The role of adenoid hypertrophy in obstructive sleep apnea outcomes post-mandibular distraction osteogenesis in patients with craniofacial microsomia.

Abstract

Study objectives: Mandibular distraction osteogenesis (MDO) is recommended for children with craniofacial microsomia (CFM) and obstructive sleep apnea (OSA). However, its efficacy remains limited, with success rates of 36.4%-60%. The role of adenoid hypertrophy (AH) in persistent OSA post-MDO has not been been fully investigated. This study aimed to evaluate the role of AH in influencing MDO outcomes and to explore its contribution to the pathophysiology and treatment of OSA in patients with CFM.

Methods: A retrospective analysis was conducted on 72 patients with CFM undergoing MDO. Preoperative adenoid size was assessed using adenoid/nasopharyngeal (A/N) ratios from cranial CT scans. Polysomnographic data, including pre- and postoperative obstructive apnea-hypopnea index (OAHI), were analyzed. Patients were classified into effective and ineffective groups based on postoperative OSA improvement. Statistical correlations between A/N ratios, OSA severity, Pruzansky-Kaban classification and treatment outcomes were examined.

Results: AH prevalence among patients with CFM with OSA was 61.1%. A/N ratios correlated with postoperative OAHI (r = 0.261, p = 0.027), but not with preoperative OAHI. The ineffective group had higher A/N ratios than the effective group (0.69 ± 0.13 vs. 0.64 ± 0.12). Overall MDO effectiveness rate was 47.22%, with greater improvement observed in patients with severe OSA. No significant association was found between the Pruzansky-Kaban classification and either OSA severity or MDO treatment outcomes.

Conclusions: Adenoid hypertrophy plays a significant role in persistent OSA post-MDO, particularly in mild to moderate cases. Routine preoperative assessment of AH, combined with targeted interventions such as adenoidectomy when indicated, may improve treatment outcomes. These findings underscore the importance of addressing both skeletal and soft tissue factors in the comprehensive management of OSA in patients with CFM.