Question: You are an expert researcher providing comprehensive, well-cited information.

Provide detailed information focusing on: 1. Key concepts and definitions with current understanding 2. Recent developments and latest research (prioritize 2023-2024 sources) 3. Current applications and real-world implementations 4. Expert opinions and analysis from authoritative sources 5. Relevant statistics and data from recent studies

Format as a comprehensive research report with proper citations. Include URLs and publication dates where available. Always prioritize recent, authoritative sources and provide specific citations for all major claims.

Disease Characteristics Research Template

Target Disease

• Disease Name: Silent Sinus Syndrome
• MONDO ID: MONDO:0019108 (if available)
• Category: Complex

Research Objectives

Please provide a comprehensive research report on Silent Sinus Syndrome covering all of the disease characteristics listed below. This report will be used to populate a disease knowledge base entry. Be thorough and cite primary literature (PMID preferred) for all claims.

For each section, suggested databases/resources are listed. These are the first places you should search for information on each topic.

1. Disease Information

Search first: OMIM, Orphanet, ICD-10/ICD-11, MeSH, PubMed

• What is the disease? Provide a concise overview.
• What are the key identifiers? (OMIM, Orphanet, ICD-10/ICD-11, MeSH, Mondo)
• What are the common synonyms and alternative names?
• Is the information derived from individual patients (e.g., EHR) or aggregated disease-level resources?

2. Etiology

• Disease Causal Factors: What are the primary causes? (genetic, environmental, infectious, mechanistic)
• Risk Factors:

  Search first: PubMed, Cochrane Library, UpToDate, clinical guidelines, ClinVar, ClinGen, GWAS Catalog, PheGenI, CTD, CDC, WHO, epidemiological databases

• Genetic risk factors (causal variants, susceptibility loci, modifier genes)
• Environmental risk factors (toxins, lifestyle, occupational exposures, age, sex, family history)
• Protective Factors:

  Search first: PubMed, Cochrane Library, clinical trial databases, GWAS Catalog, gnomAD, WHO, CDC, nutrition databases

• Genetic protective factors (protective variants, modifier alleles)
• Environmental protective factors (diet, lifestyle, exposures that reduce risk)
• Gene-Environment Interactions: How do genetic and environmental factors interact to influence disease?

  Search first: CTD, PubMed, PheGenI, GxE databases

3. Phenotypes

Search first: HPO (Human Phenotype Ontology), OMIM, Orphanet, PubMed, clinicaltrials.gov, MedDRA, SNOMED CT, DECIPHER, LOINC

For each phenotype, provide: - Phenotype type: symptoms, clinical signs, physical manifestations, behavioral changes, or laboratory abnormalities

For symptoms/signs: HPO, OMIM, Orphanet, PubMed For behavioral changes: HPO, DSM, RDoC (Research Domain Criteria), PubMed For laboratory abnormalities: LOINC, SNOMED CT, LabTests Online, PubMed - Phenotype characteristics: Search first: OMIM, Orphanet, HPO, PubMed - Age of symptom onset (neonatal, childhood, adult-onset, late-onset) - Symptom severity (mild, moderate, severe, variable) - Symptom progression (stable, progressive, episodic, fluctuating) - Frequency among affected individuals (percentage or qualitative) - Quality of life impact: Effects on daily functioning and well-being (per-phenotype when possible) Search first: EQ-5D database, SF-36, WHO QOL databases, PubMed - Suggest HPO (Human Phenotype Ontology) terms for each phenotype

4. Genetic/Molecular Information

• Causal Genes: Gene mutations or chromosomal abnormalities responsible for disease (gene symbols, OMIM IDs)

  Search first: OMIM, ClinVar, HGMD, Ensembl, NCBI Gene

• Pathogenic Variants:
• Affected genes (gene symbols, HGNC IDs) > Search first: OMIM, NCBI Gene, Ensembl, HGNC, UniProt, GeneCards
• Variant classification (pathogenic, likely pathogenic, VUS per ACMG/AMP guidelines) > Search first: ClinVar, ClinGen, ACMG/AMP guidelines, VarSome
• Variant type/class (missense, frameshift, nonsense, splice-site, structural)
• Allele frequency in population databases > Search first: gnomAD, 1000 Genomes, ExAC, TOPMed, dbSNP
• Somatic vs germline origin > Search first: COSMIC (somatic), ClinVar, ICGC, TCGA
• Functional consequences (loss of function, gain of function, dominant negative)
• Modifier Genes: Genes that modify disease severity or expression
• Epigenetic Information: DNA methylation, histone modifications, chromatin changes affecting disease

  Search first: ENCODE, Roadmap Epigenomics, MethBase, DiseaseMeth

• Chromosomal Abnormalities: Large-scale genetic changes (aneuploidy, translocations, inversions)

  Search first: DECIPHER, ClinVar, ECARUCA, UCSC Genome Browser

5. Environmental Information

• Environmental Factors: Non-genetic contributing factors (toxins, radiation, pollution, occupational exposure)

  Search first: CTD (Comparative Toxicogenomics Database), TOXNET, PubMed, EPA databases

• Lifestyle Factors: Behavioral factors (smoking, diet, exercise, alcohol consumption)

  Search first: CDC databases, WHO, PubMed, NHANES

• Infectious Agents: If applicable, pathogens causing or triggering disease (bacteria, viruses, fungi, parasites)

  Search first: NCBI Taxonomy, ViPR, BV-BRC, MicrobeDB, GIDEON

6. Mechanism / Pathophysiology

• Molecular Pathways: Specific signaling cascades or biochemical pathways involved (Wnt, MAPK, mTOR, PI3K-AKT, etc.)

  Search first: KEGG, Reactome, WikiPathways, PathBank, BioCyc

• Cellular Processes: Cell-level mechanisms (apoptosis, autophagy, cell cycle dysregulation, inflammation, etc.)

  Search first: Gene Ontology (GO), Reactome, KEGG, PubMed

• Protein Dysfunction: How protein structure or function is altered (misfolding, aggregation, loss of function, gain of function)

  Search first: UniProt, PDB (Protein Data Bank), InterPro, Pfam, AlphaFold

• Metabolic Changes: Alterations in metabolic processes (energy metabolism, lipid metabolism, amino acid metabolism)

  Search first: KEGG, BioCyc, HMDB (Human Metabolome Database), BRENDA

• Immune System Involvement: Role of immune response (autoimmunity, immunodeficiency, chronic inflammation)

  Search first: ImmPort, Immunome Database, IEDB, Gene Ontology

• Tissue Damage Mechanisms: How tissues/ are injured (oxidative stress, ischemia, fibrosis, necrosis)

  Search first: PubMed, Gene Ontology, Reactome

• Biochemical Abnormalities: Specific molecular defects (enzyme deficiencies, receptor dysfunction, ion channel defects)

  Search first: BRENDA, UniProt, KEGG, OMIM, PubMed

• Epigenetic Changes: DNA methylation, histone modifications affecting gene expression in disease

  Search first: ENCODE, Roadmap Epigenomics, MethBase, DiseaseMeth

• Molecular Profiling (if available):
• Transcriptomics/gene expression changes > Search first: GEO (Gene Expression Omnibus), ArrayExpress, GTEx, Human Cell Atlas, SRA
• Proteomics findings > Search first: PRIDE, ProteomeXchange, Human Protein Atlas, STRING, BioGRID
• Metabolomics signatures > Search first: MetaboLights, Metabolomics Workbench, HMDB, METLIN
• Lipidomics alterations > Search first: LIPID MAPS, SwissLipids, LipidHome, Metabolomics Workbench
• Genomic structural features > Search first: UCSC Genome Browser, Ensembl, NCBI, dbVar, DGV
• Advanced Technologies (if applicable):
• Single-cell analysis findings (cell-type specific mechanisms, cellular heterogeneity) > Search first: Human Cell Atlas, Single Cell Portal, GEO, CELLxGENE
• Spatial transcriptomics findings > Search first: GEO, Spatial Research, Vizgen, 10x Genomics data
• Multi-omics integration results > Search first: TCGA, ICGC, cBioPortal, LinkedOmics, PubMed
• Functional genomics screens (CRISPR, RNAi) > Search first: DepMap, GenomeRNAi, PubMed, BioGRID ORCS

For each mechanism, describe: - The causal chain from initial trigger to clinical manifestation - Which mechanisms are upstream vs downstream - What cell types and biological processes are involved - Suggest GO terms for biological processes and CL terms for cell types

7. Anatomical Structures Affected

• Organ Level:
• Primary organs directly affected
• Secondary organ involvement (complications, secondary effects)
• Body systems involved (cardiovascular, nervous, digestive, respiratory, endocrine, etc.)

  Search first: Uberon, FMA (Foundational Model of Anatomy), OMIM, HPO, ICD-11, MeSH, SNOMED CT

• Tissue and Cell Level:
• Specific tissue types affected (epithelial, connective, muscle, nervous)
• Specific cell populations targeted (with Cell Ontology terms)

  Search first: Uberon, Human Protein Atlas, Cell Ontology, Human Cell Atlas, CellMarker, PanglaoDB

• Subcellular Level:
• Cellular compartments involved (mitochondria, nucleus, ER, lysosomes) (with GO Cellular Component terms)

  Search first: Gene Ontology (Cellular Component), UniProt, Human Protein Atlas

• Localization:
• Specific anatomical sites (with UBERON terms) > Search first: FMA, Uberon, NeuroNames (for brain), SNOMED CT
• Lateralization (unilateral, bilateral, asymmetric) > Search first: HPO, clinical literature, imaging databases

8. Temporal Development

• Onset:
• Typical age of onset (congenital, pediatric, adult, geriatric)
• Onset pattern (acute, subacute, chronic, insidious)

  Search first: OMIM, Orphanet, HPO, PubMed

• Progression:
• Disease stages (early, intermediate, advanced, end-stage) > Search first: Cancer Staging Manual (AJCC), WHO classifications, PubMed
• Progression rate (rapid, slow, variable)
• Disease course pattern (episodic, relapsing-remitting, progressive, stable)
• Disease duration (self-limited, chronic lifelong)

  Search first: Disease registries, longitudinal cohort databases, natural history studies, PubMed, Orphanet, OMIM

• Patterns:
• Remission patterns (spontaneous, treatment-induced) > Search first: Clinical trial databases, disease registries, PubMed
• Critical periods (time windows of vulnerability or opportunity for intervention) > Search first: PubMed, developmental biology databases, clinical guidelines

9. Inheritance and Population

• Epidemiology:
• Prevalence (cases per 100,000 at given time)
• Incidence (new cases per 100,000 per year)

  Search first: Orphanet, CDC, WHO, GBD (Global Burden of Disease), national registries, SEER, disease registries

• For Genetic Etiology:
• Inheritance pattern (AD, AR, X-linked, mitochondrial, multifactorial, polygenic) > Search first: OMIM, Orphanet, ClinVar, GTR (Genetic Testing Registry)
• Penetrance (complete, incomplete, age-dependent) > Search first: ClinVar, OMIM, PubMed, ClinGen
• Expressivity (variable, consistent) > Search first: OMIM, ClinVar, PubMed
• Genetic anticipation (increasing severity in successive generations) > Search first: OMIM, PubMed (especially for repeat expansion disorders)
• Germline mosaicism > Search first: ClinVar, OMIM, genetic counseling literature, PubMed
• Founder effects (population-specific mutations) > Search first: gnomAD, population genetics databases, PubMed
• Consanguinity role > Search first: OMIM, population studies, genetic counseling resources
• Carrier frequency > Search first: gnomAD, carrier screening databases, GeneReviews, GTR
• Population Demographics:
• Affected populations (ethnic or demographic groups with higher prevalence) > Search first: gnomAD, 1000 Genomes, PAGE Study, PubMed, population registries
• Geographic distribution (endemic areas, regional variation) > Search first: WHO, CDC, GBD, Orphanet, geographic epidemiology databases
• Geographic distribution of specific variants
• Sex ratio (male:female) > Search first: Disease registries, OMIM, PubMed, epidemiological databases
• Age distribution of affected individuals > Search first: CDC, disease registries, SEER, Orphanet

10. Diagnostics

• Clinical Tests:
• Laboratory tests (blood, urine, tissue chemistry, specific enzyme assays) > Search first: LOINC, LabTests Online, PubMed
• Biomarkers (proteins, metabolites, genetic markers, circulating biomarkers) > Search first: FDA Biomarker List, BEST (Biomarkers, EndpointS, and other Tools), PubMed
• Imaging studies (X-ray, CT, MRI, PET, ultrasound) > Search first: RadLex, DICOM, Radiopaedia, imaging databases
• Functional tests (pulmonary function, cardiac stress tests) > Search first: LOINC, clinical guidelines, PubMed
• Electrophysiology (EEG, EMG, ECG, nerve conduction studies) > Search first: LOINC, clinical neurophysiology databases, PubMed
• Biopsy findings (histopathology, immunohistochemistry) > Search first: SNOMED CT, College of American Pathologists resources, PubMed
• Pathology findings (microscopic examination) > Search first: SNOMED CT, Digital Pathology databases, PubMed
• Genetic Testing:

  Search first: GTR (Genetic Testing Registry), GeneReviews, ClinGen

• Overview of recommended genetic testing approach
• Whole genome sequencing (WGS) utility > Search first: GTR, ClinVar, GEL (Genomics England), gnomAD
• Whole exome sequencing (WES) utility > Search first: GTR, ClinVar, OMIM, GeneMatcher
• Gene panels (which panels, which genes) > Search first: GTR, ClinVar, laboratory-specific databases
• Single gene testing > Search first: GTR, ClinVar, OMIM, GeneReviews
• Chromosomal microarray (CMA) > Search first: DECIPHER, ClinVar, dbVar, ECARUCA
• Karyotyping > Search first: Chromosome Abnormality Database, ClinVar, cytogenetics resources
• FISH > Search first: ClinVar, cytogenetics databases, PubMed
• Mitochondrial DNA testing > Search first: MITOMAP, MSeqDR, ClinVar, GTR
• Repeat expansion testing > Search first: GTR, ClinVar, repeat expansion databases, PubMed
• Omics-Based Diagnostics (if applicable):
• RNA sequencing / transcriptomics > Search first: GEO, ArrayExpress, GTEx, RNA-seq databases
• Proteomics > Search first: PRIDE, ProteomeXchange, FDA Biomarker database
• Metabolomics > Search first: MetaboLights, Metabolomics Workbench, HMDB
• Epigenomics > Search first: GEO, ENCODE, Roadmap Epigenomics, MethBase
• Liquid biopsy > Search first: COSMIC, ClinVar, liquid biopsy databases, PubMed
• Clinical Criteria:
• Standardized diagnostic criteria (DSM, ICD, society guidelines) > Search first: DSM-5, ICD-11, clinical society guidelines, UpToDate
• Differential diagnosis (other conditions to rule out, with distinguishing features) > Search first: DynaMed, UpToDate, clinical decision support systems
• Screening:
• Screening methods for asymptomatic individuals (newborn screening, carrier screening, cascade screening) > Search first: ACMG recommendations, CDC newborn screening, GTR

11. Outcome/Prognosis

• Survival and Mortality:
• Survival rate (5-year, 10-year, overall) > Search first: SEER, cancer registries, disease-specific registries, PubMed
• Life expectancy (with and without treatment if applicable) > Search first: Orphanet, disease registries, actuarial databases, PubMed
• Mortality rate > Search first: CDC, WHO, GBD, national mortality databases
• Disease-specific mortality (deaths directly attributable to disease) > Search first: Disease registries, CDC Wonder, GBD, PubMed
• Morbidity and Function:
• Morbidity (disease-related disability and health impacts) > Search first: GBD, WHO, disability databases, PubMed
• Disability outcomes (long-term functional impairments) > Search first: ICF (International Classification of Functioning), disability registries
• Quality of life measures (EQ-5D, SF-36, PROMIS, disease-specific tools) > Search first: EQ-5D database, SF-36, PROMIS, PubMed
• Disease Course:
• Complications (secondary problems: infections, organ failure, etc.) > Search first: ICD codes, disease registries, clinical databases, PubMed
• Recovery potential (likelihood and extent of recovery, with vs without treatment) > Search first: Natural history studies, rehabilitation databases, PubMed
• Prediction:
• Prognostic factors (age, disease severity, biomarkers, treatment response) > Search first: Prognostic models databases, clinical calculators, PubMed
• Prognostic biomarkers (molecular markers predicting disease course) > Search first: FDA Biomarker database, PubMed, cancer prognostic databases

12. Treatment

• Pharmacotherapy:
• Pharmacological treatments (drug names, drug classes, mechanisms of action) > Search first: DrugBank, RxNorm, ATC classification, DailyMed, FDA databases
• Pharmacogenomics (how genetic variants affect drug metabolism, efficacy, toxicity) > Search first: PharmGKB, CPIC (Clinical Pharmacogenetics), FDA Table of PGx Biomarkers
• Advanced Therapeutics:
• Gene therapy (viral vectors, CRISPR, gene replacement, gene editing) > Search first: ClinicalTrials.gov, FDA gene therapy database, ASGCT resources
• Cell therapy (stem cell transplant, CAR-T, cellular therapeutics) > Search first: ClinicalTrials.gov, FDA cell therapy database, FACT standards
• RNA-based therapies (ASOs, siRNA, mRNA therapies) > Search first: ClinicalTrials.gov, FDA approvals, PubMed
• Targeted therapies (treatments directed at specific molecular targets) > Search first: My Cancer Genome, OncoKB, ClinicalTrials.gov, FDA approvals
• Immunotherapies (checkpoint inhibitors, monoclonal antibodies) > Search first: Cancer Immunotherapy Database, FDA approvals, ClinicalTrials.gov
• Surgical and Interventional:
• Surgical interventions (types of surgery, timing, outcomes) > Search first: CPT codes, surgical registries, clinical guidelines, PubMed
• Supportive and Rehabilitative:
• Supportive care (symptom management, pain control, nutrition) > Search first: Clinical guidelines, Cochrane Library, PubMed
• Rehabilitation (physical therapy, occupational therapy, speech therapy) > Search first: Rehabilitation medicine databases, clinical guidelines, PubMed
• Experimental:
• Experimental treatments in clinical trials (with NCT identifiers if available) > Search first: ClinicalTrials.gov, EU Clinical Trials Register, WHO ICTRP
• Treatment Outcomes:
• Treatment response rates > Search first: Clinical trial databases, FDA reviews, systematic reviews, PubMed
• Side effects and adverse events > Search first: FDA Adverse Event Reporting System (FAERS), MedWatch, PubMed
• Treatment Strategy:
• Treatment algorithms (clinical pathways, decision trees) > Search first: Clinical practice guidelines, NCCN Guidelines, UpToDate
• Combination therapies > Search first: ClinicalTrials.gov, treatment guidelines, PubMed
• Personalized medicine approaches (genotype-guided treatment) > Search first: My Cancer Genome, CIViC, PharmGKB, precision medicine databases

For each treatment, suggest MAXO (Medical Action Ontology) terms where applicable.

13. Prevention

• Prevention Levels:
• Primary prevention (preventing disease occurrence: vaccination, risk factor modification) > Search first: CDC, WHO, USPSTF recommendations, Cochrane Library
• Secondary prevention (early detection and treatment: screening programs, early intervention) > Search first: USPSTF, CDC screening guidelines, WHO
• Tertiary prevention (preventing complications in those with disease) > Search first: Clinical guidelines, disease management protocols, PubMed
• Immunization: Vaccine strategies (if applicable)

  Search first: CDC vaccine schedules, WHO immunization, FDA vaccine database

• Screening and Early Detection:
• Screening programs (population-based: newborn screening, cancer screening) > Search first: CDC screening programs, USPSTF, cancer screening databases
• Genetic screening (carrier screening, preimplantation genetic diagnosis, prenatal testing) > Search first: ACMG recommendations, ACOG guidelines, GTR
• Risk stratification (identifying high-risk individuals for targeted prevention) > Search first: Risk prediction models, clinical calculators, PubMed
• Behavioral Interventions: Lifestyle modifications to reduce risk

  Search first: CDC, WHO, behavioral intervention databases, Cochrane Library

• Counseling: Genetic counseling (risk assessment, family planning guidance)

  Search first: NSGC resources, ACMG guidelines, GeneReviews

• Public Health:
• Public health interventions (sanitation, vector control, health education) > Search first: CDC, WHO, public health databases, PubMed
• Environmental interventions (reducing environmental risk factors) > Search first: EPA databases, WHO environmental health, PubMed
• Prophylaxis: Preventive medications or procedures

  Search first: Clinical guidelines, FDA approvals, PubMed

14. Other Species / Natural Disease

• Taxonomy: Species affected (with NCBI Taxon identifiers)

  Search first: NCBI Taxonomy

• Breed: Specific breeds affected (with VBO identifiers if applicable)

  Search first: VBO (Vertebrate Breed Ontology)

• Gene: Orthologous genes in other species (with NCBI Gene IDs)

  Search first: NCBI Gene

• Natural Disease:
• Naturally occurring disease in other species (companion animals, wildlife) > Search first: OMIA (Online Mendelian Inheritance in Animals), VetCompass, PubMed
• Veterinary relevance and importance in animal health > Search first: OMIA, veterinary databases, PubMed
• Comparative Biology:
• Comparative pathology (similarities and differences across species) > Search first: OMIA, comparative pathology databases, PubMed
• Evolutionary conservation of disease mechanisms > Search first: HomoloGene, OrthoMCL, Alliance of Genome Resources
• Transmission (if applicable):
• Zoonotic potential > Search first: CDC zoonotic diseases, WHO zoonoses, GIDEON
• Cross-species susceptibility > Search first: NCBI Taxonomy, veterinary databases, PubMed

15. Model Organisms

• Model Types:
• Model organism type (mammalian, invertebrate, cellular, in vitro) > Search first: Alliance of Genome Resources, model organism databases
• Specific model systems (mouse, rat, zebrafish, Drosophila, C. elegans, yeast, cell lines, organoids, iPSCs) > Search first: MGI, RGD, ZFIN, FlyBase, WormBase, SGD, ATCC, Cellosaurus
• Induced models (drug treatment, surgical intervention, environmental manipulation) > Search first: MGI, model organism databases, PubMed
• Genetic Models:
• Types available (knockout, knock-in, transgenic, conditional, humanized) > Search first: MGI, IMPC, KOMP, EuMMCR, IMSR
• Model Characteristics:
• Phenotype recapitulation (how well model reproduces human disease features) > Search first: Model organism databases, comparative studies, PubMed
• Model limitations (aspects of human disease not captured) > Search first: Model organism databases, PubMed, review articles
• Applications:
• Research applications (what aspects of disease can be studied) > Search first: Model organism databases, PubMed
• Resources:
• Model databases > Search first: MGI, RGD, ZFIN, FlyBase, WormBase, IMSR, EMMA, MMRRC

Citation Requirements

• Cite primary literature (PMID preferred) for all mechanistic and clinical claims
• Prioritize recent reviews and landmark papers
• Include direct quotes from abstracts where possible to support key statements
• Distinguish evidence source types: human clinical, model organism, in vitro, computational

Output Format

Structure your response as a comprehensive narrative organized by the sections above. For each section, provide: - Factual content with specific details (numbers, percentages, gene names, variant nomenclature) - Ontology term suggestions (HPO, GO, CL, UBERON, CHEBI, MAXO, MONDO) where applicable - Evidence citations with PMIDs - Direct quotes from abstracts to support key claims - Clear indication when information is not available or not applicable for this disease

This report will be used to populate a disease knowledge base entry with: - Pathophysiology descriptions with causal chains - Gene/protein annotations (HGNC, GO terms) - Phenotype associations (HP terms) with frequencies - Cell type involvement (CL terms) - Anatomical locations (UBERON terms) - Chemical entities (CHEBI terms) - Treatment annotations (MAXO terms) - Evidence items with PMIDs and exact abstract quotes - Epidemiology, prognosis, diagnostic, and prevention information - Animal model descriptions with phenotype recapitulation details

Silent Sinus Syndrome (SSS) — Comprehensive Disease Characteristics Report

Target disease

• Disease name: Silent sinus syndrome (SSS)
• MONDO ID: MONDO:0019108 (provided by user)
• Category: Complex (acquired/anatomic-mechanistic syndrome)

1. Disease information

1.1 Concise overview (current understanding)

Silent sinus syndrome (SSS) is a rare clinical-radiologic entity characterized by progressive collapse (atelectasis) of the maxillary sinus with associated inferior displacement (descent) of the orbital floor, producing painless, progressive ipsilateral enophthalmos and/or hypoglobus, often with minimal sinonasal symptoms. Representative definitions include: - “Spontaneous, painless enophthalmos, hypoglobus with orbital floor resorption and maxillary sinus collapse on the ipsilateral side.” (Clarós 2019; URL: https://doi.org/10.1080/00016489.2018.1542161) (claros2019silentsinussyndrome pages 1-3) - Diagnostic criteria summarized by de Dorlodot 2017 (attributed to Soparkar et al.) include “modification of facial appearance, enophthalmos and/or hypoglobus, a reduction of maxillary sinus volume on computed tomography (CT) scan, and the absence of sinonasal symptoms.” (de Dorlodot 2017; URL: https://doi.org/10.1007/s00405-017-4622-8) (dorlodot2017chronicmaxillaryatelectasis pages 1-2)

SSS is widely considered within the spectrum of chronic maxillary atelectasis (CMA), sometimes described as an advanced form (e.g., type 3 CMA in some classification systems). (claros2019silentsinussyndrome pages 1-3, dorlodot2017chronicmaxillaryatelectasis pages 1-2)

1.2 Key identifiers

• MONDO: MONDO:0019108 (user-provided)
• ICD-10 / ICD-11, MeSH, Orphanet, OMIM: Not retrievable using the provided toolchain in this run; therefore not reported here to avoid introducing uncited identifiers.

1.3 Common synonyms / alternative names

Evidence-supported synonyms and closely related terms: - Chronic maxillary atelectasis (CMA) (spectrum entity including SSS) (dorlodot2017chronicmaxillaryatelectasis pages 1-2) - Imploding antrum syndrome (used in some literature traditions; referenced indirectly via criteria attribution to Soparkar et al.) (dorlodot2017chronicmaxillaryatelectasis pages 1-2)

1.4 Evidence-source type

Most SSS knowledge is derived from aggregated clinical resources (case series, systematic reviews, narrative reviews) and individual case reports, supported by CT-based radiographic characterization. (tousidonis2024contemporarytreatmentof pages 7-8, dorlodot2017chronicmaxillaryatelectasis pages 1-2, sivasubramaniam2011silentsinussyndrome pages 1-2)

2. Etiology

2.1 Disease causal factors (mechanistic / anatomic)

Across recent reviews and classic series, the dominant etiologic model is functional obstruction of the maxillary sinus outflow pathway: - Tousidonis 2024 describes the favored model: “obstruction of the osteomeatal complex … causes hypoventilation … accumulation of secretions that creates a negative pressure that leads to atelectasis of the sinus with downward displacement of the orbital floor.” (Tousidonis 2024; published Apr 2024; URL: https://doi.org/10.7759/cureus.57577) (tousidonis2024contemporarytreatmentof pages 7-8) - Sivasubramaniam 2011 similarly describes osteomeatal occlusion → gas resorption → negative pressure → progressive maxillary atelectasis and orbital floor descent. (URL: https://doi.org/10.1017/S0022215111001952) (sivasubramaniam2011silentsinussyndrome pages 1-2)

2.2 Risk factors

Anatomic / local factors

• Ostiomeatal complex / infundibular obstruction (primary upstream factor). (tousidonis2024contemporarytreatmentof pages 7-8, lee2018silentsinussyndrome pages 1-4)

Trauma / iatrogenic (secondary SSS)

Strabbing 2025 explicitly defines secondary SSS as arising after trauma or surgery that disrupts mucociliary clearance, and reports a time-to-onset distribution: - In 9 secondary SSS patients, the interval from trauma/surgery to SSS onset ranged 1–36 months, with a median of 3 months in the post-traumatic group; 8/9 reported diplopia. (Strabbing 2025; URL: https://doi.org/10.1007/s10006-025-01391-x) (strabbing2025posttraumaticandiatrogenic pages 1-2)

Systemic inflammatory/autoimmune causes (rare)

• Kramer 2024 presents what it describes as the first reported instance of granulomatosis with polyangiitis (GPA) causing SSS via sinonasal destructive disease producing obstruction: “around 100 cases of SSS have been reported so far” and this case is “the first reported instance of GPA causing SSS.” (Kramer 2024; published May 2024; URL: https://doi.org/10.7759/cureus.61442) (kramer2024granulomatosiswithpolyangiitis pages 1-3)

2.3 Protective factors

No protective genetic or environmental factors were identified in the retrieved evidence.

2.4 Gene–environment interactions

No gene–environment interaction data were identified in the retrieved evidence.

3. Phenotypes

3.1 Core symptom/sign phenotype spectrum

Common clinical manifestations reported across series and reviews include: - Enophthalmos and hypoglobus (core defining signs) (claros2019silentsinussyndrome pages 1-3, dorlodot2017chronicmaxillaryatelectasis pages 1-2) - Orbital/facial asymmetry, superior sulcus deepening, diminished malar projection (lee2018silentsinussyndrome pages 1-4, tousidonis2024contemporarytreatmentof pages 1-4) - Diplopia (variable; common in some series) (strabbing2025posttraumaticandiatrogenic pages 1-2, sivasubramaniam2011silentsinussyndrome pages 1-2)

Recent review/case-based synthesis (Tousidonis 2024) adds less typical features that may appear: - “facial hypoesthesia,” eyelid “retraction, ptosis, absent fold,” and dry eye. (tousidonis2024contemporarytreatmentof pages 7-8)

Quantitative clinical displacement estimates from a classic series: - Sivasubramaniam 2011 cites ranges: hypoglobus 2–6 mm and enophthalmos 2–5 mm. (sivasubramaniam2011silentsinussyndrome pages 1-2)

3.2 Phenotype characteristics

• Age of onset: typically adult; often presenting in third to fifth decades in major series/reviews. (sivasubramaniam2011silentsinussyndrome pages 1-2, tousidonis2024contemporarytreatmentof pages 4-7, lee2018silentsinussyndrome pages 1-4)
• Progression: often described as slow/progressive, sometimes over years (Sivasubramaniam 2011; also reiterated in trial registry description). (sivasubramaniam2011silentsinussyndrome pages 1-2, NCT04388345 chunk 1)
• Frequency among affected individuals: high-quality population-level phenotype frequency data are not available in the retrieved evidence; in secondary SSS series, diplopia occurred in 8/9. (strabbing2025posttraumaticandiatrogenic pages 1-2)

3.3 Quality-of-life impact

The ClinicalTrials.gov registry case report notes that diagnostic delay “affected the patient lifestyle tremendously.” (NCT04388345 posted May 14, 2020; URL: https://clinicaltrials.gov/study/NCT04388345) (NCT04388345 chunk 1)

3.4 Suggested HPO terms (non-exhaustive)

(Provided as ontology suggestions; frequencies not established in retrieved sources.) - Enophthalmos — HP:0000654 - Hypoglobus — HP:0032007 - Diplopia — HP:0000651 - Facial asymmetry — HP:0000324 - Ptosis — HP:0000508 - Nasal obstruction (when present, especially in secondary or comorbid CRS) — HP:0001742

4. Genetic / molecular information

4.1 Causal genes

No validated causal genes for SSS were identified in the retrieved evidence. SSS is primarily characterized as an acquired/anatomic-mechanistic entity (ostiomeatal obstruction-driven). (tousidonis2024contemporarytreatmentof pages 7-8, dorlodot2017chronicmaxillaryatelectasis pages 1-2)

4.2 Pathogenic variants / modifier genes / epigenetics / chromosomal abnormalities

Not reported in retrieved evidence.

4.3 Notable related immunogenetic associations (not SSS-specific)

In the rare etiologic context of GPA presenting with SSS-like anatomy, Kramer 2024 notes GPA genetic associations, including “HLA-DPB1*0401 and HLA-DPB4,” but these are GPA associations rather than established SSS susceptibility loci. (kramer2024granulomatosiswithpolyangiitis pages 5-7)

5. Environmental information

5.1 Environmental/lifestyle contributors

No lifestyle/toxin/radiation/pollution associations were identified in the retrieved evidence.

5.2 Iatrogenic exposures (procedural)

Trauma and prior surgery can precipitate secondary SSS; thus, prior orbital or midface procedures constitute relevant iatrogenic “exposures.” (strabbing2025posttraumaticandiatrogenic pages 1-2)

5.3 Infectious agents

SSS itself is not presented as a primary infectious disease. Infectious colonization is discussed indirectly in GPA context (e.g., elevated S. aureus carriage in GPA patients), which may contribute to inflammation/obstruction in that systemic disease. (kramer2024granulomatosiswithpolyangiitis pages 5-7)

6. Mechanism / pathophysiology

6.1 Causal chain (upstream → downstream)

A consolidated, evidence-based mechanistic model: 1. Upstream trigger: obstruction/closure of the ostiomeatal complex / infundibulum (anatomic narrowing, inflammation, post-traumatic/iatrogenic changes). (tousidonis2024contemporarytreatmentof pages 7-8, lee2018silentsinussyndrome pages 1-4) 2. Sinus physiology change: hypoventilation with gas resorption produces subatmospheric (negative) pressure in the maxillary sinus. (tousidonis2024contemporarytreatmentof pages 7-8, sivasubramaniam2011silentsinussyndrome pages 1-2) 3. Tissue-level remodeling: inward retraction/bowing of maxillary sinus walls → maxillary atelectasis and reduced sinus volume; sinus may become opacified (secretions/transudate). (dorlodot2017chronicmaxillaryatelectasis pages 1-2, sivasubramaniam2011silentsinussyndrome pages 1-2) 4. Orbital consequences: inferior displacement/thinning/dehiscence of orbital floor → increased orbital volume → enophthalmos/hypoglobus and sometimes diplopia. (dorlodot2017chronicmaxillaryatelectasis pages 1-2, sivasubramaniam2011silentsinussyndrome pages 1-2)

6.2 Cellular and bone remodeling hypotheses

Sheptulin 2024 summarizes competing hypotheses (pressure-driven remodeling vs subclinical inflammation). It cites animal evidence that a pressure drop of ~2 mmHg could increase osteoclast activity, suggesting a potential pressure–bone remodeling link, while their sampled orbital-floor specimen showed no osteoclastic activity in that late-stage sample (implying remodeling may be earlier). (Sheptulin 2024; published Dec 2024; URL: https://doi.org/10.15275/rusomj.2024.0413) (sheptulin2024clinicalandmorphological pages 2-3, sheptulin2024clinicalandmorphological pages 3-3)

6.3 Suggested ontology mappings (mechanism)

GO biological process terms (suggestions)

• Negative regulation of ventilation / gas exchange in cavity (conceptual; no direct GO mapping in retrieved texts)
• Bone remodeling — GO:0046849
• Osteoclast differentiation — GO:0030316 (hypothesized involvement) (sheptulin2024clinicalandmorphological pages 2-3)
• Inflammatory response — GO:0006954 (subclinical inflammation hypothesis) (sheptulin2024clinicalandmorphological pages 2-3)

CL (cell types; suggestions)

• Osteoclast — CL:0000092 (hypothesized, stage-dependent) (sheptulin2024clinicalandmorphological pages 2-3)
• Osteoblast — CL:0000062 (implied by bone remodeling context)
• Respiratory epithelial cell — CL:0002633 (sinus mucosa)

7. Anatomical structures affected

7.1 Organ/tissue level

Primary anatomical sites: - Maxillary sinus (collapse/atelectasis; opacification; reduced volume) (dorlodot2017chronicmaxillaryatelectasis pages 1-2, tousidonis2024contemporarytreatmentof pages 1-4) - Orbit, especially orbital floor (inferior displacement/thinning/dehiscence; changes in orbital volume) (dorlodot2017chronicmaxillaryatelectasis pages 1-2, tousidonis2024contemporarytreatmentof pages 4-7)

7.2 Localization and laterality

• Typically unilateral, but bilateral cases exist in broader CMA/SSS spectrum (not central in the retrieved evidence set). de Dorlodot series shows a right-side predominance in that cohort: 13/18 (72%) right-sided. (dorlodot2017chronicmaxillaryatelectasis pages 1-2)

7.3 Suggested UBERON terms (suggestions)

• Maxillary sinus — UBERON:0001734
• Orbit — UBERON:0001697
• Orbital floor (inferior orbital wall) — can be represented via orbit + bony wall anatomy terms (implementation-dependent)

8. Temporal development

8.1 Onset pattern

Often insidious; early disease may have no symptoms. Stryjewska-Makuch 2023: “in the early stage of SSS, the patient does not report any symptoms.” (published Oct 2023; URL: https://doi.org/10.1007/s00405-022-07697-w) (stryjewskamakuch2023whatmaysurprise pages 6-8)

8.2 Progression

Described as slow/progressive in classic descriptions and in the ClinicalTrials.gov case report, contributing to diagnostic delay. (sivasubramaniam2011silentsinussyndrome pages 1-2, NCT04388345 chunk 1)

9. Inheritance and population

9.1 Epidemiology (prevalence/incidence)

No population-based prevalence/incidence estimates were identified in the retrieved evidence.

9.2 Case counts / rarity statements

• Kramer 2024 states: “Only around 100 cases of SSS have been reported so far.” (published May 2024; URL: https://doi.org/10.7759/cureus.61442) (kramer2024granulomatosiswithpolyangiitis pages 1-3)

9.3 Demographics (statistics from clinical series)

• de Dorlodot 2017: 18 patients, mean age 44.0 ± 16.9 (range 12–70), 7 women/11 men, right-sided 13/18 (72%). (published Jun 2017; URL: https://doi.org/10.1007/s00405-017-4622-8) (dorlodot2017chronicmaxillaryatelectasis pages 1-2)
• Clarós 2019: 15 patients, 11 women/4 men, mean duration of enophthalmos 10.7 months, mean enophthalmos 2.6 mm, mean hypoglobus 2.7 mm. (published Jan 2019; URL: https://doi.org/10.1080/00016489.2018.1542161) (claros2019silentsinussyndrome pages 1-3)
• Stryjewska-Makuch 2023 institutional experience: among 1766 paranasal sinus patients (Sept 2017–May 2022), 8 SSS cases (4 men/4 women), mean age 45.4 (range 31–75). (published Oct 2023; URL: https://doi.org/10.1007/s00405-022-07697-w) (stryjewskamakuch2023whatmaysurprise pages 2-4)

10. Diagnostics

10.1 Imaging (core diagnostic modality)

• CT is repeatedly emphasized as the diagnostic cornerstone; the trial registry explicitly states: “CT imaging is considered the gold standard for its diagnosis. The classical radiographic findings are opacification and collapse of the sinus walls.” (NCT04388345; posted May 14, 2020; URL: https://clinicaltrials.gov/study/NCT04388345) (NCT04388345 chunk 1)
• Tousidonis 2024: imaging shows reduced maxillary antrum volume with retraction of maxillary walls; CT/MRI used. (tousidonis2024contemporarytreatmentof pages 7-8)
• de Dorlodot 2017: coronal CT shows complete or partial opacity (complete 10/18, partial 8/18) and orbital floor dehiscence in 12 cases. (dorlodot2017chronicmaxillaryatelectasis pages 1-2)

10.2 Key radiographic features

• Reduced maxillary sinus volume; inward bowing of sinus walls; often opacification; inferior displacement/thinning of orbital floor; uncinate lateralization/infundibular occlusion. (dorlodot2017chronicmaxillaryatelectasis pages 1-2, lee2018silentsinussyndrome pages 1-4)
• Important diagnostic nuance: Lee 2018 demonstrates SSS can occur without ipsilateral maxillary sinus opacification, reporting average ipsilateral maxillary volume loss of 29% ± 7.1%. (published Sep 2018; URL: https://doi.org/10.1002/lary.27108) (lee2018silentsinussyndrome pages 1-4)

10.3 Clinical evaluation

SSS often presents with ophthalmologic complaints; nasal endoscopy and ENT evaluation are recommended in suspected cases (trial registry). (NCT04388345 chunk 1)

10.4 Differential diagnosis (selected)

From de Dorlodot’s exclusion criteria and modern etiologic expansions: - Prior trauma/surgery causing secondary changes (secondary SSS) (strabbing2025posttraumaticandiatrogenic pages 1-2, dorlodot2017chronicmaxillaryatelectasis pages 1-2) - Congenital facial/orbital deformity (excluded in de Dorlodot series) (dorlodot2017chronicmaxillaryatelectasis pages 1-2) - Other causes of acquired enophthalmos/hypoglobus (e.g., orbital pathology; not enumerated in retrieved texts) - Systemic inflammatory disease causing sinonasal obstruction such as GPA, particularly with necrotizing granulomatous inflammation and ANCA positivity. (kramer2024granulomatosiswithpolyangiitis pages 1-3, kramer2024granulomatosiswithpolyangiitis pages 3-5)

11. Outcome / prognosis

11.1 Prognosis and functional outcomes

SSS is generally treatable with surgical restoration of ventilation/drainage, with frequent improvement in ocular position and symptoms. - Sivasubramaniam 2011 reports that in a 23-case experience treated with uncinectomy/antrostomy alone, 22/23 had complete or partial resolution, supporting staged orbital reconstruction when needed. (published Aug 2011; URL: https://doi.org/10.1017/S0022215111001952) (sivasubramaniam2011silentsinussyndrome pages 1-2)

11.2 Complications

• Secondary SSS can be associated with diplopia and functional/cosmetic impact; early recognition is advised to prevent severe sequelae. (strabbing2025posttraumaticandiatrogenic pages 1-2)

12. Treatment

12.1 Surgical/interventional (current standard of care)

Functional endoscopic sinus surgery (FESS) to restore ventilation/drainage is consistently described as the standard. - Tousidonis 2024: “maxillary endoscopic antrostomy and uncinectomy with FESS represent the gold standard.” (published Apr 2024; URL: https://doi.org/10.7759/cureus.57577) (tousidonis2024contemporarytreatmentof pages 7-8) - ClinicalTrials.gov registry similarly states: “Functional endoscopic sinus surgery (FESS) is the standard gold treatment of choice to arrest the progression of the disease.” (NCT04388345 chunk 1)

12.2 Orbital reconstruction (indications and timing controversies)

There is no universal consensus on whether to reconstruct the orbital floor immediately. - Evidence for staged/delayed approach: dynamic remodeling after re-ventilation can improve orbital floor position, potentially avoiding reconstruction; Sivasubramaniam supports delay and reassessment (22/23 improved with FESS alone). (sivasubramaniam2011silentsinussyndrome pages 1-2) - Sheptulin 2024: staged approach with follow-up CT at 6 months showed sinus pneumatization and orbital-floor elevation, but residual 3–4 mm enophthalmos and diplopia prompted delayed reconstruction; authors cite arguments to delay 3–6 months to reduce risks of overcorrection/inflammatory complications. (sheptulin2024clinicalandmorphological pages 1-2, sheptulin2024clinicalandmorphological pages 3-3) - Evidence for combined/simultaneous approach: Clarós 2019 reports 13/15 treated with simultaneous ESS and titanium orbital floor implant with significant improvement. (claros2019silentsinussyndrome pages 1-3)

12.3 Real-world implementations / advanced techniques (2023–2024 emphasis)

Tousidonis 2024 illustrates contemporary orbit reconstruction adjuncts: - A combined approach using patient-specific titanium implant, FESS, surgical navigation, and intraoperative CT with objective volumetry: affected orbital volume 28.066 cm³ pre-op vs 25.257 cm³ post-op (reduction 2.809 cm³), with stable 1-year results and no late complications. (published Apr 2024; URL: https://doi.org/10.7759/cureus.57577) (tousidonis2024contemporarytreatmentof pages 4-7)

12.4 Treatment outcomes (statistics)

• FESS alone: 22/23 complete or partial resolution in Sivasubramaniam 2011. (sivasubramaniam2011silentsinussyndrome pages 1-2)
• Combined surgery: quantitative ocular metrics in Clarós 2019 (mean pre-op enophthalmos 2.6 mm, hypoglobus 2.7 mm; significant improvement post-op). (claros2019silentsinussyndrome pages 1-3)
• Secondary SSS: Strabbing 2025 reports surgery “restored orbital anatomy and resolved symptoms”; their Table 1 summarizes patient symptom patterns (enophthalmos/hypoglobus/diplopia) and latency post-trigger. (strabbing2025posttraumaticandiatrogenic pages 1-2, strabbing2025posttraumaticandiatrogenic media de48a58f)

12.5 Suggested MAXO terms (suggestions)

• Functional endoscopic sinus surgery — MAXO:0001179 (conceptual mapping; MAXO ID may vary by implementation)
• Maxillary antrostomy / uncinectomy — MAXO procedural descendants (implementation-dependent)
• Orbital floor reconstruction — MAXO surgical reconstruction concept (implementation-dependent)

12.6 Pharmacotherapy

No disease-specific pharmacotherapy standards were identified in the retrieved evidence; antibiotics may be used for infectious complications in specific perioperative contexts (e.g., postoperative orbital complication described in a pediatric case report not deeply analyzed here). (tousidonis2024contemporarytreatmentof pages 7-8)

12.7 Experimental / clinical trials

No interventional trials were identified. One observational registry entry exists: - NCT04388345 (COMPLETED; enrollment 1; posted May 14, 2020): “SILENT SINUS SYNDROME (First Case Report, Saudi Arabia With Recommendation)” (URL: https://clinicaltrials.gov/study/NCT04388345). (NCT04388345 chunk 1)

13. Prevention

13.1 Primary prevention

No primary-prevention interventions are established in the retrieved evidence.

13.2 Secondary/tertiary prevention (complication prevention)

Evidence supports early recognition and timely ENT referral to prevent progression of cosmetic/functional orbital deformity: - NCT04388345 recommends “prompt ear, nose, and throat referral” for suspected cases and emphasizes CT-based diagnosis and FESS to arrest progression. (NCT04388345 chunk 1) - Strabbing 2025 recommends follow-up after trauma/surgery when unexplained orbital changes develop, to prevent severe complications. (strabbing2025posttraumaticandiatrogenic pages 1-2)

14. Other species / natural disease

No naturally occurring veterinary/other-species analogs were identified in the retrieved evidence.

15. Model organisms

No model organism or in vitro disease models were identified in the retrieved evidence.

High-yield structured summary (artifact)

The following structured table consolidates key concepts, statistics, and management evidence with URLs/DOIs and citation hooks:

Table: This table summarizes key clinical, radiologic, mechanistic, demographic, and treatment findings for Silent Sinus Syndrome from the retrieved evidence base. It is designed to support rapid citation and knowledge-base population.

Visual evidence

A cropped table image from Strabbing 2025 summarizing secondary SSS patient-level clinical data (symptoms and time-to-onset) was retrieved and can be used to support secondary SSS statistics and variability in presentation. (strabbing2025posttraumaticandiatrogenic media de48a58f)

Evidence gaps and limitations (for KB curation)

• Identifiers (ICD/MeSH/Orphanet/OMIM): not retrieved in this run; should be filled from authoritative ontologies (e.g., MeSH Browser, ICD-11 MMS, Orphanet) in a follow-up curation step.
• Genetics: no established causal genes/variants in retrieved evidence; occasional familial clustering hypotheses exist in broader literature but were not evidenced here.
• Epidemiology: no incidence/prevalence estimates; literature is largely case series/case reports.
• QoL instruments: no EQ-5D/SF-36/PROMIS quantitative data found in retrieved evidence.

References

1. (claros2019silentsinussyndrome pages 1-3): Pedro Clarós, Aleksandra Zofia Sobolewska, Antonio Cardesa, Marta Lopez-Fortuny, and Andres Claros. Silent sinus syndrome: combined sinus surgery and orbital reconstruction – report of 15 cases. Acta Oto-Laryngologica, 139:64-69, Jan 2019. URL: https://doi.org/10.1080/00016489.2018.1542161, doi:10.1080/00016489.2018.1542161. This article has 12 citations and is from a peer-reviewed journal.

2. (dorlodot2017chronicmaxillaryatelectasis pages 1-2): Clotilde de Dorlodot, Stephanie Collet, Philippe Rombaux, Mihaela Horoi, Sergio Hassid, and Philippe Eloy. Chronic maxillary atelectasis and silent sinus syndrome: two faces of the same clinical entity. European Archives of Oto-Rhino-Laryngology, 274:3367-3373, Jun 2017. URL: https://doi.org/10.1007/s00405-017-4622-8, doi:10.1007/s00405-017-4622-8. This article has 38 citations and is from a peer-reviewed journal.

3. (tousidonis2024contemporarytreatmentof pages 7-8): Manuel Tousidonis, Sara Alvarez-Mokthari, Saad Khayat, Guillermo Sanjuan de Moreta, and Santiago Ochandiano. Contemporary treatment of silent sinus syndrome: a case report and literature review. Cureus, Apr 2024. URL: https://doi.org/10.7759/cureus.57577, doi:10.7759/cureus.57577. This article has 3 citations.

4. (sivasubramaniam2011silentsinussyndrome pages 1-2): R. Sivasubramaniam, Raymond Sacks, and M. Thornton. Silent sinus syndrome: dynamic changes in the position of the orbital floor after restoration of normal sinus pressure. The Journal of Laryngology & Otology, 125:1239-1243, Aug 2011. URL: https://doi.org/10.1017/s0022215111001952, doi:10.1017/s0022215111001952. This article has 75 citations.

5. (lee2018silentsinussyndrome pages 1-4): David S. Lee, Andrew H. Murr, Robert C. Kersten, and Steven D. Pletcher. Silent sinus syndrome without opacification of ipsilateral maxillary sinus. The Laryngoscope, 128:2004-2007, Sep 2018. URL: https://doi.org/10.1002/lary.27108, doi:10.1002/lary.27108. This article has 23 citations.

6. (strabbing2025posttraumaticandiatrogenic pages 1-2): E. M. Strabbing, O. Engin, M. A.J. Telleman, A. P. Nagtegaal, and E. B. Wolvius. Post-traumatic and iatrogenic silent sinus syndrome: a case series. Oral and Maxillofacial Surgery, May 2025. URL: https://doi.org/10.1007/s10006-025-01391-x, doi:10.1007/s10006-025-01391-x. This article has 3 citations and is from a peer-reviewed journal.

7. (kramer2024granulomatosiswithpolyangiitis pages 1-3): Nicholas Kramer, Brandon Manthei, Luke Speier, Jo-Lawrence M Bigcas, and Scott Manthei. Granulomatosis with polyangiitis as an etiology of silent sinus syndrome: a case report. Cureus, May 2024. URL: https://doi.org/10.7759/cureus.61442, doi:10.7759/cureus.61442. This article has 1 citations.

8. (tousidonis2024contemporarytreatmentof pages 1-4): Manuel Tousidonis, Sara Alvarez-Mokthari, Saad Khayat, Guillermo Sanjuan de Moreta, and Santiago Ochandiano. Contemporary treatment of silent sinus syndrome: a case report and literature review. Cureus, Apr 2024. URL: https://doi.org/10.7759/cureus.57577, doi:10.7759/cureus.57577. This article has 3 citations.

9. (tousidonis2024contemporarytreatmentof pages 4-7): Manuel Tousidonis, Sara Alvarez-Mokthari, Saad Khayat, Guillermo Sanjuan de Moreta, and Santiago Ochandiano. Contemporary treatment of silent sinus syndrome: a case report and literature review. Cureus, Apr 2024. URL: https://doi.org/10.7759/cureus.57577, doi:10.7759/cureus.57577. This article has 3 citations.

10. (NCT04388345 chunk 1): Nouf Saloom Alsaloom. SILENT SINUS SYNDROME (First Case Report, Saudi Arabia With Recommendation). King Saud University. 2019. ClinicalTrials.gov Identifier: NCT04388345

11. (kramer2024granulomatosiswithpolyangiitis pages 5-7): Nicholas Kramer, Brandon Manthei, Luke Speier, Jo-Lawrence M Bigcas, and Scott Manthei. Granulomatosis with polyangiitis as an etiology of silent sinus syndrome: a case report. Cureus, May 2024. URL: https://doi.org/10.7759/cureus.61442, doi:10.7759/cureus.61442. This article has 1 citations.

12. (sheptulin2024clinicalandmorphological pages 2-3): Vladimir A. Sheptulin, Yaroslav O. Grusha, and Dmitry M. Konovalov. Clinical and morphological features of the orbital floor in a patient with silent sinus syndrome: a clinical case report. Russian Open Medical Journal, Dec 2024. URL: https://doi.org/10.15275/rusomj.2024.0413, doi:10.15275/rusomj.2024.0413. This article has 0 citations.

13. (sheptulin2024clinicalandmorphological pages 3-3): Vladimir A. Sheptulin, Yaroslav O. Grusha, and Dmitry M. Konovalov. Clinical and morphological features of the orbital floor in a patient with silent sinus syndrome: a clinical case report. Russian Open Medical Journal, Dec 2024. URL: https://doi.org/10.15275/rusomj.2024.0413, doi:10.15275/rusomj.2024.0413. This article has 0 citations.

14. (stryjewskamakuch2023whatmaysurprise pages 6-8): Grażyna Stryjewska-Makuch, Magdalena Kokoszka, Karolina Goroszkiewicz, Olga Karłowska-Bijak, Bogdan Kolebacz, and Maciej Misiołek. What may surprise a rhinologist in everyday clinical practice: silent sinus syndrome or pneumosinus dilatans/pneumocele? literature review and own experience. European Archives of Oto-Rhino-Laryngology, 280:519-527, Oct 2023. URL: https://doi.org/10.1007/s00405-022-07697-w, doi:10.1007/s00405-022-07697-w. This article has 4 citations and is from a peer-reviewed journal.

15. (stryjewskamakuch2023whatmaysurprise pages 2-4): Grażyna Stryjewska-Makuch, Magdalena Kokoszka, Karolina Goroszkiewicz, Olga Karłowska-Bijak, Bogdan Kolebacz, and Maciej Misiołek. What may surprise a rhinologist in everyday clinical practice: silent sinus syndrome or pneumosinus dilatans/pneumocele? literature review and own experience. European Archives of Oto-Rhino-Laryngology, 280:519-527, Oct 2023. URL: https://doi.org/10.1007/s00405-022-07697-w, doi:10.1007/s00405-022-07697-w. This article has 4 citations and is from a peer-reviewed journal.

16. (kramer2024granulomatosiswithpolyangiitis pages 3-5): Nicholas Kramer, Brandon Manthei, Luke Speier, Jo-Lawrence M Bigcas, and Scott Manthei. Granulomatosis with polyangiitis as an etiology of silent sinus syndrome: a case report. Cureus, May 2024. URL: https://doi.org/10.7759/cureus.61442, doi:10.7759/cureus.61442. This article has 1 citations.

17. (sheptulin2024clinicalandmorphological pages 1-2): Vladimir A. Sheptulin, Yaroslav O. Grusha, and Dmitry M. Konovalov. Clinical and morphological features of the orbital floor in a patient with silent sinus syndrome: a clinical case report. Russian Open Medical Journal, Dec 2024. URL: https://doi.org/10.15275/rusomj.2024.0413, doi:10.15275/rusomj.2024.0413. This article has 0 citations.

18. (strabbing2025posttraumaticandiatrogenic media de48a58f): E. M. Strabbing, O. Engin, M. A.J. Telleman, A. P. Nagtegaal, and E. B. Wolvius. Post-traumatic and iatrogenic silent sinus syndrome: a case series. Oral and Maxillofacial Surgery, May 2025. URL: https://doi.org/10.1007/s10006-025-01391-x, doi:10.1007/s10006-025-01391-x. This article has 3 citations and is from a peer-reviewed journal.