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Do ortho extractions lead to SDB or OSA?

April 9, 2022
With an increased awareness of SDB/OSA, Alina Fintineanu, RDH, says we must be careful in claiming causation and allowing misinformation to guide our orthodontic treatment decision-making process.

Sleep-disordered breathing (SDB) is defined as “a syndrome of upper airway dysfunction during sleep that is characterized by snoring and/or increased respiratory effort secondary to greater upper airway resistance and pharyngeal collapsibility. Obstructive sleep apnea (OSA) is a sleep disorder that involves a significant decrease or cessation of airflow in the presence of breathing effort.”1

In more recent years, speculation has been rife about a causative relationship between extractions for orthodontics and SDB/OSA. It has been suggested that removing teeth, typically first or second premolars, will narrow the arch and therefore decrease the size of the airway, leading to or causing SDB or OSA. This theory has led some dental professionals to avidly oppose dental extractions for orthodontics, and instead push to “expand, expand, expand.” They urge their patients to seek third, fourth, and 10th opinions until they reach an “airway focused” practitioner who will agree to proceed without extractions. Ultimately, what does the scientific evidence say about this hot button topic?

Why do we extract in orthodontics?

Patients aren’t excited about the prospect of removing (typically) healthy teeth, and neither are we. While it is true that correcting a transverse deficiency through expansion has the potential to improve existing OSA, there is no evidence that it prevents its development in the future.

A large comparison study was done in 2015 on over 5,000 patients, assessing those who were treated without extractions and those who had four premolars extracted (during the years when the rate of extractions was around 35%–40% of cases, whereas now it is closer to 15%). No statistical difference was found in the prevalence of OSA in subjects who were treated with or without extractions.2

Related reading: Using Kobe Bryant's mamba mentality in your dental hygiene career

The truth is that not all cases are suitable for expansion. Let’s look at the basics: the upper arch has the anatomical feature of the midpalatal suture. In growing patients usually up to 15 years of age, this suture is not fused and contains soft cartilage. A rapid palatal expander (RPE) can be used to gradually separate the two halves of the palate; then it is kept in place for several more months until bone fills in the expanded area.

In nongrowing patients, the midpalatal suture is already matured. If we were to attempt to expand with an RPE, the crowns of the posterior teeth would tip outward, rather than true expansion occurring. If palatal expansion is needed in nongrowing patients, then it must be completed by Surgically Assisted Rapid Palatal Expansion (SARPE) or Microimplant Assisted Rapid Palatal Expansion (MARPE).

Why can’t everyone just be expanded?

The short answer here is arch coordination—the lower arch does not have a suture that can be expanded. Any “expansion” of the lower arch is just tooth movement; the actual result is uprighting or flaring outward of the teeth, and not actually moving bone.3 In order to resolve significant crowding on the lower teeth, we have two options: upright/flare the teeth outward or extract. The supporting structures of the teeth, bone, and gums must dictate the most stable course of treatment. In the goal of arch coordination, we cannot simply expand the upper arch by surgical or nonsurgical means; it must still “fit” the lower arch.

How do extractions affect the face?

Do extractions ruin faces? No, but poor orthodontic diagnosis and treatment planning has the potential to ruin faces with or without extractions. Dental, skeletal, periodontal, and facial soft tissue parameters need to be considered for exceptional outcomes. In patients with bimaxillary protrusion (often seen in the Asian demographic), the upper and lower incisors are proclined, typically combined with lip incompetence, anterior open bite, strain on the mentalis muscle, and a gummy smile. The treatment plan is extraction of four premolars, followed by retraction and retroclination of the anteriors.4 In these cases, extractions can significantly improve facial profile.

In severe crowding cases, if teeth are not removed to make space, then the anteriors (and lips) will flare outward, and patients may even look worse than before treatment. It is common for the ardent “nonextractionist” to push teeth outside of their bony housing, causing fenestration, dehiscence, and ultimately, long-term recession and periodontal attachment loss. Furthermore, studies show bicuspid extractions do not affect vertical facial height.5

Diagnosing OSA and gold standard treatment

The American Association of Orthodontists (AAO) released a white paper on the topic of orthodontics and sleep apnea, and I will summarize the significant findings here. Although dentists and orthodontists can screen for it, only a physician can definitively diagnose and treat OSA.

The gold standard treatment for adult OSA is continuous positive airway pressure (CPAP). Additional measures could include positional/medicinal therapy, hypoglossal nerve stimulation,6 weight reduction, management of nasal congestion and rhinitis, various surgeries of the oral soft tissues (tonsils, adenoids, tongue, frena), palatal/orthognathic surgery, genioglossus advancement, hyoid suspension, and avoidance of alcohol and sedatives before sleep.

For patients who cannot tolerate CPAP or do not respond to it, mandibular advancing oral appliances (OAm) and tongue-retaining devices can be effective in up to two-thirds of cases.7 Over time, however, these appliances can move the teeth and cause development of anterior crossbite, posterior open bite, reduction in overjet and overbite, and changes in facial height.

In pediatric patients, normal facial growth results in an increase in the anterior, posterior, and inferior skeletal boundaries of the airway, which combine with a decrease in soft tissue mass. This causes a huge increase in the airway starting from infancy and through childhood and the teen years. In direct correlation, multiple studies have shown that during phases of growth, childhood OSA remits without intervention.

Finally, the AAO states that “these changes in airway due to growth far exceed any orthodontic or orthopedic effects on airway shape and/or size.” In pediatric patients, hypertrophic adenoids and tonsils are the highest risk factors for OSA, with the first line of treatment being tonsillectomy and adenoidectomy.

Assessing airway function

One additional topic of note is the validity of cephalometric and cone beam computed tomography (CBCT) to assess airway function. While 3D imaging is more accurate in assessing airway bony structure and possible sites of constriction, CBCT provides no information on the function of the airway, susceptibility to collapse, or neuromuscular tone. The image is taken in an upright position with the patient awake, which defeats the purpose of considering the pathophysiology of OSA; therefore, CBCT cannot be used to accurately screen for SDB or OSA.

Do extractions cause or lead to SDB?

Finally, let’s return to our original question: do extractions for orthodontics cause or lead to SDB? It is important to understand and “has been demonstrated that a narrow airway does not result in OSA, but rather it is an inability for a patient’s airway muscles to compensate adequately that leads to obstruction and sleep-disordered breathing.”8,9

In patients where extractions have been performed to alleviate crowding or improve occlusion, no change in airway dimensions has been found. The mesial movement of molars increases space for the tongue and upper airway dimensions. Cross-sectional reductions have only been observed in patients with significant bimaxillary protrusion requiring extractions.10

In children and adolescents undergoing orthodontic treatment, an increase in airway volume and cross-sectional areas have been found in both extraction and nonextraction cases, likely the result of normal growth. In adults, it has been found that “dental extractions in conjunction with orthodontic treatment have a negligible effect on the upper airway.”11 Furthermore, no constriction of the oropharyngeal airway has been found during extraction or nonextraction orthodontic treatment, and there is “no quantitative evidence that reducing arch perimeter has any effect on oropharyngeal size.”12

The AAO concludes: “Overall it can be stated that existing evidence in the literature does not support the notion that arch constriction or retraction of the anterior teeth facilitated by dental extractions, and which may (or may not) be the objective of orthodontic treatment, has a detrimental effect on respiratory function.”8

Orthodontic treatment planning is complex and multifactorial. With the increasing awareness of SDB/OSA, there is nothing inherently wrong in looking for connections or wanting to prevent future airway issues. Where we must be careful, however, is in claiming causation and allowing misinformation to guide our decision-making process. Advising patients to avoid extraction orthodontic treatment at all costs due to the belief that it will cause/lead to SDB/OSA is mistaken at best and could significantly compromise results and stability in the short and long term. 

Editor's note: This article appeared in the April 2022 print edition of RDH magazine. Dental hygienists in North America are eligible for a complimentary print subscription. Sign up here.

References

  1. Memon J, Manganaro SN. Obstructive sleep-disordered breathing. In: StatPearls (internet). StatPearls Publishing; 2022. Updated August 14, 2021. Accessed January 8, 2022.
  2. Larsen AJ, Rindal DB, Hatch JP, et al. Evidence supports no relationship between obstructive sleep apnea and premolar extraction: an electronic health records review. J Clin Sleep Med. 2015;11(12):1443-1448. doi:10.5664/jcsm.5284
  3. Jorgensen G. Can orthodontic expanders be used on the lower teeth to avoid extractions? Jorgensen Orthodontics. August 15, 2019. Accessed January 8, 2022. https://www.jorgensenorthodontics.com/blog/can-orthodontic-expanders-be-used-on-the-lower-teeth-to-avoid-extractions
  4. Chu YM, Bergeron L, Chen YR. Bimaxillary protrusion: an overview of the surgical-orthodontic treatment. Semin Plast Surg. 2009;23(1):32-39. doi:10.1055/s-0028-1110099
  5. Zafarmand AH, Zafarmand MM. Premolar extraction in orthodontics: does it have any effect on patient’s facial height? J Int Soc Prev Community Dent. 2015;5(1):64-68. doi:10.4103/2231-0762.151980
  6. Maresch KJ. Hypoglossal nerve stimulation: effective longterm therapy for obstructive sleep apnea. AANA J. 2018;86(5):412-416.
  7. Sutherland K, Vanderveken OM, Tsuda H, et al. Oral appliance treatment for obstructive sleep apnea: an update. J Clin Sleep Med. 2014;10(2):215-227. doi:10.5664/jcsm.3460
  8. Behrents RG, Shelgikar AV, Conley RS, et al. American Association of Orthodontists. White paper: Obstructive sleep apnea and orthodontics. Updated March 15, 2019. Accessed January 9, 2022. https://www2.aaoinfo.org/wp-content/uploads/2019/03/sleep-apnea-white-paper-amended-March-2019.pdf
  9. Cheng S, Brown EC, Hatt A, Butler JE, Gandevia SC, Bilston LE. Healthy humans with a narrow upper airway maintain patency during quiet breathing by dilating the airway during inspiration. J Physiol. 2014;592(21):4763-4774. doi:10.1113/jphysiol.2014.279240
  10. Hu Z, Yin X, Liao J, Zhou C, Yang Z, Zou S. The effect of teeth extraction for orthodontic treatment on the upper airway: a systematic review. Sleep Breath. 2015;19(2):441-451. doi:10.1007/s11325-015-1122-1
  11. Pliska BT, Tam IT, Lowe AA, Madson AM, Almeida FR. Effect of orthodontic treatment on the upper airway volume in adults. Am J Orthod Dentofacial Orthop. 2016;150(6):937-944. doi:10.1016/j.ajodo.2016.05.013
  12. Shannon TP. Oropharyngeal airway volume following orthodontic treatment: premolar extraction versus non-extraction. (2012). Theses and Dissertations (ETD). Paper 231. http://dx.doi.org/ 10.21007/etd.cghs.2012.0284