How well do we manage the odontogenic keratocyst? A multicenter study.

OBJECTIVE: The aim of this study was to answer the following clinical questions: Among patients treated for odontogenic keratocysts (OKCs), what is the overall 5-year disease-free rate, and what factors are associated with disease recurrence? STUDY DESIGN: We implemented a multicenter retrospective cohort study composed of patients presenting for the evaluation and management of previously untreated OKCs. The predictor variables were grouped into demographic, medical, radiographic, and operative categories. The primary outcome variable was time to lesion recurrence. Data analyses were performed by using bivariate analysis and univariate or multivariate Cox proportional hazards models. RESULTS: The study sample was composed of 231 OKCs. Of these, 57 (24.7%) were treated with decompression with residual cystectomy, 86 (37.2%) with enucleation without adjuvant therapy, and 78 (33.8%) with enucleation with peripheral ostectomy. There were 44 recurrences (19%), with a median time to recurrence of 26.7 months (range 15.8-49.8). CONCLUSIONS: This multicenter study is the largest study analyzing disease recurrence after treatment of OKCs by using appropriate statistical analysis for a time-to-event outcome (disease recurrence). The 5-year disease-free estimate was 29%. Mandibular lesions, multilocular lesions, and lesions treated with decompression and residual cystectomy were associated with recurrence.

Kv2.1 cell surface clusters are insertion platforms for ion channel delivery to the plasma membrane.

Voltage-gated K(+) (Kv) channels regulate membrane potential in many cell types. Although the channel surface density and location must be well controlled, little is known about Kv channel delivery and retrieval on the cell surface. The Kv2.1 channel localizes to micron-sized clusters in neurons and transfected human embryonic kidney (HEK) cells, where it is nonconducting. Because Kv2.1 is postulated to be involved in soluble N-ethylmaleimide-sensitive factor attachment protein receptor-mediated membrane fusion, we examined the hypothesis that these surface clusters are specialized platforms involved in membrane protein trafficking. Total internal reflection-based fluorescence recovery after photobleaching studies and quantum dot imaging of single Kv2.1 channels revealed that Kv2.1-containing vesicles deliver cargo at the Kv2.1 surface clusters in both transfected HEK cells and hippocampal neurons. More than 85% of cytoplasmic and recycling Kv2.1 channels was delivered to the cell surface at the cluster perimeter in both cell types. At least 85% of recycling Kv1.4, which, unlike Kv2.1, has a homogeneous surface distribution, is also delivered here. Actin depolymerization resulted in Kv2.1 exocytosis at cluster-free surface membrane. These results indicate that one nonconducting function of Kv2.1 is to form microdomains involved in membrane protein trafficking. This study is the first to identify stable cell surface platforms involved in ion channel trafficking.

Serial histologic and immunohistochemical changes in anterior digastric myocytes in response to distraction osteogenesis.

PURPOSE: To document histologic and immunohistochemical changes in the anterior digastric muscle during distraction osteogenesis (DO). MATERIALS AND METHODS: Nineteen Yucatan minipigs with mixed dentition were used for these experiments. Group A (n = 16) underwent unilateral mandibular distraction at a rate of 1 mm/day (no latency) for 12 days. Animals were killed at mid-DO (n = 5), end-DO (n = 5), mid-fixation (n = 4), and end-fixation (n = 2). Group B (n = 2) underwent acute 12-mm advancement, and group C (n = 1) dissection and osteotomy. Animals from groups B and C were killed at the end-DO time point. Digastric muscles from treatment and contralateral sides of all animals were harvested and embedded in paraffin. Specimens were stained with hematoxylin/eosin or immunohistochemically for proliferating cell nuclear antigen (PCNA; total cell proliferation), paired Box-7 gene protein (Pax7; satellite cells), or myogenic differentiation 1 protein (MyoD; differentiating myoblasts). Descriptive and bivariate statistics were computed to compare groups (P ≤ .05 statistically significant). RESULTS: All animals survived the operation and observation period; there were no device failures. Two animals (1 at mid-DO, 1 at mid-fixation) were eliminated from the study because of postoperative infection. There was minimal digastric inflammation, fibrosis, and muscle fiber size variability during active DO. Immunohistochemical analysis showed statistically significant increases in PCNA (cellular proliferation), Pax7 (satellite cells), and MyoD (differentiating myoblasts) positive nuclei in digastrics at mid-DO and end-DO. CONCLUSIONS: Results of this study indicate that there are minimal pathologic changes but significant increases in PCNA, Pax7, and MyoD positive nuclei during active distraction. This supports the hypothesis that the digastric muscle response to DO consists of proliferation and hypertrophy.