What is the etiology of antrochoanal polyp in patients with a history of respiratory infections, allergies, and asthma?

Etiology of Antrochoanal Polyp

The etiology of antrochoanal polyps remains incompletely understood, but chronic inflammatory conditions—particularly chronic sinusitis and allergic rhinitis—combined with anatomical variations that disrupt maxillary sinus airflow, appear to be the primary predisposing factors. 1, 2, 3

Primary Etiological Factors

Chronic Inflammatory Pathologies

• Chronic sinusitis is present in approximately 20.5% of patients with antrochoanal polyps, representing one of the most common predisposing factors 1
• Allergic rhinitis occurs in 44.1% of antrochoanal polyp patients, suggesting a significant inflammatory contribution to polyp formation 1
• The relationship between chronic inflammation and ACP formation requires further investigation, as the exact pathophysiological mechanisms linking these conditions remain unclear 2

Anatomical Variations and Mechanical Factors

• Disrupted airflow in well-developed maxillary sinus cavities due to anatomical variations appears to be an effective factor in ACP formation 3
• Maxillary sinus volume is significantly larger on the ACP side (17.88 ± 5.16 mm³) compared to the non-ACP side (16.37 ± 4.55 mm³), suggesting that increased sinus volume may predispose to polyp development 3
• Nasal septal deviation is present in 50% of ACP patients, potentially contributing to altered airflow patterns 1
• Concha bullosa occurs in 42.6% of ACP patients on the affected side, representing another anatomical factor that may obstruct normal sinus drainage 3
• Agger nasi cells are present in 87% of ACP patients on the affected side, indicating that anterior ethmoid pneumatization may play a role 3

Anatomical Origin and Pathway

Maxillary Sinus Origin

• Antrochoanal polyps arise from the edematous mucosa of the maxillary sinus, typically originating from the posterior or lateral wall 2, 4
• The polyps have a characteristic cystic intramaxillary portion and a solid intranasal portion, distinguishing them from bilateral nasal polyposis 2
• Microscopically, ACPs resemble maxillary mucosal cysts, suggesting a cystic transformation of the sinus mucosa as part of the pathogenesis 2

Exit Route Through Ostia

• In 97.05% of cases, the polyp exits the maxillary sinus through an accessory ostium rather than the natural ostium 1
• In a pediatric series, 78% of polyps passed through the main ostium, while 14% used the accessory ostium, suggesting age-related differences in drainage patterns 4
• The presence of accessory ostia appears nearly universal in ACP patients, raising questions about whether these represent a predisposing anatomical variant or a consequence of the disease process 1

Associated Conditions

Concurrent Sinonasal Pathology

• Turbinate hypertrophy is present in 32.3% of ACP patients 1
• Mucous retention cysts occur in 32.3% of cases, suggesting underlying mucosal dysfunction in the maxillary sinus 1
• Hyperpneumatized ethmoid bulla is observed in 25.9% of ACP patients on the affected side 3

Respiratory Comorbidities

• While asthma is strongly associated with bilateral nasal polyposis (occurring in 7-15% of adults with asthma), the specific association between asthma and antrochoanal polyps has not been well-established in the literature 5, 6
• The inflammatory profile of ACPs differs from bilateral nasal polyposis, suggesting distinct pathophysiological mechanisms despite some shared risk factors 2

Key Distinguishing Features from Bilateral Nasal Polyposis

• ACPs are typically unilateral, whereas bilateral nasal polyposis is associated with allergic rhinitis, asthma, and aspirin sensitivity 2
• ACPs appear in younger patients (mean age 22-25 years in most series), contrasting with bilateral nasal polyps that typically occur after age 40 1, 2
• The role of allergy in ACP formation is unclear, unlike bilateral nasal polyposis where eosinophilic inflammation and IgE-mediated mechanisms are well-established 5, 2

Critical Knowledge Gaps

Important caveat: The exact pathophysiological mechanisms of ACP formation remain poorly understood, and further research is needed to establish 2:

• The precise relationship between chronic sinusitis and ACP development
• The role of inflammatory mediators (histamine, IgE, adhesion molecules) in ACP pathogenesis
• The contribution of metalloproteases and tissue remodeling to polyp formation
• Whether anatomical variations are causative or merely associated findings