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Clinical Challenges
October 2005

Adenoid Facies and Nasal Airway Obstruction: Cause and Effect?

Author Affiliations




Arch Otolaryngol Head Neck Surg. 2005;131(10):919-920. doi:10.1001/archotol.131.10.919

Adenotonsillectomy remains one of the most commonly performed surgical procedures in the pediatric age group, with the 2 most frequent indications for surgery being obstructive sleep apnea and chronic adenotonsillitis. As nicely exemplified by Clark, there is an on-going argument in the literature about whether prevention of craniofacial dysmorphologic traits constitutes an additional indication for adenotonsillectomy.

Can severe nasal airway obstruction (NAO) and mouth breathing lead to abnormal craniofacial growth? This argument arises from the description of the so-called adenoid facies. Adenoid facies has been vaguely defined as a long, thin face with malar hypoplasia, high-arched palate, narrow maxillary arch, and angle class II malocclusion. At the root of the dispute is cause and effect: Can children with adenoid facies have NAO, or can NAO lead to adenoid facies? The answer to the first question is unquestionably yes. However, the answer to the second question is unknown.

Ravindhra G. Elluru, MD, PhD

Ravindhra G. Elluru, MD, PhD

What arguments support the claim that NAO can lead to craniofacial dysmorphology? Children with NAO tend to be mouth breathers when awake or asleep. With the mouth open, the tongue places less pressure on the palate. Furthermore, with the mouth in a chronically open position, the forces on the mandible, temporal-mandibular joint, and dental arches are altered. These small pressure or force changes are thought to lead to aberrant growth of the craniofacial skeleton. This line of thought is based on the multitude of known examples in which small perturbations in pressure applied to the facial skeleton lead to alterations in growth. Orthodontics is based on the principle of applying small forces to alter the growth of the facial skeleton and dentition. A constant and localized pressure to the skull, such as those incurred in children with preferred head position during supine sleep, leads to nonsynostotic plagiocephaly.1-3 Finally, pressure changes applied from chronic thumb sucking lead to craniofacial skeletal changes.4-6

Unfortunately, the first studies that implied a causal relationship between NAO and mouth breathing are antiquated and difficult to access for evaluation. Recent studies7-10 have only superficially explored this issue by demonstrating a temporal correlation between NAO and craniofacial dysmorphologic traits, but none have demonstrated a cause-and-effect relationship between NAO and abnormal craniofacial growth. The difficulty in directly addressing the causal relationship between NAO and craniofacial dysmorphologic traits may lie in the fact that it would be both difficult and unethical to design a long-term longitudinal study of children with untreated NAO. The closest approximation to such a study is that by Linder-Aronson,11 who demonstrated that the craniofacial skeleton of children successfully treated for NAO returned to more normal dimensions. However, the results of Linder-Aronson’s study11 should not be overinterpreted given that this study may have lacked the appropriate controls.

Animal models of nasal airway obstruction have been developed. Specifically, Vargervik and Harvold12 created NAO in young rhesus monkeys by using silicon splints and demonstrated the development of craniofacial changes similar to those described for adenoid facies. For the most part, these craniofacial changes returned to normal after relief of the nasal airway obstruction. However, there are important differences in primate and human craniofacial development; the results from this study, too, should not be overinterpreted.

In summary, all practicing otolaryngologists are familiar with the concept of adenoid facies. Current knowledge supports the correlation between NAO and adenoid facies. However, little to no data exist that currently validate the hypothesis that NAO leads to abnormal craniofacial development. Given the other known morbidities associated with NAO and the efficacy with which patients with NAO are currently treated, the quest to answer Clark’s hypothesis may have minimal practical implications.

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Article Information

Correspondence: Ravindhra G. Elluru, MD, PhD, Department of Pediatric Otolaryngology, Cincinnati Children’s Hospital Medical Center, 3333 Burnet Ave, MLC 2018, Cincinnati, OH 45229 (ravi.elluru@cchmc.org).

Financial Disclosure: None.

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