Patients presenting with nasal obstruction after rhinoplasty are frequently found to have collapse and/or weakening of their upper lateral cartilages with resulting nasal valve dysfunction. The conchal cartilage "butterfly" graft is a technique which, when properly performed during revision rhinoplasty, yields predictable functional and cosmetic results with minimal morbidity.

IMPORTANCE Nasal valve compromise is a major cause of nasal obstruction, and multiple methods have been developed to address it. OBJECTIVE To compare nasal airflow resistance, airflow partitioning, and mucosal cooling (heat flux) before and after 2 surgical interventions, butterfly and spreader graft placement, used to treat nasal valve compromise. DESIGN, SETTING, AND PARTICIPANTSIn this cadaveric tissue study, 4 fresh cadaveric heads underwent both spreader graft and butterfly graft surgical procedures in alternating sequence in March 2016. Preoperative and postoperative computed tomographic scans were used to generate 3-dimensional (3-D) models of the nasal airway. These models were then used in steady state computational fluid dynamics simulations of airflow and heat transfer during inspiration. INTERVENTION Butterfly and spreader graft techniques.MAIN OUTCOMES AND MEASURES Nasal airflow resistance, airflow partitioning, and heat flux.RESULTS Donors 1, 2, and 3 were white males; donor 4, a white female. Computational fluid dynamics simulations during inspiration in 3-D models generated from preoperative and postoperative computed tomographic scans of the 4 cadaveric heads indicated reductions from preoperative values in nasal airflow resistance associated with both butterfly grafts (range, 20%-51%) and spreader grafts (range, 2%-29%). Butterfly grafts were associated with a greater reduction in nasal airflow resistance in models of all 4 cadaveric heads. Changes from preoperative values for heat flux, a biophysical variable that correlates with the subjective sensation of nasal patency, were more variable, ranging from −11% to 4% following butterfly grafts and −9% to 10% following spreader grafts. The preoperative airflow allocation in the left and right nostrils improved consistently with the butterfly graft. With the spreader graft, there were improvements for donors 1 and 4, but the allocations were worse for donors 2 and 3. CONCLUSIONS AND RELEVANCEThe results of this study suggest that the more recently developed butterfly graft technique may be associated with a similar level of improved nasal airflow as that observed with the use of a spreader graft in nasal valve compromise. Both interventions were associated with comparable changes in heat flux. Because this study addressed only static internal nasal valve stenosis, even greater differences in air flow and heat flux between the 2 techniques may be anticipated in a dynamic model. Further investigation in patients is warranted.LEVEL OF EVIDENCE NA.

In this series of patients, a novel surgical protocol was used. The extruded implant was removed and immediate reconstruction with irradiated rib cartilage was done. All patients were evaluated for postoperative infection, graft extrusion, and satisfaction with cosmetic result. There was one major complication in this series of 18 patients, warping of the IHCC, which necessitated removal and replacement. This approach appears to be a reasonable method for reconstruction of extruded nasal alloplasts.

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CCR2 is considered a proinflammatory mediator in many inflammatory diseases such as rheumatoid arthritis. However, mice lacking CCR2 develop exacerbated collagen-induced arthritis. To explore the underlying mechanism, we investigated whether autoimmune-associated Th17 cells were involved in the pathogenesis of the severe phenotype of autoimmune arthritis. We found that Th17 cells were expanded approximately 3-fold in the draining lymph nodes of immunized CCR2−/− mice compared to WT controls (p = 0.017), whereas the number of Th1 cells and regulatory T cells are similar between these two groups of mice. Consistently, levels of the Th17 cell cytokine IL-17A and Th17 cell-associated cytokines, IL-6 and IL-1β were approximately 2–6-fold elevated in the serum and 22–28-fold increased in the arthritic joints in CCR2−/− mice compared to WT mice (p = 0.04, 0.0004, and 0.01 for IL-17, IL-6, and IL-1β, respectively, in the serum and p = 0.009, 0.02, and 0.02 in the joints). Furthermore, type II collagen-specific antibodies were significantly increased, which was accompanied by B cell and neutrophil expansion in CCR2−/− mice. Finally, treatment with an anti-IL-17A antibody modestly reduced the disease severity in CCR2−/− mice. Therefore, we conclude that while we detect markedly enhanced Th17-cell responses in collagen-induced arthritis in CCR2-deficient mice and IL-17A blockade does have an ameliorating effect, factors additional to Th17 cells and IL-17A also contribute to the severe autoimmune arthritis seen in CCR2 deficiency. CCR2 may have a protective role in the pathogenesis of autoimmune arthritis. Our data that monocytes were missing from the spleen while remained abundant in the bone marrow and joints of immunized CCR2−/− mice suggest that there is a potential link between CCR2-expressing monocytes and Th17 cells during autoimmunity.