Search

Abstract Objective Surgical resection is associated with higher overall survival (OS) than definitive radiotherapy (RT) or chemoradiotherapy (CRT) in cT4b sinonasal squamous cell carcinoma (SCC). Our study investigates the survival benefit of surgical resection in cT4b sinonasal non‐SCC. Methods The 2004 to 2019 National Cancer Database was queried for patients with cT4b sinonasal non‐SCC undergoing definitive treatment with (1) surgical resection + additional therapy (RT, chemotherapy, or both), (2) RT alone, or (3) CRT. Surgical resection + additional therapy and definitive RT/CRT were compared with Kaplan–Meier and multivariable Cox regression models. Results Of 629 patients satisfying inclusion criteria, 513 (81.6%) underwent surgical resection + additional therapy and 116 (18.4%) underwent definitive RT/CRT. The most frequent histologic types were undifferentiated carcinoma (23.7%), adenoid cystic carcinoma (22.6%), and adenocarcinoma (20.7%). Few patients presented with clinical nodal metastasis (15.7%). There were 4 (0.8%) mortalities within 90 days of surgical resection. Patients undergoing surgical resection with positive surgical margins had higher 5‐year OS than those undergoing definitive RT/CRT (56.3% vs. 39.4%, p = .039) and similar 5‐year OS as those with negative margins (56.3% vs. 63.9%, p = .059). Patients undergoing neoadjuvant chemotherapy had similar 5‐year OS as those undergoing definitive RT/CRT (60.9% vs. 39.5%, p = .053). Age at diagnosis, tumor diameter, and surgical resection + additional therapy (aHR 0.64, 95% CI 0.45–0.91) were associated with OS (p

Abstract Objective Functional endoscopic sinus surgery is a commonly performed otolaryngologic procedure that often uses the microdebrider device for tissue removal. Given the ubiquitous nature of the instrument, we sought to better define the patterns of device failure using the postmarket surveillance openFDA database. Methods The openFDA database was queried for all microdebrider‐related adverse events from January 1, 2000 to November 1, 2020. Descriptive information on the nature of device failure and any associated patient injury was compiled. Reports not directly related to device failure were excluded from the analysis. Results A total of 641 events were included in the analysis. The most common device failure was overheating (n = 348, 54.3%), followed by material separation (n = 173, 27%), and inconsistent device activation (n = 52, 8.1%). Of the reported events, the vast majority did not result in patient harm (n = 579, 90.3%). On review of the remaining cases, only 24 events (3.7%) resulted in true harm to the patient, defined as a temporary or permanent injury or >30 min of additional anesthesia time. Of these cases, the need to reschedule surgical cases (n = 5, 0.8%), retained foreign body (n = 5, 0.8%), and thermal tissue injury (n = 3,0.5%) were the most common. Five patients suffered an injury due to surgeon error unrelated to device malfunction (n = 5, 0.8%). Conclusions Microdebrider device failures are extremely rare. When they do occur, less than 10% result in patient harm. In cases of patient harm related to microdebrider failure, preoperative testing of the device before use could prevent many of the reported malfunctions.

Abstract Objectives The use of topical corticosteroids to manage postoperative sinonasal symptoms after endoscopic skull base surgery (ESBS) has not been well studied. We quantified long‐term impact of postoperative steroid irrigations (SIs) on quality of life of patients after ESBS. Methods Retrospective review of patients at the University of Pennsylvania undergoing ESBS from 2010 to 2019. Data on patient demographics and postoperative treatment with nasal saline irrigation twice daily with and without dissolved steroids (mometasone or budesonide) was collected. Preoperative, and 1‐, 3‐, 6‐, 12‐, 18‐, and 24‐month postoperative Sino‐Nasal Outcome Test (SNOT‐22) scores were assessed. Results A total of 727 patients were assessed (53.4% males), with 479 patients in the no SI group and 248 patients in the SI group. Preoperative SNOT‐22 scores did not differ significantly (P = 0.19). 1‐, 3‐, 6‐, 12‐, 18‐, and 24‐month post‐op SNOT‐22 scores did not significantly differ between groups. However, mometasone irrigations resulted in significantly lower postoperative 2‐year SNOT‐22 scores compared to budesonide (P

Abstract Background Carcinosarcomas are rare, aggressive malignancies that can arise in the nasal cavity and paranasal sinuses. There are limited outcome data available. Accordingly, we sought to use the National Cancer Database (NCDB) to characterize patient demographics and outcomes. Method A retrospective analysis of the NCDB from 2004 to 2016 for patients with sinonasal carcinosarcoma was conducted. Results Thirty patients were included. The patients were predominantly male (n = 20), white (n = 23), and privately insured (n = 15), with an average age of 62.4 years. The nasal cavity was the most common subsite (n = 14), followed by the maxillary sinus (n = 8). Most patient were treated with surgery followed by radiation (n = 23), with the remaining undergoing surgery alone (n = 4), radiation alone (n = 2), or no treatment (n = 1). One‐third (n = 10) received adjuvant chemotherapy. The 1‐ and 5‐year overall survival (OS) in the cohort were 79.2% and 43.3%, respectively. Univariate log‐rank testing showed OS varied based on intervention (P

Akt is an important kinase in metabolism. Akt also phosphorylates and activates endothelial and neuronal nitric oxide (NO) synthases (eNOS and nNOS, respectively) expressed in M0 (unpolarized) macrophages. We showed that e/nNOS NO production downstream of bitter taste receptors enhances macrophage phagocytosis. In airway epithelial cells, we also showed that the activation of Akt by a small molecule (SC79) enhances NO production and increases levels of nuclear Nrf2, which reduces IL-8 transcription during concomitant stimulation with Toll-like receptor (TLR) 5 agonist flagellin. We hypothesized that SC79’s production of NO in macrophages might likewise enhance phagocytosis and reduce the transcription of some pro-inflammatory cytokines. Using live cell imaging of fluorescent biosensors and indicator dyes, we found that SC79 induces Akt activation, NO production, and downstream cGMP production in primary human M0 macrophages. This was accompanied by a reduction in IL-6, IL-8, and IL-12 production during concomitant stimulation with bacterial lipopolysaccharide, an agonist of pattern recognition receptors including TLR4. Pharmacological inhibitors suggested that this effect was dependent on Akt and Nrf2. Together, these data suggest that several macrophage immune pathways are regulated by SC79 via Akt. A small-molecule Akt activator may be useful in some infection settings, warranting future in vivo studies.

IntroductionBitter taste receptors (T2Rs) are G protein-coupled receptors identified on the tongue but expressed all over the body, including in airway cilia and macrophages, where T2Rs serve an immune role. T2R isoforms detect bitter metabolites (quinolones and acyl-homoserine lactones) secreted by gram negative bacteria, including Pseudomonas aeruginosa, a major pathogen in cystic fibrosis (CF). T2R activation by bitter bacterial products triggers calcium-dependent nitric oxide (NO) production. In airway cells, the NO increases mucociliary clearance and has direct antibacterial properties. In macrophages, the same pathway enhances phagocytosis. Because prior studies linked CF with reduced NO, we hypothesized that CF cells may have reduced T2R/NO responses, possibly contributing to reduced innate immunity in CF.MethodsImmunofluorescence, qPCR, and live cell imaging were used to measure T2R localization, calcium and NO signaling, ciliary beating, and antimicrobial responses in air-liquid interface cultures of primary human nasal epithelial cells and immortalized bronchial cell lines. Immunofluorescence and live cell imaging was used to measure T2R signaling and phagocytosis in primary human monocyte-derived macrophages.ResultsPrimary nasal epithelial cells from both CF and non-CF patients exhibited similar T2R expression, localization, and calcium signals. However, CF cells exhibited reduced NO production also observed in immortalized CFBE41o- CF cells and non-CF 16HBE cells CRISPR modified with CF-causing mutations in the CF transmembrane conductance regulator (CFTR). NO was restored by VX-770/VX-809 corrector/potentiator pre-treatment, suggesting reduced NO in CF cells is due to loss of CFTR function. In nasal cells, reduced NO correlated with reduced ciliary and antibacterial responses. In primary human macrophages, inhibition of CFTR reduced NO production and phagocytosis during T2R stimulation.ConclusionsTogether, these data suggest an intrinsic deficiency in T2R/NO signaling caused by loss of CFTR function that may contribute to intrinsic susceptibilities of CF patients to P. aeruginosa and other gram-negative bacteria that activate T2Rs.

Abstract Background The non-cancerous functions of Akt in the airway are understudied. In some tissues, Akt phosphorylates and activates endothelial nitric oxide synthase (eNOS) to produce nitric oxide (NO) that has anti-inflammatory effects. NO production has antibacterial and antiviral effects in the airway, and increasing NO may be a useful anti-pathogen strategy. Akt also stimulates the nuclear factor erythroid 2–related factor 2 (Nrf-2) transcription factor, which transcribes antioxidant genes. Therefore, we hypothesized that activation of the Akt/eNOS pathway, which also activates Nrf-2, may have protective effects in human airway cells against injury. Methods To directly test the effects of Akt signaling in the airway, we treated A549 and 16HBE cells as well as primary bronchial, nasal, and type II alveolar epithelial cells with small molecule Akt activator SC79. We examined the effects of SC79 on eNOS activation, NO production, Nrf-2 target levels, and interleukin-8 (IL-8) transcription during exposure to TNF-α or Pseudomonas flagellin (TLR5 agonist). Additionally, air–liquid interface bronchial cultures were treated with cadmium, an oxidative stressor that causes airway barrier breakdown. Results SC79 induced a ~ twofold induction of p-eNOS and Nrf-2 protein levels blocked by PI3K inhibitor LY294002. Live cell imaging revealed SC79 increased acute NO production. Quantitative RT-PCR showed a ~ twofold increase in Nrf-2 target gene transcription. TNF-α or flagellin-induced IL-8 levels were also significantly reduced with SC79 treatment. Moreover, the transepithelial electrical resistance decrease observed with cadmium was ameliorated by SC79, likely by an acute increase in tight junction protein ZO-1 levels. Conclusions Together, the data presented here demonstrate SC79 activation of Akt induces potentially anti-pathogenic NO production, antioxidant gene transcription, reduces IL-8 transcription, and may protect against oxidative barrier dysfunction in a wide range of airway epithelial cells.

Abstract Background BNO 1016 is an ethanolic extract of a mixture of five herbs that has been sold in different formulations for decades in the European market and more recently, in the United States market as an over-the-counter treatment for rhinosinusitis. Previous studies indicated activation of chloride secretion and increase in ciliary beat frequency by BNO 1016 but the functional consequences on mucociliary transport velocity and airway surface liquid homeostasis are unknown. This study intends to examine the effects of BNO 1016 on these properties in vitro. Results Human sinonasal epithelial cells were grown at an air-liquid interface, with addition of BNO 1016 basolaterally in each experiment. Polystyrene fluorescent microspheres were added to the apical surface of the culture, and distance traveled across the surface of the culture over a fixed time period was measured using live imaging. BNO 1016 concentrations of 50 μg/ml and 500 μg/ml were tested. Basolateral application of compound resulted in a non-dose-dependent increase in culture surface liquid height compared to controls at 30 min, and this effect persisted through the one-hour duration of the experiment (p

Abstract Background Epithelial solitary chemosensory cell (tuft cell) bitter taste signal transduction occurs through G protein coupled receptors and calcium-dependent signaling pathways. Type II taste cells, which utilize the same bitter taste signal transduction pathways, may also utilize cyclic adenosine monophosphate (cAMP) as an independent signaling messenger in addition to calcium. Methods In this work we utilized specific pharmacologic inhibitors to interrogate the short circuit current (Isc) of polarized nasal epithelial cells mounted in Ussing chambers to assess the electrophysiologic changes associated with bitter agonist (denatonium) treatment. We also assessed release of human β-defensin-2 from polarized nasal epithelial cultures following treatment with denatonium benzoate and/or potassium channel inhibitors. Results We demonstrate that the bitter taste receptor agonist, denatonium, decreases human respiratory epithelial two-pore potassium (K2P) current in polarized nasal epithelial cells mounted in Ussing chambers. Our data further suggest that this occurs via a cAMP-dependent signaling pathway. We also demonstrate that this decrease in potassium current lowers the threshold for denatonium to stimulate human β-defensin-2 release. Conclusions These data thus demonstrate that, in addition to taste transducing calcium-dependent signaling, bitter taste receptor agonists can also activate cAMP-dependent respiratory epithelial signaling pathways to modulate K2P currents. Bitter-agonist regulation of potassium currents may therefore serve as a means of rapid regional epithelial signaling, and further study of these pathways may provide new insights into regulation of mucosal ionic composition and innate mechanisms of epithelial defense.

Introduction: To describe a case of an isolated clival mucocele presenting asymptomatically after previous endoscopic sinus surgery and review the existing literature on the clinical characteristics associated with these lesions. Methods: Case report and literature review. Results: We present a case of a clival mucocele that was found incidentally in a 66-year-old female undergoing hearing loss evaluation and had previously undergone endoscopic sphenoidotomy 17 years prior. The lesion was drained via an expanded endonasal endoscopic approach without complication and pathology confirmed the diagnosis of mucocele. Conclusion: This case demonstrates the efficacy of a surgical approach to cystic lesions of the clivus and highlights the importance of regular follow-up after endoscopic sinus surgery to detect these potentially subtle lesions and prevent their symptomatic progression.

T1Rs are expressed in solitary chemosensory cells of the upper airway where they detect apical glucose levels and repress bitter taste receptor Ca2+ signaling pathways. Microbial growth leads to a decrease in apical glucose levels. T1Rs detect this change and liberate bitter taste receptor signaling, initiating an innate immune response to both kill and expel pathogens through releasing antimicrobial peptides and increasing nitric oxide production and ciliary beat frequency. However, chronic inflammation due to disease, smoking, or viral infections causes a remodeling of the epithelial airway. The resulting squamous metaplasia causes a loss of multi-ciliated cells and solitary chemosensory cells, replaced by basal epithelial cells. To understand how T1R function is altered during disease, we used basal epithelial cells as a model to study the function of T1R3 on Ca2+ signaling dynamics. We found that both T1R1 and T1R3 detect amino acids and signal via cAMP, increasing the responsiveness of the cells to Ca2+ signaling stimuli. Either knocking down T1R1/3 or treating wild-type cells with MEM amino acids caused a reduction in ER Ca2+ content through a non-cAMP signaled pathway. Treatment with amino acids led to a reduction in downstream denatonium-induced Ca2+-signaled caspase activity. Thus, amino acids may be used to reduce unwanted apoptosis signaling in treatments containing bitter compounds.

Human airway sweet (T1R2 + T1R3), umami (T1R1 + T1R3), and bitter taste receptors (T2Rs) are critical components of the innate immune system, acting as sensors to monitor pathogenic growth. T2Rs detect bacterial products or bitter compounds to drive nitric oxide (NO) production in both healthy and diseased epithelial cell models. The NO enhances ciliary beating and also directly kills pathogens. Both sweet and umami receptors have been characterized to repress bitter taste receptor signaling in healthy and disease models. We hypothesized that the sweet/umami T1R3 antagonist lactisole may be used to alleviate bitter taste receptor repression in airway basal epithelial cells and enhance NO production. Here, we show that lactisole activates cAMP generation, though this occurs through a pathway independent of T1R3. This cAMP most likely signals through EPAC to increase ER Ca2+ efflux. Stimulation with denatonium benzoate, a bitter taste receptor agonist which activates largely nuclear and mitochondrial Ca2+ responses, resulted in a dramatically increased cytosolic Ca2+ response in cells treated with lactisole. This cytosolic Ca2+ signaling activated NO production in the presence of lactisole. Thus, lactisole may be useful coupled with bitter compounds as a therapeutic nasal rinse or spray to enhance beneficial antibacterial NO production in patients suffering from chronic inflammatory diseases such as chronic rhinosinusitis.

T2R bitter taste receptors in airway motile cilia increase ciliary beat frequency (CBF) and nitric oxide (NO) production. Polymorphisms in some T2Rs are linked to disease outcomes in chronic rhinosinusitis (CRS) and cystic fibrosis (CF). We examined the expression of cilia T2Rs during the differentiation of human nasal epithelial cells grown at air–liquid interface (ALI). The T2R expression increased with differentiation but did not vary between CF and non-CF cultures. Treatment with Pseudomonas aeruginosa flagellin decreased the expression of diphenhydramine-responsive T2R14 and 40, among others. Diphenhydramine increased both NO production, measured by fluorescent dye DAF-FM, and CBF, measured via high-speed imaging. Increases in CBF were disrupted after flagellin treatment. Diphenhydramine impaired the growth of lab and clinical strains of P. aeruginosa, a major pathogen in CF and CF-related CRS. Diphenhydramine impaired biofilm formation of P. aeruginosa, measured via crystal violet staining, as well as the surface attachment of P. aeruginosa to CF airway epithelial cells, measured using colony-forming unit counting. Because the T2R agonist diphenhydramine increases NO production and CBF while also decreasing bacterial growth and biofilm production, diphenhydramine-derived compounds may have potential clinical usefulness in CF-related CRS as a topical therapy. However, utilizing T2R agonists as therapeutics within the context of P. aeruginosa infection may require co-treatment with anti-inflammatories to enhance T2R expression.

Bitter taste receptors (T2Rs) are G protein-coupled receptors (GPCRs) expressed in various cell types including ciliated airway epithelial cells and macrophages. T2Rs in these two innate immune cell types are activated by bitter products, including those secreted by Pseudomonas aeruginosa, leading to Ca2+-dependent activation of endothelial nitric oxide (NO) synthase (eNOS). NO enhances mucociliary clearance and has direct antibacterial effects in ciliated epithelial cells. NO also increases phagocytosis by macrophages. Using biochemistry and live-cell imaging, we explored the role of heat shock protein 90 (HSP90) in regulating T2R-dependent NO pathways in primary sinonasal epithelial cells, primary monocyte-derived macrophages, and a human bronchiolar cell line (H441). Immunofluorescence showed that H441 cells express eNOS and T2Rs and that the bitter agonist denatonium benzoate activates NO production in a Ca2+- and HSP90-dependent manner in cells grown either as submerged cultures or at the air–liquid interface. In primary sinonasal epithelial cells, we determined that HSP90 inhibition reduces T2R-stimulated NO production and ciliary beating, which likely limits pathogen clearance. In primary monocyte-derived macrophages, we found that HSP-90 is integral to T2R-stimulated NO production and phagocytosis of FITC-labeled Escherichia coli and pHrodo-Staphylococcus aureus. Our study demonstrates that HSP90 serves as an innate immune modulator by regulating NO production downstream of T2R signaling by augmenting eNOS activation without impairing upstream Ca2+ signaling. These findings suggest that HSP90 plays an important role in airway antibacterial innate immunity and may be an important target in airway diseases such as chronic rhinosinusitis, asthma, or cystic fibrosis.

Abstract Background Pan-bacterial 16S rRNA microbiome surveys performed with massively parallel DNA sequencing technologies have transformed community microbiological studies. Current 16S profiling methods, however, fail to provide sufficient taxonomic resolution and accuracy to adequately perform species-level associative studies for specific conditions. This is due to the amplification and sequencing of only short 16S rRNA gene regions, typically providing for only family- or genus-level taxonomy. Moreover, sequencing errors often inflate the number of taxa present. Pacific Biosciences’ (PacBio’s) long-read technology in particular suffers from high error rates per base. Herein, we present a microbiome analysis pipeline that takes advantage of PacBio circular consensus sequencing (CCS) technology to sequence and error correct full-length bacterial 16S rRNA genes, which provides high-fidelity species-level microbiome data. Results Analysis of a mock community with 20 bacterial species demonstrated 100% specificity and sensitivity with regard to taxonomic classification. Examination of a 250-plus species mock community demonstrated correct species-level classification of > 90% of taxa, and relative abundances were accurately captured. The majority of the remaining taxa were demonstrated to be multiply, incorrectly, or incompletely classified. Using this methodology, we examined the microgeographic variation present among the microbiomes of six sinonasal sites, by both swab and biopsy, from the anterior nasal cavity to the sphenoid sinus from 12 subjects undergoing trans-sphenoidal hypophysectomy. We found greater variation among subjects than among sites within a subject, although significant within-individual differences were also observed. Propiniobacterium acnes (recently renamed Cutibacterium acnes) was the predominant species throughout, but was found at distinct relative abundances by site. Conclusions Our microbial composition analysis pipeline for single-molecule real-time 16S rRNA gene sequencing (MCSMRT, https://github.com/jpearl01/mcsmrt) overcomes deficits of standard marker gene-based microbiome analyses by using CCS of entire 16S rRNA genes to provide increased taxonomic and phylogenetic resolution. Extensions of this approach to other marker genes could help refine taxonomic assignments of microbial species and improve reference databases, as well as strengthen the specificity of associations between microbial communities and dysbiotic states.

Bitter taste receptors (T2Rs) are G-protein-coupled receptors (GPCRs) expressed on the tongue but also in various locations throughout the body, including on motile cilia within the upper and lower airways. Within the nasal airway, T2Rs detect secreted bacterial ligands and initiate bactericidal nitric oxide (NO) responses, which also increase ciliary beat frequency (CBF) and mucociliary clearance of pathogens. Various neuropeptides, including neuropeptide tyrosine (neuropeptide Y or NPY), control physiological processes in the airway including cytokine release, fluid secretion, and ciliary beating. NPY levels and/or density of NPYergic neurons may be increased in some sinonasal diseases. We hypothesized that NPY modulates cilia-localized T2R responses in nasal epithelia. Using primary sinonasal epithelial cells cultured at air–liquid interface (ALI), we demonstrate that NPY reduces CBF through NPY2R activation of protein kinase C (PKC) and attenuates responses to T2R14 agonist apigenin. We find that NPY does not alter T2R-induced calcium elevation but does reduce T2R-stimulated NO production via a PKC-dependent process. This study extends our understanding of how T2R responses are modulated within the inflammatory environment of sinonasal diseases, which may improve our ability to effectively treat these disorders.

BackgroundBitter (T2R) and sweet (T1R) taste receptors in the airway are important in innate immune defense, and variations in taste receptor functionality in one T2R (T2R38) correlate with disease status and disease severity in chronic rhinosinusitis (CRS). Quinine is a bitter compound that is an agonist for several T2Rs also expressed on sinonasal cells, but not for T2R38. Because of this property, quinine may stimulate innate immune defense mechanisms in the airway, and functional differences in quinine perception may be reflective of disease status in CRS.MethodsDemographic and taste intensity data were collected prospectively from CRS patients and non-CRS control subjects. Sinonasal tissue from patients undergoing rhinologic surgery was also collected and grown at an air–liquid interface (ALI). Nitric oxide (NO) production and dynamic regulation of ciliary beat frequency in response to quinine stimulation were assessed in vitro.ResultsQuinine reliably increased ciliary beat frequency and NO production in ALI cultures in a manner consistent with T2R activation (p

Background Malar augmentation is a common cosmetic procedure utilizing silastic materials. We describe an uncommon complication of a silastic implant eroding into the anterior maxillary sinus wall resulting in chronic rhinosinusitis (CRS). Methods A literature review is presented describing the presentation, surgical management and outcome of this uncommon adverse event. Results An 80 year old female with a history of bilateral cosmetic malar implants placed approximately 25 years ago presented to our office with a 4–5 month history of left-sided symptoms consistent with chronic sinusitis, and was found to have intrasinus penetration of her left malar implant. Only one other case series of 5 cases in 4 patients is reported in the literature. Conclusions Intrasinus malar implant migration is a rare complication of malar augmentation. The present experience suggests that removal of the offending foreign body often results in successful symptom resolution.

Background There is preliminary evidence that patients with chronic rhinosinusitis (CRS) and comorbid obstructive sleep apnea (OSA) have reduced quality-of-life (QOL) improvements after functional endoscopic sinus surgery (FESS) compared with patients without OSA. The effect of OSA severity on QOL improvement after FESS is unknown. Objectives To better characterize the QOL improvement after FESS for patients with comorbid OSA and to assess whether QOL improvement is dependent on OSA severity. Methods This multi-institution, retrospective cohort study evaluated adult patients with CRS who underwent FESS between 2007 and 2015. Preoperative, 1-month, 3-month, 6-month, and 1-year postoperative 22-Item Sino-Nasal Outcome Test scores were used to evaluate QOL. We compared patients without OSA with patients with stratified OSA based on the preoperative apnea-hypopnea index. A multilevel, mixed-effects linear regression model was used for the analysis. Results Of 480 participants, 83 (17%) had OSA, and 47 of these patients had polysomnography results available for review. Both patients with OSA and patients without OSA reported significant QOL improvement after surgery (p < 0.0001) relative to baseline. In the unadjusted model, the subjects with OSA demonstrated a statistically worse outcome in 22-Item Sino-Nasal Outcome Test scores at each time point (2.4 points higher per time point, p = 0.006). When controlling for covariates, the adjusted model showed no difference in QOL outcome based on OSA status (p = 0.114). When stratified by OSA disease severity, the adjusted model showed no difference in the QOL outcome. Conclusions Patients with CRS and comorbid OSA had worse QOL outcomes after FESS; however, when controlling for patient factors, there was no difference in QOL outcome. OSA disease severity did not seem to predict QOL improvement after FESS.

Objectives Odontogenic chronic rhinosinusitis (CRS) is an epidemiologically important disease process due, in part, to the increasingly commonplace use of dental restorative procedures such as zygomatic implantation. Traditional management of this clinical entity typically entails extraction of the infected hardware via an open or endoscopic approach. We describe a novel management strategy of odontogenic CRS following bilateral zygomatic implantation for oral rehabilitation that we surgically salvaged via a modified endoscopic medial maxillectomy. Methods We describe the presentation and management of a case of metachronous development of bilateral CRS subsequent to zygomatic implantation. Results The patient's postoperative course was characterized by marked endoscopic, radiologic, and symptomatic improvement as measured by the 22-item Sino-Nasal Outcome Test. Conclusion We describe a novel treatment strategy for the management of odontogenic sinusitis resulting from erroneous zygomatic implant placement. Modified endoscopic medial maxillectomy in this clinical context facilitates mucosal normalization of the affected sinus, while permitting preservation of oral function through salvage of the displaced implant.