How has our interest in the airway changed over 100 years?

Since the beginning of our specialty, our understanding of the link between function and facial growth and development has progressively improved. Today, we know that children with sleep-related breathing problems will often develop distinctive facial characteristics. In adults, sleep apnea can result in serious morbidity and mortality. Orthodontists can ask sleep-related questions in the health history to help identify sleep breathing disorders. Treating these patients presents unique opportunities for orthodontists to collaborate with other medical specialties to improve a patient’s health and treatment outcome. Research presented in our Journal in the next century may shed new light that will help us better identify the problem and aid the specialty in developing more effective evidence-based treatment. Additional efforts are needed to understand the physiology, neurology, and genetics of sleep breathing disorders.


  • Children with sleep-breathing disorders (SBDs) often develop distinctive facial features.

  • In adults, sleep apnea can result in serious morbidity and mortality.

  • Orthodontists can ask sleep-related questions in the health history.

  • Additional efforts are needed to understand the physiology, neurology, and genetics of SBDs.

Well before the functional matrix theory of Moss, some people already recognized the possible link between function and facial growth. The Danish otorhinolaryngologist Wilhelm Meyer in 1868 in describing children with sleep-related breathing problems noted that they often have a different facial appearance than do children without these problems. In the first issue of this Journal 100 years ago, M’Kenzie wrote an article entitled “Some points of common interest to the rhinologist and the orthodontist.” He described the development of a narrow palate and several osseous malformations resulting from mouth breathing and the presence of enlarged adenoids. Since then, the effect on facial growth of the respiratory function has become one of the more heated controversies in the modern orthodontics.

Harvold et al completed a landmark study using monkeys to show the relationship between the modification of facial growth and simulated mouth breathing. Many studies have suggested that a vertical growth pattern is associated with mouth breathing and obstruction of the pharyngeal airway. However, the relationship between mouth breathing and the development of certain types of malocclusion is still debatable.

Our interest in the airway has been expanded into sleep breathing disorders (SBDs). According to the third edition of the International Classification of Sleep Disorders, SBDs are classified into 3 basic categories: central sleep apnea, obstructive sleep apnea (OSA), and sleep-related hypoventilation/hypoxia. Public awareness of health problems related to OSA has led many orthodontists to take an interest in this condition.

It has been known that untreated OSA can result in serious morbidity and mortality mostly caused by cardiovascular disease and traffic accidents. It has been suggested that children with OSA have poor learning skills, behavioral problems, attention deficit hyperactivity disorder, and depression.

Anatomic compromise, pharyngeal dilator muscle dysfunction, lowered arousal threshold, ventilatory control instability, or reduced lung volume tethering have been proposed as the pathophysiologic mechanisms leading to OSA. Surface tension of the liquid lining of the upper airway can also be a contributing factor. OSA patients have higher surface forces acting on the upper airway compared with healthy persons. Several studies have suggested that there is a potential link between specific genomes and OSA. Anatomy (obesity, craniofacial structures), the size of the upper airway soft tissues, ventilatory control abnormalities, and respiratory responses to resistive loading during sleep can be affected by genetic factors.

Chronic inflammation in the upper airway has negative effects on the airway dilator muscles through the alteration of the biomechanical properties of the upper airway and its sensory neuronal output. One study suggested that prolonged untreated OSA might lead to sensory impairment of the upper airway structures. Trauma from snoring may contribute to neurogenic lesions of the upper airway that lead to increased collapsibility and increased risk for SBDs. There have been some efforts to provide a potential molecular signature for the presence and consequences of OSA.

Diagnosis is based on a comprehensive sleep evaluation, which includes a history and physical examination, and findings identified by a sleep study or polysomnography. Multiple questionnaires have been developed to screen for further testing, but none is accurate enough to replace polysomnography, which is considered the standard for diagnosing OSA. However, polysomnography does not provide information regarding the site of the upper airway obstruction or whether there are multiple sites of obstruction. Several diagnostic imaging techniques have been used for identifying the obstruction site in SBDs, such as cephalometric radiography, acoustic reflection, fluoroscopy, magnetic resonance imaging, computed tomography, cone-beam computed tomography (CBCT), and nasopharyngoscopy.

Cephalometric radiography is widely available, inexpensive, and the most commonly used for airway evaluation. On the other hand, it is a 2-dimensional representation of a 3-dimensional space and has limitations to providing volumetric information. Many studies, however, have stressed the value of cephalometric radiographs in the assessment of airways. It has been suggested to use the cephalometric radiograph as a screening tool for determining whether more intensive follow-up is needed.

CBCT has been used to evaluate the common sites of obstruction in 3 dimensions with OSA patients. Many studies have shown that OSA patients have smaller airway cross-sectional areas and volumes than do normal subjects. However, CBCT is static, not dynamic, imaging, and static imaging correlates poorly with OSA. Few studies have shown significant dynamic airway changes in OSA patients with dynamic 3-dimensional computed tomography imaging. Most current CBCT images are taken when a patient is in an upright position, not in a supine position. Differences exist in upper airway geometry and functionality between the supine and upright positions. The patient’s wakefulness must also be considered because the airway and surrounding soft tissue structures differ between sleep and wakefulness. Considering these limitations, even though the obstruction or the constriction in the upper airway is observed in cephalometric radiographs or CBCT images, further comprehensive evaluation is needed to confirm SBDs.

Orthodontists can identify the early signs of SBDs by adding sleep-related questions in the health history and evaluating airway structures in the cephalometric radiographs. If there are high-risk factors related to SBDs such as obesity, allergy, increased neck girth, and certain cephalometric characteristics, it is important to refer a patient to a sleep specialist for the comprehensive evaluation.

Behavioral treatment such as weight loss, avoidance of alcohol and sedatives before bedtime, positional therapy, positive airway pressure therapy, oral appliances, and surgical procedures are treatment options for OSA. The most common treatment for OSA uses oral appliances, which have been considered a simple, least invasive, tolerable, and effective treatment option for mild-to-moderate OSA, or for severe OSA patients who refuse or do not tolerate continuous positive airway pressure therapy. Since clinical symptoms for OSA seem obvious and it is easy to identify a constricted upper airway on cephalometric radiographs or CBCT, orthodontists often encounter a dilemma in diagnosing OSA without polysomnography, and offer oral appliances as a treatment tool. However, polysomnography needs to be done before treatment with oral appliances to confirm the OSA and establish the baseline information for the subsequent treatment. Many oral appliances, especially mandibular anterior repositioning appliances, are similar to Class II removable functional appliances. Many reports have suggested that long-term use of oral appliances with mandibular advancement can cause occlusal and skeletal changes, and these changes need to be monitored periodically. Patients with severe OSA who cannot tolerate or who are unwilling to adhere to positive airway pressure therapy may be indicated for surgical treatment. Depending on the obstruction sites, the surgical techniques include nasal, oropharyngeal, maxillofacial, and bariatric surgeries by different specialties. Maxillomandibular advancement is currently the most effective surgical procedure after tracheotomy for the treatment of OSA in adults. A few reports suggest that maxillomandibular advancement should be considered for the initial or the sole surgical approach in treating OSA. However, the optimum amount of advancement to maximize the treatment effect and minimize the negative esthetic effect is not clear.

For patients with a large skeletal Class III malocclusion, to decrease the risk of OSA, some suggest that it would be better to consider maxillary advancement along with a small amount of mandibular setback instead of a large amount of mandibular setback.

Rapid palatal expansion increases both nasal and pharyngeal airway dimensions. Some evidence supports a breathing pattern change from oral to nasal and improvement in nasal patency after rapid palatal expansion. However, other researchers question the breathing benefit from rapid palatal expansion.

The effects of rapid palatal expansion on the nasal airway should not be used to advocate altering a normal maxilla to an excessively expanded maxilla. Currently, rapid palatal expansion is not recommended alone as a treatment tool for SBDs or improving nasal breathing without an orthodontic indication.

A number of studies have shown how different orthodontic treatment modalities affect the upper airway, including protraction facemask, cervical headgear, orthodontic extraction, and Class II functional appliances. However, based on the current literature, it is difficult to draw evidence-based conclusions about how each orthodontic treatment affects the upper airway. More randomized controlled trials are needed.

The ideal treatment approach for any disease is identifying the etiology, understanding the pathophysiology, and removing the etiology. Most treatments focus on structural changes to increase the airway space. As previously mentioned, many etiologic factors and possible pathophysiologic processes lead to SBDs. If there is no clear understanding of how each treatment alters anatomy, structures, and physiology, it may lead to ineffective treatment or unnecessarily invasive treatment. Additional efforts are needed to understand the nature of SBDs, not only from the structural standpoint, but also from the physiologic, neurologic, and genetic points of view, to improve diagnosis and treatment.

SBD is not a simple problem. However, it can be a great opportunity for orthodontists to collaborate with other medical specialties to improve a patient’s health and treatment outcome. Since the beginning of our specialty, there has been a continual progression of improved understanding of the link between function and facial growth and development. Future research presented in our Journal in the next century may shed a light for us to better identify the problem and aid our specialty in developing more effective evidence-based treatments.

Orthodontists today still agree with the following statement written by M’Kenzie, as he concluded his article, “Thus in your orthodontic work you are engaged in a great labor for the prevention of disease not only in childhood but also later in life, and your efforts, when successful, make for the prolongation of life.”


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Apr 6, 2017 | Posted by in Orthodontics | Comments Off on How has our interest in the airway changed over 100 years?
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