As an ortho student, you keep hearing “check adenoids, check tonsils, check breathing.” By the end of this blog, you should be able to predict the likely malocclusion pattern just from knowing where the child’s airway is obstructed – and explain the logic behind it to parents and ENTs, not just quote it.
The core question Nunes asked
Nunes & Di Francesco (2010) studied 114 mouth-breathing, snoring children (3–12 years) with tonsillar and/or adenoid enlargement, all seen in an ENT clinic.
They asked a very simple but powerful question:
“Is the site of lymphoid obstruction (adenoids, tonsils, or both) associated with specific patterns of malocclusion (sagittal / transverse / vertical)?”
Obstruction was graded objectively: tonsils (Brodsky 1-4), adenoids (cephalometric 0-100%). Orthodontic exams classified sagittal (I/II/III), transverse (normal/crossbite), and vertical (normal/open/deep) relationships.
The groups:
- Non-obstructive (small tonsils/adenoids)
- Isolated obstructive tonsils
- Isolated obstructive adenoids
- Combined obstructive adenoids + tonsils
LIKELY AIRWAY OBSTRUCTION → EXPECTED MALOCCLUSION
A. Adenoid + Tonsil Hypertrophy
- 🔹 Common occlusion: Class II
- 🔹 Transverse: Posterior crossbite common
- 🔹 Skeletal pattern: Vertical growth tendency
- 🔹 Clinical hint: Retropositioned mandible, narrow maxilla
B. Isolated Tonsillar Hypertrophy
- 🔹 Common occlusion: Class III tendency
- 🔹 Mechanism: Forward tongue posture
- 🔹 Watch for: Lower incisor proclination
C. Isolated Adenoid Hypertrophy
- 🔹 Usually Class I or mild Class II
- 🔹 Often associated with maxillary constriction
TRANSVERSE DIMENSION (KEY RED FLAG 🚩)
- Posterior crossbite prevalence ↑ in all airway obstruction types
- Early maxillary expansion = functional + airway benefit
VERTICAL RELATIONSHIP
- ☐ Open bite / Deep bite
- ⚠️ Not directly site-dependent
- Influenced by:
- Facial type
- Oral habits (thumb sucking, tongue thrust)
Is this malocclusion causing airway issues, or is the airway issue causing this malocclusion?
Airway obstruction causes the malocclusion. Nunes 2010 shows enlarged adenoids/tonsils (64.9% combined obstructive) drive specific patterns: combined → Class II (43.2%) via backward mandibular rotation for airflow; tonsils only → Class III (37.5%) via forward tongue thrust. Mouth breathing narrows palate → 36.8% posterior crossbite (vs 6.9-16.4% controls/population). Reverse (malocclusion → airway) not supported—it’s functional matrix disruption (Moss theory).
If I correct the teeth without correcting the airway, will this case relapse?
Yes, high relapse risk. Obstruction persists → ongoing tongue displacement, mandibular posture changes, dolichofacial growth continue post-ortho. Adenotonsillectomy normalizes GH → mandibular growth boost, but without it, ortho stability fails as functional drivers (mouth breathing) remain. Early ENT + ortho (pre-spurt) prevents irreversibility.
Am I seeing a dental problem or a functional growth problem?
Functional growth problem. 36.8% crossbite, site-specific sagittal shifts (P=.02) signal airway-altered craniofacial development, not isolated dental misalignment. Class I appears “normal” but hides constricted arches → future crowding; true dental issues lack this obstruction-malocclusion signature.
Will correcting the airway allow self-correction of growth?
Partial self-correction possible pre-spurt: surgery normalizes GH, boosts condylar/mandibular base apposition → some malocclusion improvement. Not full—ortho often needed for transverse (crossbite), residual sagittal discrepancies.
In Class II: Is the mandible retruded due to posture or true deficiency?
Posture-driven retrusion from airway obstruction. Nunes shows combined adenoid+tonsil enlargement (64.9% sample) correlates with Class II (43.2% vs population 12.6%), caused by backward mandibular rotation—child opens posture for airflow through narrow palate, displacing mandible posteriorly. Not primary skeletal deficiency; functional adaptation becomes skeletal if untreated pre-spurt.
In Class II: Is the head posture influencing jaw position?
Yes, head posture reinforces retrusion. Mouth breathing → forward head tilt + downward chin to compensate airway restriction, locking mandible in distal position and promoting dolichofacial growth (vertical dominance). Nunes links this cycle: obstruction → tongue flop → posture change → Class II signature (P=.02 sagittal association).
In Class III: Is tongue pressure from tonsillar obstruction contributing?
Yes, directly. Isolated tonsillar enlargement (7%) drives Class III (37.5% vs population 1.9%)—tonsils narrow oropharynx, forcing tongue forward/downward against lower anteriors, proclining incisors and shifting mandible mesially. Adenoids alone (12% Class III) lack this lower-level pressure effect.
In Class III: Is this a true skeletal Class III or a pseudo-Class III?
Pseudo-Class III (functional). Forward tongue thrust from tonsils creates mesial molar relation + lower incisor procline, mimicking skeletal but reversing post-tonsillectomy via normalized tongue posture and mandibular growth (GH normalization). True skeletal lacks airway trigger; differentiate via tonsil grade + tongue eval



