RPE reduces the size of adenoids and tonsils? I don’t think so!
Some orthodontists heavily promote maxillary expansion for the treatment of paediatric sleep apnoea. However, the evidence for the effects of this treatment is relatively weak. The authors of this new paper claim that RPE reduces the size of the tonsils. But does it?
It appears that adenoid and tonsillar enlargement may lead to obstructive sleep apnea in children. The first-line treatment for this condition is tonsillectomy. It is also claimed that maxillary expansion by orthodontists leads to a reduction in airway resistance and other changes that alleviate OSA. However, as we have discussed before, the evidence is weak as there are no clinical trials in this area. The authors of this paper suggest that RPE may alleviate adenoid and tonsillar hypertrophy and reduce OSA. They carried out a study to look at this interesting question.
A team from Stanford University did this study. Sleep Medicine published the paper.
Impact of rapid palatal expansion on the size of adenoids and tonsils in children*
Audrey Yoon et al. Sleep Medicine. 92: 96-102.
What did they ask?
The aim of their study was to;
“Evaluate volumetric changes in adenoid and palatine tonsil size following RPE in a paediatric patient population”.
What did they do?
They did a retrospective evaluation of the case records of patients treated in two specialist orthodontic practices.
The team collected the records of 60 paediatric patients and divided these into a treatment (expansion) and untreated control group.
The treatment group had RPE to correct narrow maxilla, posterior crossbite, arch length discrepancy and a transverse skeletal discrepancy between the maxilla and the mandible. The clinician did this treatment with a hyrax expander activated 0.25mm per day for 4-6 weeks.
The control group did not have treatment because of the patients’ personal and financial reasons. This is an important issue, and I will return to this later.
The clinicians took CBCT images at the start of treatment and 13.8 months later. They also collected Paediatric Sleep questionnaire data and BMI at each time point.
Two blinded calibrated examiners measured the CBCT images to record the volumes of the palatine tonsils and adenoids. They did not report any other measurements from the scans.
What did they find?
They presented data in several tables. I was confused about their statistical analysis because they did not make a comparison between the groups. The only statistics that they presented were within-group comparisons. They found a statistically significant change in the size of the tonsils and adenoids for the expansion group. However, there was no change in the control group. As a result, I looked at their data closely and compared the tonsil and adenoids at time 2 between the groups. This is the data that I found.
|Control||2786 (2260-3310)||5829 (4610-7050)|
|Expansion||2241 (1930-2520)||3531 (2970-4100)|
|Difference||-545 (-2.32 to 1091) (NS)||-2298 (-3344 to-1251) (p<0.001)|
They also reported a significant reduction in PSQ scores for the expansion group from 5.81 to 3.75 (p<0.001). However, they did not report this data for the untreated group.
Their overall conclusions were;
“This study demonstrated that RPE led to a significant reduction in the size of adenoids and palatine tonsils, revealing another long-term benefit of treatment”.
“Furthermore, the significant reduction in the volumes of the adenoids and tonsils can be attributed to an increase in nasal volume. This decreases air velocity and resistance in the nasal cavity, thereby improving the irritation of the lymphoid tissues”.
Their reference to this statement was from their paper on the DOME technique. I am not sure that they can extrapolate this statement to RPE?
What did I think?
Regular readers of this blog will know that I rarely review retrospective and other poor studies. However, I will review these papers when their findings may be used to promote treatments that lack an evidence base. This is my main reason for looking at this paper.
I am sorry to say that I struggled to find anything good about this piece of research. For the following reasons:
- The control group was selected on their ability to pay for their care. This is likely to mean a difference in socioeconomic status (SES) between the treatment and control groups. As a result, they completely ignored a massive confounder. This is a fundamental flaw.
- The authors selectively reported findings. For example, they did not report the PSQ for the control group.
- They misquoted the literature (see above)
- They carried out within-group comparisons and did not compare between the groups. This is a classic “spinning” of research findings. We have discussed this before.
- They did not do a sample size calculation, and the groups were of different sizes.
- They took CBCT images for the control group at the end of the observation period. I could not think of a good clinical reason for doing this.
- We do not know the amount of expansion that they achieved.
- CBCT has a poor contrast resolution for soft tissues. To reduce the effects of this, they used hard tissue landmarks. However, they concede that this method may overestimate the adenoid volume.
- They did not collect data on patients’ use of allergy medication. This may have been different between the two groups.
I cannot help thinking that much better research than this is needed to support the efforts of our airway orthodontic physicians.
Emeritus Professor of Orthodontics, University of Manchester, UK.
Have your say!
I believe that there is a basic flaw in directly relating RPE to the observed reductions in adenoidal and tonsillar tissue
The cause of adenotonsillar hypertrophy is a combination of excess volumes of unfiltered and untreated air passing over the lymph nodes and causing them to become inflamed and engorged.
These lymph nodes are normally flushed by the lymphatic system which is largely driven by the diaphragm,
Mouth breathing children are almost universally upper chest breathers so the diaphragmatic movement is vestigial at best.
It is the combination of overloading and under flushing these nodes that causes them to hypertrophy.
By lowering the roof of the mouth – which is also the floor of the nose – RPE will free up some nasal space making it easier to breathe nasally. On its own I struggle to see a direction connection – other than an accidental benefit.
RME “reduces” the size of the adenoids and tonsils is wrong.
RME “decreases” the size of enlarged adenoids and tonsils to its normal size is true.
I really glad to see these kind of studies investigating the issue which is not touched yet neither by the orthodontists nor by the ENT or the other doctors.
There are hundereds of studies evaluating the dental and skeletal effects of RME, and it is time to investigate the medical effects of this procedure.
The RME helps “normalization” of the upper airway system by increasing the upper airway volume and the quality of air passing to the lungs.
The main outcome in RME treatment is “normalization” of related struructures and so the systems. Similarly in this study the authors found that the enlarged adenoids and tonsils return to its normal size after RME.
Thanks a lot to the authors for this valuable study. 🙏
Thank you Dr. O’Brien for sharing this study.
I completely agree with Dr. Babacan’s observations that: A. The authors of the study you’d critiqued have provided a valuable service in that they’d dare to test their hypothesis that posits at least one defensible/supportable reason for why RME (when applied to transverse deficient maxillas) has been observed to improve QOL and general health as is reported in myriad med-dent journals over the past century or so; and B. You, yourself sir, did us all a similar favor by publishing your critique……thank you.
You might want to explore other published papers Kevin that are of a ‘controlled observational trial’ research design, as were ALL published scientific papers prior to the Nuremberg Trials of WW II btw, that show secular trends towards RME as being a mitigating intervention for not only transverse malocclusion phenotypes, but often also for naso-respiratory systemic co-morbidities; maybe start with this one: (Yoon Chang, Lisa J. Koenig, Jessica E. Pruszynski et al ‘Dimensional changes of upper airway after rapid maxillary expansion: A prospective cone-beam computed tomography study. Am J Orthod Dentofacial Orthop 2013;143:462-70). The authors of this paper concluded from a small sample of 13 year-olds with Dx: MTD and Naso-respiratory co-morbidities, ‘These results confirm the findings of previous studies of the effect of rapid maxillary expansion on the maxilla. Additionally, we found that only the cross-sectional area of the upper airway at the posterior nasal spine to basion level significantly gains a moderate increase after rapid maxillary expansion.’ I think if some of your readers who might be comfortable with treating kids in the deciduous, early/middle/late-mixed dentition and/or the early permanent dentition, will find a similar T-1/T-2 dimensional change at the Bason-PNS line, and also likely at the Linder-Aronson Ad-1/Ad-2 ‘adenoid spaces(Linder-Aronson S. Adenoids: their effect on mode of breathing and nasal airflow and their relationship to characteristics of the facial skeleton and the dentition. Acta Otolaryngol 1970;(Supp 265):1-132.), as a Tx response from RME for Dx:MTD (with/without posterior crossbite)…..and normalization of tonsils and adenoids size might/mightn’t be a concurrent Tx effect.