Adenoiditis pathophysiology

Adenoiditis Microchapters
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Mahshid Mir, M.D. [2]

Overview

The pathogenesis of adenoiditis is characterized by its inflammation. This process is primarily due to an elevated rate of trafficking of lymphocytes into adenoid from the blood, exceeding the rate of outflow from the adenoid. Adenoids are involved in the production of mostly secretory IgA, which is transported to the surface where it provides local immune protection. Adenoids can be infected by either bacterial and viral pathogens leading to adenoiditis.

Pathophysiology

• Adenoids are on the posterior nasopharynx, posterior to the nasal cavity. They are a component of the Waldeyer's ring of lymphoid tissue, which is a ring of lymphoid tissue and includes adenoids and tonsils.

• Adenoids are developed from lymphocytes infiltration in subendothelium of nasopharynx during the 16th week of gestation.

• After the birth adenoids begin to enlarge.
• By the time children are aged 6 months, lactobacilli, anaerobic streptococci, actinomycosis, Fusobacterium species, and Nocardia species are present in the mucosal flora.
• Normal flora found in the mature adenoid tissue consists:
  • Alpha-hemolytic streptococci
  • Enterococci
  • Corynebacterium species
  • Coagulase-negative staphylococci
  • Neisseria species
  • Haemophilus species
  • Micrococcus species
  • Stomatococcus species
• It is normal to find symptomatic adenoids in children aged 18-24 months.
• They continue their grow until individuals are aged 5-7 years.

• Adenoids start to shrink by the age 6-7.
• By the time children reach 10-12, the adenoids are usually small enough for the child to become asymptomatic.

Pathogenesis

• Adenoids are involved in the production of mostly secretory IgA, which is transported to the surface providing local immune protection. Studies suggest that a reduction in IgA will happen postoperative of adenoidectomy.

• Adenoiditis can happen as a result of infection and harbor pathogenic bacterial activity, which may lead to the development of disease of the ears, nose, and sinuses. Adenoiditis can progress to chronic disease if remain untreated for a long term.

• Parental history of tonsillectomy and atopy hold significant predictive power in pediatric adenoiditis.
• The pathogenesis of adenoiditis is characterized by its inflammation. This process is primarily due to an elevated rate of trafficking of lymphocytes into adenoid from the blood, exceeding the rate of outflow from the adenoid.
• The persistence of tonsillitis beyond 3 months is known as chronic tonsillitis. In case of chronic bacterial tonsillitis the bacteria persist in the tonsils and lead to chronic inflammation. This persistent infection and inflammation leads to chronic tonsillitis. Manifestations appear whenever the patient has decline in immunity.
• The immune response between the antigen and lymphocyte that leads to cellular proliferation and enlargement of the adeoid especially in paracortex area which lead to excess enlargement of the adenoids.
• Bacterial adenoiditis is primarily caused by group A β-hemolytic streptococcus (GABHS) Streptococcus pyogenes infection.
  • S. pyogenes and taxonomically-similar bacteria infiltrate the adenoidal epithelium, successfully penetrating the protective mucosal films in the oral and nasal cavity.
    • Colonization begins when the bacteria adheres to the adenoid surface proteins through lipoteichoic acid (LTA), depositing fibronectin molecules that bind to the adenoidal epithelium.
• Adenoid paracortex may also be enlarged secondarily as a result of the activation and proliferation of antigen-specific T and B cells (clonal expansion).

Gross pathology

• On gross pathology, characteristic findings of adenoiditis, include:

• Enlarged adenoids
• Soft greasy yellow areas within capsule

Microscopic Pathology

• On microscopic histopathological analysis, characteristic findings of adenoiditis
• Recurrent bacterial tonsillitis is caused primarily by Staphylococcus aureus.
  • S. aureus invades the adenoids through microbial surface components recognizing adhesive matrix molecules (MSCRAMMs)
  • Following invasion, S. aureus is internalized by non-phagocytic cells through fibronectin-binding protein and beta-integrins.
  • Invasion of non-eukaryotic cells results in the up-regulation of cytokines, resulting in adenoiditis