ABSTRACT
OBJECTIVE: This study aimed to longitudinally assess the risk of facial nerve injury (FNI) in the surgical repair of mandibular condylar neck and subcondylar fractures (CN/SCFs) and to explore its predictors. MATERIALS AND METHODS: In a retrospective cohort study, the outcome was defined as FNI at 1 week and 1, 3, and 6 months postoperatively. Potential predictors included age, sex, etiology, fracture site and pattern (dislocation/non-dislocation), concomitant facial fractures, interval to surgery, surgeons' experience, plate types, and the marginal mandibular branch-traversing approach (deep/superficial group). We employed generalized estimating equations (GEEs) for repeated measurements throughout the 6-month follow-up period. RESULTS: Among 102 patients with 114 fractures, 27 patients (26.5%) developed FNI within 1 week. Prolonged FNI (≥ 1 month) occurred in 19 (19.2%) of 99 patients. Multivariate GEE analyses revealed that deep surgical approaches (i.e., traditional submandibular and retroparotid approaches; odds ratio [OR], 18.90; p = 0.011), fractures with dislocation (OR, 3.60; p = 0.025), and female gender (OR, 2.71; p = 0.040) were independently associated with the overall FNI risk. Additionally, the deep approaches (OR, 15.91; p = 0.014) and female gender (OR, 3.41; p = 0.035) were correlated with a prolonged FNI risk. Sensitivity analyses for the outcomes identified the same predictors. CONCLUSION: The predictors longitudinally associated with FNI in CN/SCF surgeries included a deep MMB-traversing approach, dislocated fracture, and female gender. CLINICAL RELEVANCE: The superficial surgical approaches (i.e., transparotid, transmasseteric anteroparotid, and high perimandibular approaches) should be adopted for CN/SCF treatment to minimize postoperative morbidity, especially for female patients with dislocated condyles.
Subject(s)
Facial Nerve Injuries/etiology , Fracture Fixation, Internal/adverse effects , Mandibular Fractures/surgery , Adult , Aged , Facial Nerve , Female , Humans , Longitudinal Studies , Male , Mandibular Condyle , Middle Aged , Retrospective Studies , Risk Factors , Treatment Outcome , Young AdultABSTRACT
BACKGROUND: In our department, patients with oral squamous cell carcinoma(OSCC)received preoperative chemotherapy containing S-1 to prevent the growth and dissemination of tumors during the waiting time before definitive surgery. We retrospectively evaluated the usefulness of this treatment. PATIENTS AND METHODS: One hundred and five patients comprising stages T1(26), T2(64), T3(7), and T4(8 cases)were enrolled in this study from July 2001 to June 2013. In principle, patients were administered S-1(80mg/m / 2/day, days 1-14)and followed by a drug holiday(days 15-21), continuing until 1 week before surgery. RESULTS: The median administration period was 14 days(256 days). Ninety-eight patients underwent definitive surgery, but 7 patients who revealed clinical CR underwent only biopsy and showed histological CR. The histological responses of all patients were CR(24), PR(22), and NC(59), and the response rate was 43.8%. Almost all adverse effects were Grade 1 or 2, except 1 case of neutropenia(Grade 3)and 1 case of urticaria(Grade 3). The 5-year overall survival rates were 86.7% in all cases, 95.3% in CR/PR cases, and 79.7% in NC cases. CONCLUSION: Preoperative S-1 administration during the waiting time was a safe and very effective method and was considered beneficial for patients with OSCC.
Subject(s)
Antineoplastic Combined Chemotherapy Protocols/therapeutic use , Carcinoma, Squamous Cell , Mouth Neoplasms , Carcinoma, Squamous Cell/drug therapy , Drug Combinations , Humans , Mouth Neoplasms/drug therapy , Oxonic Acid , Retrospective Studies , Tegafur , Waiting ListsABSTRACT
Neurofibromatosis type 1 (NF1) was first described in 1882 as a hamartomatous disorder of neural crest derivation. We present the imaging of a 65-year-old woman with NF1. Computed tomography revealed that there were three major findings presented: skeletal deformity, an area of fat (probably related to mesodermal dysplasia), and benign neoplasm within the masticator space. Moreover, masticatory muscles were hypoplastic.
ABSTRACT
It is necessary to explore new treatments for recurrent head and neck malignancies (HNM) to avoid severe impairment of oro-facial structures and functions. Boron neutron capture therapy (BNCT) is tumor-cell targeted radiotherapy that has significant superiority over conventional radiotherapies in principle. We have treated with BNCT 42 times for 26 patients (19 squamous cell carcinomas (SCC), 4 salivary gland carcinomas and 3 sarcomas) with a recurrent and far advanced HNM since 2001. Results of (1) (10)B concentration of tumor/normal tissue ratios (T/N ratio) of FBPA-PET studies were SCC: 1.8-5.7, sarcoma: 2.5-4.0, parotid tumor: 2.5-3.7. (2) Therapeutic effects were CR: 12 cases, PR: 10 cases, PD: 3 cases NE (not evaluated): 1 case. Response rate was 85%. (3) Improvement of QOL such as a relief of severe pain, bleeding, and exudates at the local lesion, improvement of PS, disappearance of ulceration, covered with normal skin and preserved oral and maxillofacial functions and tissues. (4) Survival periods after BNCT were 1-72 months (mean: 13.6 months). Six-year survival rate was 24% by Kaplan-Meier analysis. (5) Adverse-events were transient mucositis and alopecia in most of the cases; three osteomyelitis and one brain necrosis were recognized. These results indicate that BNCT represents a new and promising treatment approach for advanced HNM.
Subject(s)
Boron Neutron Capture Therapy , Head and Neck Neoplasms/radiotherapy , Neoplasm Recurrence, Local/radiotherapy , Adult , Aged , Aged, 80 and over , Boron Neutron Capture Therapy/adverse effects , Carcinoma, Squamous Cell/mortality , Carcinoma, Squamous Cell/radiotherapy , Female , Head and Neck Neoplasms/diagnostic imaging , Head and Neck Neoplasms/mortality , Humans , Kaplan-Meier Estimate , Male , Middle Aged , Neoplasm Recurrence, Local/diagnostic imaging , Neoplasm Recurrence, Local/mortality , Positron-Emission Tomography , Salivary Gland Neoplasms/mortality , Salivary Gland Neoplasms/radiotherapy , Sarcoma/mortality , Sarcoma/radiotherapyABSTRACT
BACKGROUND: It was reported that elevation of the intracellular concentration of free Ca2+ ([Ca2+]i) by a calcium ionophore increased the release of herpes simplex virus type 1 (HSV-1). Freely diffusible hydrogen peroxide (H2O2) is implied to alter Ca2+ homeostasis, which further enhances abnormal cellular activity, causing changes in signal transduction, and cellular dysfunction. Whether H2O2 could affect [Ca2+]i in HSV-1-infected cells had not been investigated. RESULTS: H2O2 treatment increased the amount of cell-free virus and decreased the proportion of viable cells. After the treatment, an elevation in [Ca2+]i was observed and the increase in [Ca2+]i was suppressed when intracellular and cytosolic Ca2+ were buffered by Ca2+ chelators. In the presence of Ca2+ chelators, H2O2-mediated increases of cell-free virus and cell death were also diminished. Electron microscopic analysis revealed enlarged cell junctions and a focal disintegration of the plasma membrane in H2O2-treated cells. CONCLUSION: These results indicate that H2O2 can elevate [Ca2+]i and induces non-apoptotic cell death with membrane lesions, which is responsible for the increased release of HSV-1 from epithelial cells.
Subject(s)
Calcium/metabolism , Epithelial Cells/virology , Herpesvirus 1, Human/drug effects , Hydrogen Peroxide/pharmacology , Cell Communication , Cell Death , Cell Line, Tumor , Cell Survival/drug effects , Chelating Agents/pharmacology , DNA Fragmentation , Egtazic Acid/pharmacology , Epithelial Cells/cytology , Epithelial Cells/ultrastructure , Flow Cytometry , Herpesvirus 1, Human/metabolism , HumansABSTRACT
p34(cdc2) is a protein kinase that plays an important role in the control of the cell cycle and regulation of activity of the tumor suppressor gene. Previously, we demonstrated that cisplatin (CDDP) induced growth suppression resulting in differentiation of teratocarcinoma F9 cells. In the present study, we investigated the mechanism of cell cycle retardation by CDDP in F9 cells, focusing on p34(cdc2). After the induction of differentiation with CDDP, F9 cells were arrested at the late S+G2/M. After treatment with CDDP, the level of the expression of cdc2 mRNA did not change. However, the half-life of p34(cdc2) was greatly reduced, thus, the level of p34(cdc2) protein was decreased. These findings suggest that the cell cycle arrest by CDDP is due partly to the induced instability of p34(cdc2) in F9 cells.