Adenoid hypertrophy (AH) is a common upper airway obstruction in children, with prevalence rates ranging from 42 % to 70 %, highlighting its public health significance [1]. Clinically, AH commonly presents with nasal obstruction, snoring, and mouth breathing, which can lead to obstructive sleep apnea, chronic hypoxia, and associated issues such as poor sleep, recurrent infections, and cognitive impairment [2]. More importantly, AH is also linked to craniofacial abnormalities and an increased risk of malocclusion, which is more prevalent in affected children than in healthy peers [3]. Because upper-airway obstruction and craniofacial growth vary across childhood, the dentofacial impact of AH may differ by developmental stage. Therefore, this study aimed to characterize dentition-stage–specific craniofacial changes associated with AH across three pediatric age groups (3–5, 5–8, and 8–11 years).

Extensive evidence shows that AH disrupts nasal breathing and significantly affects craniofacial growth [1,4]. The primary mechanism is chronic mouth breathing, which promotes mandibular retrusion and limits maxillary growth, producing the characteristic “adenoid facies” with increased lower facial height and an altered mandibular angle [5]. Cephalometrics in children with AH often reveal reduced SNB, increased ANB, and a steeper MP/SN angle, consistent with vertical growth and a skeletal Class II pattern [6–8]. AH may also induce dentoalveolar compensation and occlusal adaptation, contributing to clinically relevant malocclusion features [7].

The influence of AH on craniofacial morphology appears to be age-dependent, and both onset timing and symptom duration have been associated with the magnitude of dentofacial alterations [6,9]. Thus, dentition stage–based analyses are needed to determine when AH-related skeletal and dentoalveolar changes become detectable [6,7,9].

Despite growing evidence linking AH to craniofacial abnormalities, age-stratified analyses of related skeletal and dentoalveolar changes across dentition stages remain limited [6,7,9]. Many studies combine wide pediatric age ranges and/or assess only a few cephalometric variables, which may mask stage-specific patterns [6,10]. Therefore, participants were stratified by dentition stage (3–5, 5–8 and 8–11 years), and an integrated panel of skeletal (SNA, SNB, ANB), dentoalveolar (NA–Apo), functional/occlusal (NPo–FH) and clinical (overjet) indices was evaluated to determine when adenoidal hypertrophy–associated dentofacial changes become detectable and clinically relevant. This age-stage–specific approach is intended to inform the timing of airway assessment and individualized orthodontic planning.

AH is commonly associated with upper airway obstruction and mouth breathing, which may influence craniofacial development. During early childhood (3–5 years), skeletal morphology remains largely unchanged, owing to the inherent plasticity of maxillomandibular growth and the compensatory mechanisms of the deciduous dentition phase [6,9]. In children aged 5 to 8 years and 8 to 11 years with AH, SNB angles are significantly lower, indicating mandibular retrusion. ANB angles are significantly higher, reflecting maxillary protrusion or mandibular retrusion. These findings are consistent with a progressive skeletal Class II pattern [6,7]. Altered breathing patterns and oral posture have been proposed to affect craniofacial growth direction and jaw posture.(1,4) Multivariate regression indicates that the AH/Np ratio correlates significantly with SNA and SNB changes, with snoring duration and mouth breathing serving as primary drivers of craniofacial morphological alterations [9]. Previous studies also link AH to sagittal skeletal discrepancies, particularly mandibular retrusion and altered craniofacial proportions [6]. Overall, these findings highlight early mixed dentition as a key window for monitoring and interdisciplinary evaluation [4].

Our age-stratified analyses revealed a stage-dependent pattern. No measurable skeletal or dentoalveolar differences were detected at 3–5 years. Early mixed dentition (5–8 years) was characterized by emerging mandibular retrusion and dentoalveolar compensation (SNB↓, NA-Apo↑). By 8–11 years, a broader deterioration was observed, with reductions in both SNA and SNB, an increased ANB, posterior occlusal plane inclination, and greater overjet. This within-cohort gradient may reflect an age- and duration-related worsening of AH-associated dentofacial alterations, rather than a uniform phenotype across childhood.

Craniofacial adaptations induced by AH extend to the dentoalveolar structures. In both the 5–8 and 8–11 year age groups, children with AH exhibited significantly increased NA-Apo angles, indicative of upper incisor proclination, a compensatory mechanism for mandibular retrusion [9]. In the 8–11 year cohort, the NPo-FH angle was significantly reduced, indicating posterior occlusal plane inclination, which may be related to tongue depression and altered masticatory force distribution from mouth breathing [6,7]. An open-mouth posture upsets perioral muscle balance, reducing lip pressure on the upper incisors and increasing tongue thrust, which worsens incisor proclination. Additionally, abnormal mandibular positioning alters occlusal loading patterns, ultimately influencing alveolar bone morphology [1,11]. AH patients consistently exhibit anterior alveolar protrusion alongside increased mandibular plane angles (MP/SN), highlighting concurrent sagittal and vertical discrepancies [6]. Early orthodontic assessment should identify these dentoalveolar compensations, and myofunctional therapy (e.g., lip-seal training) may help slow malocclusion progression.

Although maxillomandibular lengths (ANS-Ptm, Co-Gn) remain unchanged in children with AH, overjet increases steadily after age 5, peaking in the 8–11-year group [7,9]. These changes reflect mandibular retrusion and compensatory upper incisor proclination rather than skeletal hypoplasia, together worsening horizontal dental discrepancies [12]. Previous studies have demonstrated significantly higher rates of deep overjet in AH populations compared to controls (p < 0.05), with overjet positively correlated with maxillary protrusion and incisor inclination [13,14]. Furthermore, the prevalence of AH among patients with skeletal Class II malocclusion has been reported as high as 80 %, supporting overjet as an early clinical indicator of AH-related craniofacial abnormalities [15,16]. Overjet assessment should be incorporated into AH screening protocols. In patients presenting with Class II malocclusion, airway obstruction should be carefully evaluated [12,15]. Importantly, in our cohort the mean overjet increased to 4.9 mm (5–8 years) and 5.6 mm (8–11 years) in the AH group, compared with 3.1 mm and 2.8 mm in controls, supporting that the observed differences are not only statistically significant but also clinically noticeable.

Consistent with this stage-dependent progression, previous work suggests that symptom duration is a key predictor of dentofacial changes [9]. Age-specific analyses show that vertical discrepancies peak at 6–9 years, while sagittal discrepancies intensify at 9–12 years [17]. Postpubertal cases often exhibit a shift in OSA etiology from AH to obesity [18]. During the deciduous phase, nasal patency should be optimized, whereas in the mixed dentition phase, airway management should be combined with functional growth-modulating appliances [19].

Our findings are consistent with age-stratified reports showing that AH is associated with sagittal skeletal disharmony, driven mainly by mandibular retrusion and an increased ANB, with the signal most evident during the mixed-dentition stages [6,7]. The age-related worsening observed in our cohort is also in line with evidence that longer symptom duration (for example, habitual snoring and chronic mouth breathing) is associated with larger shifts in SNA and SNB [9]. Notably, although mandibular size or length differences have been described in some age windows, no group differences were detected for ANS-Ptm or Co-Gn in the present sample. This pattern suggests that, in prepubertal children, AH may preferentially influence jaw position and rotational pattern, accompanied by dentoalveolar compensation, rather than producing a primary deficiency in skeletal length. Our restriction to prepubertal skeletal maturity (CS1-CS2) and the use of ANS-Ptm/Co-Gn as length surrogates may also partly explain why skeletal length differences observed in other cohorts were not detected here. Between-study differences may reflect variation in age ranges, diagnostic definitions (isolated AH vs. adenotonsillar hypertrophy), population background, and whether vertical growth measures were included.

Dentoalveolar compensation varies by skeletal class. In Class I, vertical alveolar adaptation fine-tunes incisor inclination to preserve occlusion [20,21]. In Class II, early use of functional appliances before puberty limits maxillary growth and enhances mandibular compensation, improving alignment and stability [22,23]. Children with AH often exhibit increased mandibular plane angle (MP/SN) and alveolar height, leading to an elongated facial profile and more severe malocclusion [7,13]. AH also reshapes the airway and displaces the hyoid bone posteriorly [24,25], elevating obstructive sleep apnea risk in older children, especially when obesity and mandibular anatomy (height, SNB) are contributory [18,26].

Lateral cephalometry is the standard for AH diagnosis, though accuracy depends on obstruction severity [27]. Effective management requires collaboration between ENT specialists, pediatric dentists, and orthodontists to ensure early intervention and reduce malocclusion risk. Adenoidectomy or other surgical treatments may be indicated [28,29]. Tonsillar hypertrophy often coexists, further reducing bite force and airway volume [28], but dentoalveolar compensation can partly mitigate skeletal imbalances [30,31]. The strong association between AH, mouth breathing, and facial growth highlights the necessity of personalized treatment planning.

Clinically, the age-stratified analyses indicate that AH-associated dentofacial deviations become evident from early mixed dentition (5–8 years) and appear to progress by 8–11 years. In particular, overjet increased from 3.1 mm (controls) to 4.9 mm (AH) at 5–8 years and from 2.8 mm to 5.6 mm at 8–11 years (Table 2), corresponding to mean differences of 1.8–2.8 mm with moderate effect sizes. Increased overjet and NA-Apo, together with a reduced SNB angle, may provide pragmatic screening cues that warrant targeted upper-airway evaluation. Since jaw lengths (ANS-Ptm and Co-Gn) did not differ between groups, the craniofacial effects likely reflect positional changes and dentoalveolar compensation rather than true skeletal length deficiency. These findings support early airway management and coordinated interceptive orthodontic and myofunctional intervention during the mixed-dentition period. Children with persistent mouth breathing or snoring who develop a Class II trend (e.g., reduced SNB with overjet rising to ∼5–6 mm) may benefit from earlier ENT–orthodontic referral, especially at 5–8 years when changes first appear.

This study still has several limitations. First, the retrospective design precludes drawing causal links between adenoid hypertrophy and craniofacial changes. Second, the use of two-dimensional lateral cephalograms may introduce measurement inaccuracies due to projection and landmark identification errors; the lack of 3D imaging restricts the precision of anatomical evaluation. Third, the absence of longitudinal follow-up in treated cases precludes evaluation of treatment effects on craniofacial development. Fourth, selection bias is possible because AH cases came from a clinical database, whereas controls were recruited from a health examination center. Fifth, despite matching for age, sex, and BMI and restricting analyses to CS1-CS2, unmeasured confounding may remain. Sixth, because multiple outcomes were tested across age groups, the findings are exploratory and need confirmation in prospective studies. Thus, prospective longitudinal studies using advanced imaging techniques are warranted to validate these findings.

Future work should prioritize (i) prospective longitudinal follow-up across dentition stages to define developmental trajectories and improve causal inference; (ii) pre–post intervention analyses (for example, after medical therapy/adenoidectomy and/or myofunctional or functional orthopedic-orthodontic treatment) to assess reversibility of positional and dentoalveolar changes; (iii) integration of objective airway and sleep measures with cephalometric phenotyping; and (iv) selective use of CBCT to refine anatomic assessment while limiting radiation exposure.

In this retrospective, age-stratified analysis, adenoid hypertrophy was associated with age-dependent mandibular retrusion, dentoalveolar protrusion, posterior occlusal plane inclination and increased overjet, whereas maxillary and mandibular lengths (ANS-Ptm and Co-Gn) did not differ between groups. These results suggest that, in prepubertal children, AH is linked mainly to jaw position/rotation and dentoalveolar compensation rather than skeletal length deficiency. Early recognition of airway obstruction and interdisciplinary evaluation during mixed dentition may help limit progression of dentofacial discrepancies, but prospective longitudinal studies are required to confirm causality and treatment effects.

The study was approved by Children’s Hospital of Nanjing Medical University (#202405006–1). The study was performed in strict accordance with the Declaration of Helsinki, Ethical Principles for Medical Research Involving Human Subjects.

All patients signed the informed written consent.

None.

Not applicable.

The data that support the findings of this study are available from Jian-Ya Zhang upon request.

Xue-Ru Zhang: Data curation, Formal analysis, Funding acquisition, Validation, Supervision, Writing – original draft. Jian-Ya Zhang: Data curation, Formal analysis, Funding acquisition, Validation, Supervision, Writing – original draft.