Gagat Ragil Andaru Pratomo, Feri Trihandoko
Adenoid hypertrophy and chronic adenoiditis appear to be associated with pediatric CRS through combined obstructive, microbial, biofilm- related, inflammatory, and immunological pathways, although causal relationships cannot be established from the available evidence. Adenoidectomy appears beneficial in selected refractory cases, although further prospective mechanistic studies are needed.
OBJECTIVE: To synthesize available evidence on the mechanistic role of adenoid hypertrophy and chronic adenoiditis in the pathogenesis of pediatric chronic rhinosinusitis (CRS), given that the mechanistic relationship between adenoid disease and pediatric CRS remains incompletely synthesized.
DATA SOURCES: PubMed/MEDLINE, Embase, Scopus, Web of Science Core Collection, and Cochrane Library were systematically searched in accordance with PRISMA 2020 guidelines.
METHODS OF REVIEW: Eligible studies included children with CRS and evaluated adenoid- related mechanisms, including mechanical obstruction, impaired drainage, microbial reservoir function, biofilm formation, immune dysregulation, epithelial dysfunction, mucociliary impairment, or clinical outcomes after adenoidectomy. Study quality was appraised using the JBI Critical Appraisal Tools. Due to heterogeneity in study design, diagnostic criteria, and reported outcomes, a narrative synthesis was performed.
RESULTS: Nine studies involving 927 pediatric participants were included. Evidence for mechanical obstruction was mixed, as adenoid size did not consistently correlate with CRS severity. Stronger evidence supported the role of the adenoid as a microbial reservoir and biofilm- bearing tissue, with studies reporting pathogenic bacterial colonization and extensive adenoidal biofilm in children with CRS. Limited molecular evidence suggested reduced surfactant protein- D expression, while epithelial barrier dysfunction and mucociliary impairment were supported mainly by indirect findings. Adenoidectomy improved symptoms and quality of life in selected children with medically refractory CRS.
CONCLUSION: Adenoid hypertrophy and chronic adenoiditis appear to be associated with pediatric CRS through combined obstructive, microbial, biofilm- related, inflammatory, and immunological pathways, although causal relationships cannot be established from the available evidence. Adenoidectomy appears beneficial in selected refractory cases, although further prospective mechanistic studies are needed.