Faculty Bibliography

Immediate breast reconstruction relies on healthy mastectomy flaps for success. Tissue perfusion of these mastectomy flaps is dependent on multiple patient-, operative-, and surgeon-specific factors, which must be optimized. Unfortunately, tissue perfusion is also notoriously difficult to accurately assess and investigate. In this review, we discuss the importance of tissue perfusion in successful reconstructive breast surgery with an emphasis on perfusion assessment and techniques to ensure that anatomic mastectomy flap perfusion is maintained for immediate breast reconstruction after mastectomy. Preoperative and patient-specific factors should be considered with operative plans modified to minimize ischemic risk. Intraoperatively, incision planning and mastectomy dissection will dictate skin flap perfusion. Most importantly, mastectomy dissection in a plane at the breast capsule will maximize preservation of the subdermal plexus and subcutaneous perforators that supply the breast skin envelope while also maximizing oncologic parenchymal resection. Such anatomic dissection has been demonstrated to decrease risk of ischemic complications in immediate breast reconstruction. Postoperatively, any potential or actual areas of impaired perfusion and ischemia must be diagnosed appropriately and managed proactively to ensure a successful reconstruction. It is also important for surgeons to be aware of imaging modalities and adjunctive technologies that can help promote and assess optimal mastectomy flap tissue perfusion. Plastic surgeons and breast surgeons must actively and collaboratively work together to ensure their mutual goals are met, and optimal outcomes are attained for patients undergoing immediate breast reconstruction after mastectomy.

OBJECTIVE:To evaluate the reliability and failure mode of zirconia-reinforced lithium silicate (ZLS) molar crowns of different thicknesses. METHODS:Monolithic ZLS molar crowns (0.5mm, 1.0mm, and 1.5 mm thickness) were modeled and milled using a CAD/CAM system (n = 21/group). Crowns were cemented on dentin-like epoxy resin replicas with a resin cement. The specimens were subjected to single load-to-failure test for step-stress profiles designing. Mouth-motion step-stress accelerated-life test was performed under water by sliding an indenter 0.7 mm lingually down on the distobuccal cusp until specimen fracture or suspension. Use level probability Weibull curves and reliability were calculated and plotted. Polarized-light optical microscope and scanning electron microscope (SEM) were used to characterize fracture patterns. RESULTS:Irrespective of crown thickness, beta (β) values were higher than 1 and fatigue accelerated failures. While 0.5 mm ZLS crowns exhibited a significant reduction in the probability of survival at 200N, 300N and 400 N mission loads (69%, 41% and 19%, respectively), no significant difference was observed between 1.0 mm and 1.5 mm crowns. Both thicknesses have maintained the survivability at approximately 90%. Failure primarily comprised bulk fracture where radial cracks originated from the cementation surface beneath the indenter loading trail and propagated towards the cervical margin. SIGNIFICANCE/CONCLUSIONS:1.5 mm- and 1.0 mm-thickness monolithic ZLS crowns presented higher probability of survival compared to 0.5 mm crowns. Bulk fracture was the chief failure mode, regardless of thickness.

The study evaluated the effects of a Supercritical CO₂ (scCO₂ ) on a commercially available decellularized/delipidized naturally derived porcine pericardium collagen membrane, Vitala®. The Vitala® and scCO₂ treated experimental membranes were evaluated for guided tissue regeneration (GTR) of periodontal tissue in class III furcation defects utilizing a dog model. Physical material characterization was performed by scanning electron microscopy (SEM), thermogravimetric analysis (TGA), and differential scanning calorimetry (DSC). The in vivo portion of the study was allocated to three-time points (6, 12, and 24-weeks) using standardized class III furcation defects created in the upper second and third premolars. The experimental defects (n = 5) were covered with either a collagen membrane (positive control), scCO₂ -treated collagen membrane (experimental) or no membrane (negative control). Following sacrifice, histologic serial sections were performed from cervical to apical for morphologic/morphometric evaluation. Morphometric evaluation was carried out by ranking the presence of collagen membrane, amount of bone formation within the defect site and inflammatory cell infiltrate content. SEM showed the experimental scCO₂ -treated membrane to have a similar gross fibrous appearance and chemical structure in comparison to the Vitala® Collagen membrane. A significant increase in membrane thickness was noted in the scCO₂ -treated membranes (366 ± 54 μm) vs non-treated membranes (265 ± 75 μm). TGA and DSC spectra indicated no significant qualitative differences between the two membranes. For the in vivo results, both membranes indicated significantly greater amounts of newly formed bone (scCO₂ : 2.85 ± 1.1; Vitala®: 2.80 ± 1.0) within the covered defects relative to uncovered controls (0.8 ± 0.27) at 24 weeks. Both membrane types gradually degraded as time elapsed in vivo from 6 to 12 weeks, and presented nearly complete resorption at 24 weeks. The inflammatory infiltrate at regions in proximity with the membranes was commensurate with healthy tissue levels from 6 weeks in vivo on, and periodontal ligament regeneration onset was detected at 12 weeks in vivo. The effect of the supplementary scCO₂ treatment step on the collagen membrane was demonstrated to be biocompatible, allowing for the infiltration of cells and degradation over time. The treated membranes presented similar performance in GTR to non-treated samples in Class III furcation lesions. Defects treated without membranes failed to achieve regeneration of the native periodontium. © 2018 Wiley Periodicals, Inc. J Biomed Mater Res B Part B: Appl Biomater 00B: 000-000, 2018.

Facial transplantation is emerging as a therapeutic option for self-inflicted gunshot wounds. The self-inflicted nature of this injury raises questions about the appropriate role of self-harm in determining patient eligibility. Potential candidates for facial transplantation undergo extensive psychosocial screening. The presence of a self-inflicted gunshot wound warrants special attention to ensure that a patient is prepared to undergo a demanding procedure that poses significant risk, as well as stringent lifelong management. Herein, we explore the ethics of considering mechanism of injury in the patient selection process, referring to the precedent set forth in solid organ transplantation. We also consider the available evidence regarding outcomes of individuals transplanted for self-inflicted mechanisms of injury in both solid organ and facial transplantation. We conclude that while the presence of a self-inflicted gunshot wound is significant in the overall evaluation of the candidate, it does not on its own warrant exclusion from consideration for a facial transplantation.

BACKGROUND: Delayed immediate (DI) autologous breast reconstruction consists of immediate postmastectomy tissue expander placement, radiation therapy, and subsequent autologous reconstruction. The decision between timing of reconstructive methods is challenging and remains to be elucidated. We aim to compare patient reported outcomes and quality of life between delayed and DI reconstruction. METHODS: A retrospective review of all patients, who underwent autologous breast reconstruction at Montefiore Medical Center from January 2009 to December 2016, was conducted. Patients who underwent postmastectomy radiotherapy were divided into two cohorts: delayed and DI autologous breast reconstruction. Patients were mailed a BREAST-Q survey and their responses, demographic information, complications, and need for revisionary procedures were analyzed. RESULTS: = 30) in the DI group. Responses showed similar satisfaction with their breasts, well-being, and overall outcome. CONCLUSIONS: Delayed and DI autologous breast reconstruction yield similar patient-reported satisfaction; however, patients undergoing DI reconstruction have higher rates of major mastectomy necrosis. Furthermore, patients in the DI group risk premature tissue expander removal.

Pain is rated by oral cancer patients as the worst symptom and significantly impairs a patient's ability to eat, talk, and drink. Mediators, secreted from oral cancer microenvironment, excite primary afferent neurons, which in turn generate pain. Oral cancer cells release TNFalpha which induces acute inflammation and nociception in mice. We hypothesize that TNFalpha activates Schwann cells to amplify pain signals. First, we confirmed the involvement of TNFalpha in oral cancer pain in patients and animal models. We found that oral cancer tissues collected from patients have higher TNFalpha concentration compared to anatomically matched normal tissues. Differences in TNFalpha concentration between the tumor and anatomically matched normal tissues correlate positively with total pain scores. In a Nitroquinoline 1-oxide (4NQO) mouse oral cancer model we demonstrated reduced mechanical hypersensitivity (P<0.05, N=8) with the dolognawmeter gnawing assay when TNFalpha was neutralized with C-87. Using a non-contact co-culture model, we found that HSC-3 cells induced a more activated human primary Schwann cells phenotype with increased proliferation (P<0.05) and migration (P<0.05); introduction of C-87 in the co-culture reduced Schwann cell proliferation (P<0.05) and migration (P<0.05) induced by HSC-3 cells. After removal of the co-cultured cancer cells, cancer-activated Schwann cells secrete greater amounts of TNFalpha and nerve growth factor (NGF), another known nociceptive mediator in the oral cancer microenvironment, compared to Schwann cells initially co-cultured with DOK (P<0.05) or naive Schwann cells (P<0.05). To determine whether activated Schwann cells mediate oral cancer pain, we cultured Schwann cells in hypoxic conditions - a known cancer stimulus that induces robust Schwann cell activation. Schwann cell supernatant was then collected and injected into the mouse cheek. Supernatant from hypoxia-activated Schwann cells induced greater facial allodynia (measured with von Frey filaments) in mice (P<0.05, N=7), compared to supernatant from Schwann cells cultured in normoxic conditions (N=5). C-87 significantly reduced facial allodynia caused by hypoxiaactivated Schwann cells (P<0.05, N=5). We infer from our results that TNFalpha plays a role in the activation of Schwann cells and that cancer-activated Schwann cells are a source of nociceptive mediators in the cancer microenvironment. Inhibition of Schwann cell activation might be clinically useful for alleviating oral cancer pain