow-up, respectively. Graft hypertrophy occurred in the ramal segment in 2 patients. Multivariate analysis showed a significantly higher rate of graft atrophy in women than in men at later follow-up (P = .033). Fibula grafts showed long-term stability, and in 2 cases even a gain in bone height, in this elderly population. Female gender was identified as a risk factor for atrophy of the fibula bone graft in the body segment of the reconstructed mandible.

The mandible is an independent and protruding bone structure in the lower third portion of the human facial skeleton. Because of its prominent and unprotected position, the mandible is a primary site of facial trauma. Previous studies have not comprehensively discussed the association between the mandibular fractures and concomitant fractures of facial bones, the trunk, or limbs. This study analyzed the epidemiology of mandibular fractures and their correlation with concomitant fractures. The present study enrolled 118 patients with a total of 202 mandibular fracture sites during at any time from January 1, 2012, to December 31, 2021, in northern Taiwan. According to the study results, the patients between 21 and 30 years of age had the highest occurrence of trauma, and road traffic accidents (RTAs) constituted the primary cause of mandibular fractures. Fall-related injuries were significant in patients >30 years of age. By the analysis of Pearson's contingency coefficient, the number of mandibular fractures was not significantly associated with concomitant fractures of the extremities or the trunk. However, accompanying maxillary fractures can be regarded as an indication of concomitant extremity or trunk fractures in patients with mandibular fractures. Three-site mandibular fractures are not necessarily accompanied by extremity and trunk fractures; however, clinicians should implement multidisciplinary examination and management in patients with mandibular fractures accompanied by maxillary fractures. Maxillary fractures can be regarded as an indication of concomitant fractures of other facial bones, the extremities, or the trunk.

Oral submucous fibrosis (OSF) is a premalignant disorder that is associated with betel nut chewing. The purpose of the study was to establish the role of histone deacetylase (HDAC) 8, one of histone deacetylases, in the regulation of fibrotic conditions to provide a therapeutic potential for OSF. First, we examined the expression of HDAC8 in fibrotic buccal mucosal fibroblasts (fBMFs) and OSF tissues. Markers of myofibroblasts and TGF-β signaling were conducted in fBMFs with HDAC8 knockdown were examined. Furthermore, epithelial-mesenchymal transition (EMT) markers, collagen gel contraction and migration ability were also examined in fBMFs transfected with sh-HDAC8. HDAC8 inhibitor was used to analyze the collagen gel contraction and wound healing ability in fBMFs. We observed the mRNA expression of HDAC8 was significantly increased in fBMFs. Compared to normal tissues, the protein level of HDAC8 was upregulated in OSF. Next, mRNA and protein expression of HDAC8 was significantly decreased, accompanying downregulation of α-SMA and COL1A1 in fBMFs infected with sh-HDAC8. To determine the critical role of HDAC8 in OSF fibrogenesis, results revealed that TGF-β secretion and the expression of EMT transcription factor SNAIL and p-Smad were significantly decreased in HDAC8-knockdown fBMFs. We further demonstrated that collagen gel contraction and migration ability were significantly decreased in fBMFs transfected with sh-HDAC8. Last, results revealed that significantly reduced collagen gel contraction and wound healing ability in fBMFs with HDAC8 inhibitor treatment. We concluded that downregulation of HDAC8 alleviated the activities of myofibroblasts and TGF-β/Smad signaling pathway in OSF.