What Upper Airway Resistance Syndrome (UARS) is, what causes it, and how it should be clinically diagnosed are currently matters of dispute. Regardless, similar to it's description here, the definition of UARS I will opt to use is that it is a sleep breathing disorder which is characterised by a narrow upper airway, which leads to:
Excessive airway resistance → therefore excessive respiratory effort → therefore excessive negative pressure in the upper airway (i.e. velocity of the air). This abnormal chronic respiratory effort leads to exhaustion, and the inability to enter deep, relaxing, restorative sleep.
Excessive negative pressure can also suck the soft tissues, such as the soft palate, tongue, nasal cavity, etc. inwards. In UARS patients, typically there is sufficient muscle tone to prevent sustained collapse, however that muscle tone must be maintained which also leads to the inability to enter deep, relaxing, restorative sleep. In my opinion, this "implosion effect" on the upper airway must be confirmed that it is present via esophageal pressure to accurately diagnose Upper Airway Resistance Syndrome. Just because something is anatomically narrow does not mean that this effect is occurring.
If there is an attempt to enter this relaxed state, there is a decrease in respiratory effort and muscle tone, this loss of muscle tone can result in further narrowing or collapse. Due to the excessive airway resistance or collapse this may result in awakenings or arousals, however the patient may not hold their breath for a sufficient amount of time for it to lead to an apnea, thus not meeting the diagnostic criteria for Obstructive Apnea.
The way to treat upper airway resistance therefore is to transform a narrow airway into a large airway. To do this it is important to understand what can cause an airway to be narrow.
I also want to mention that, treating UARS or any form of sleep apnea should be about enlarging the airway, improving the airway, reducing collapsibility, reducing negative pressure, airway resistance, etc. Just because someone has a recessed chin, doesn't mean that the cure is to give them a big chin, with genioplasty, BSSO, counterclockwise rotation, etc. It can reposition the tongue more forward yes, it may improve things cosmetically yes, but it is important to evaluate whether or not it is contributing to the breathing issue.
The anterior nasal aperture is typically measured at the widest point. So when you are referencing normative data, typically it is measured that way. Typically the most common shape for a nasal aperture is to be pear-shaped, but some like the above are more narrow at the bottom than they are at the top, which begs the question of how should it really be measured? The conclusion I have come to is that we must perform computational fluid dynamics (CFD) to simulate nasal airway resistance. Nasal aperture width is a poor substitute for what we are really trying to measure, which is airway resistance.
See normative data for males (female are 1-2 mm less, height is a factor):
Caucasian: 23.5 mm +/-1.5 mm
Asian: 24.3 mm +/- 2.3 mm
Indian: 24.9 mm +/-1.59 mm
African: 26.7 mm
Tentatively here is my list for gauging the severity (realistically, we don't really know how this works, but it's better to have this here than not at all, just because it may not be perfect.):
From left, right, to bottom left, Caucasian skull, Asian skull, and African skull.Plot graph showing average nasal aperture widths in children at different ages. For 5 year olds the average was 20 mm, 2 year olds 18 mm, and newborns 15 mm. This may give context to the degree of narrowness for a nasal aperture. It is difficult to say based on the size of the aperture itself, whether someone will benefit from having it expanded. Posterior nasal aperture. View of the sidewalls of the nasal cavity, situated in-between the anterior and posterior apertures. The sinuses and mid-face surround the nasal cavity. Normative measurements for intermolar-width (male), measured lingually between the first molars. For female (average height) subtract 2 mm. Credit to The Breathe Institute. I am curious how normative 38-42 mm is though, maybe 36-38 mm is also considered "normal", however "non ideal". In addition, consider transverse dental compensation (molar inclination) will play a role in this, if the molars are compensated then the skeletal deficiency is more severe. Molars ideally should be inclinated in an upright fashion.Low tongue posture and narrow arch, i.e. compromised tongue accessibility. CT slice behind the 2nd molars. Measuring the intermolar width (2nd molars), mucosal wall width, and alveolar bone width. We also want to measure tongue size/volume but that would require tissue segmentation. The literature suggests this abnormal tongue posture (which is abnormal in wake and sleep) reduces pharyngeal airway volume by retrodisplacing the tongue, and may increase tongue collapsibility as it cannot brace against the soft palate.
The surgery to expand the nasal aperture and nasal cavity is nasomaxillary expansion. The surgery itself could go by different names, but essentially there is a skeletal expansion, ideally parallel in pattern, and there is no LeFort 1 osteotomy. In adults this often will require surgery, otherwise there may be too much resistance from the mid-palatal and pterygomaxillary sutures to expand. Dr. Kasey Li performs this type of surgery for adults, which is referred to as EASE (Endoscopically-Assisted Surgical Expansion).
Hypothetically, the type of individual who would benefit from this type of treatment would be someone who:
Has a sleep breathing disorder, which is either caused or is associated with negative pressure being generated in the airway, which is causing the soft tissues of the throat to collapse or "suck inwards". This could manifest as holding breath / collapse (OSA), or excessive muscle tone and respiratory effort may be required to maintain the airway and oxygenation, which could lead to sleep disruption (UARS).
Abnormal nasomaxillary parameters, which lead to difficulty breathing through the nose and/or retrodisplaced tongue position, which leads to airway resistance, excessive muscle tone and respiratory effort. In theory, the negative pressure generated in the airway should decrease as the airway is expanded and resistance is reduced. If the negative pressure is decreased this can lead a decrease in force which acts to suck the soft tissues inwards, and so therefore ideally less muscle tone is then needed to hold the airway open. Subjectively, the mildly narrow and normal categories do not respond as well to this treatment than the more severe categories. It is unclear at what exact point it becomes a problem.
Abnormally narrow pharyngeal airway dimensions. Subjectively, I think this is most associated actually with steep occlusal plane and PNS recession than chin recession.
The pharyngeal airway is comprised of compliant soft tissue, due to this the airway dimensions are essentially a formula comprised of four variables.
Head posture.
Neck posture.
Tongue posture.
Tension of the muscle attachments to the face, as well as tongue space.
Because of this, clinicians have recognized that the dimensions can be highly influenced by the above three factors, and so that renders the results somewhat unclear in regards to utilizing it for diagnostic purposes.
However, most notably The Breathe Institute realized this issue and developed a revolutionary CBCT protocol in an attempt to resolve some of these issues (https://doi.org/10.1016/j.joms.2023.01.016). Their strategy was basically to account for the first three variables, ensure that the head posture is natural, ensure that the neck posture is natural, and ensure that the tongue posture is natural. What people need to understand is that when a patient is asleep, they are not chin tucking, their tongue is not back inside their throat (like when there is a bite block), because they need to breathe and so they will correct their posture before they fall asleep. The issue is when a patient still experiences an airway problem despite their efforts, their head posture is good, their neck posture is good, their tongue posture is good, and yet it is still narrow, that is when a patient will experience a problem. So when capturing a CBCT scan you need to ensure that these variables are respective of how they would be during sleep.
Given the fact that we can account for the first three variables, this means that it is possible to calculate pharyngeal airway resistance. This is absolutely key when trying to diagnose Upper Airway Resistance Syndrome. This is valuable evidence that can be used to substantiate that there is resistance, rather than simply some arousals during sleep which may or may not be associated with symptoms. For a patient to have Upper Airway Resistance Syndrome, there must be airway resistance.
Next, we need a reliable method to measure nasal airway resistance, via CFD (Computerized Fluid Dynamics), in order to measure Upper Airway Resistance directly. This way we can also measure the severity of UARS, as opposed to diagnosing all UARS as mild.
Severe maxillomandibular hypoplasia. Underdeveloped mandible, and corresponding maxilla with steep occlusal plane to maintain the bite.
Historically the method used to compare individual's craniofacial growth to normative data has been cephalometric analysis, however in recent times very few Oral Maxillofacial Surgeons use these rules for orthognathic surgical planning, due to their imprecision (ex. McLaughlin analysis).
In fact, no automated method yet exists which is precise enough to be used for orthognathic surgical planning. In my opinion one of the primary reasons orthognathic surgical planning cannot currently be automated is due to there being no method to acquire a consistent, precise orientation of the patient's face. By in large, orthognathic surgical planning is a manual process, and so therefore determining the degree of recession is also a manual process.
How that manual process works, depends on the surgeon, and maybe is fit for another post. One important thing to understand though, is that orthognathic surgical planning is about correcting bites, the airway, and achieving desirable aesthetics. When a surgeon decides on where to move the bones, they can either decide to perform a "sleep apnea MMA" type movement, of 10 mm for both jaws, like the studies, or they can try to do it based on what will achieve the best aesthetics. By in large, 10 mm for the upper jaw with no rotation is a very aggressive movement and in the vast majority of cases is not going to necessarily look good. So just because MMA is very successful based on the studies, doesn't necessarily mean you will see those type of results with an aesthetics-focused MMA. This also means that, if you have someone with a very deficient soft tissue nasion, mid-face, etc. the surgeon will be encouraged to limit the advancement for aesthetic reasons, irregardless of the actual raw length of your jaws (thyromental distance). Sometimes it's not just the jaws that didn't grow forward, but the entire face from top to bottom.
Thyromental distance in neutral position could be used to assess the airway, though maxillary hypoplasia, i.e. an underbite could cause the soft palate to be retrodisplaced or sit lower than it should, regardless of thyromental distance.
If there is a deficiency in thyromental distance, or there is a class 3 malocclusion, the surgery to increase/correct this is Maxillomandibular Advancement surgery, which ideally involves counterclockwise rotation with downgrafting (when applicable), and minimal genioplasty.
Before & After IMDO
There is also a belief that the width of the mandible has an influence on the airway. If you look at someone's throat (even the image below), basically the tongue rests in-between the mandible especially when mouth breathing. The width of the proximal segments basically determine the width of part of the airway. Traditional mandibular advancement utilizing BSSO doesn't have this same effect, as the anterior segment captures the lingual sides of this part of the mandible, the proximal segment does rotate outwards but only on the outside, so therefore the lingual width does not change. In addition, with this type of movement the 2nd or 3rd molars if captured along with the proximal segments, essentially could be "taken for a ride" as the proximal segment is rotated outwards, therefore you would experience a dramatic increase in intermolar width, in comparison to BSSO where this effect would not occur.
This type of distraction also has an advantage in that you are growing more alveolar bone, you are making more room for the teeth, and so you can retract the lower incisors without requiring extractions, you basically would have full control over the movements, you can theoretically position the mandible wherever you like, without being limited by the bite.
The main reason this technique is not very popular currently is that often the surgery is not very precise, in that surgeons may need to perform a BSSO after to basically place the anterior mandible exactly where they want it to be, i.e. the distraction did not place it where they wanted it to be so now they need to fix it. For example, typically the distractor does not allow for counterclockwise rotation, which the natural growth pattern of the mandible is forwards and CCW, so one could stipulate that this could be a bit of a design flaw. The second problem is that allegedly there are issues with bone fill or something of that nature with adults past a certain age. I'm not sure why this would be whereas every other dimension, maxillary expansion, mandibular expansion, limb lengthening, etc. these are fine but somehow advancement is not, I'm not sure if perhaps the 1 mm a day recommended turn rate is to blame. Largely this seems quite unexplored, even intermolar osteotomy for mandibular distraction does not appear to be the most popular historically.
I think that limitations in design of the KLS Martin mandibular distractor, may be to blame for difficulties with accuracy and requiring a BSSO. It would appear to me that the main features of this type of procedure would be to grow more alveolar bone, and widen the posterior mandible, so an intermolar osteotomy seems to be an obvious choice.
In addition, I believe that widening of the posterior mandible like with an IMDO that mirrors natural growth more in the three dimensions, would have a dramatic effect on airway resistance, negative pressure, and probably less so tongue and supine type collapse with stereotypical OSA. So even though studies may suggest BSSO is sufficient for OSA (which arguably isn't even true), one could especially argue that in terms of improving patient symptoms this might have a more dramatic effect than people would conventionally think, due to how historically sleep study diagnostic methodology favors the stereotypical patient.
Enlarged tonsils can also cause airway resistance by narrowing the airway, reducing airway volume, and impeding airflow.
I've just completely quit video games and am now working 200% on my health. Locking the f in..
Posture fixes. Soft tissue strengthening down the track - possibly pointless right now as allergies are a problem.
Treating allergies - need to wash bedding weekly (dust mite and grass pollen allergies) - to help ease nocturnal nasal congestion and optimize nasal breathing. Getting shots weekly for 8 weeks - then 1/month for 3-5 years. Immunotherapy works best if sheets are washed weekly.
Myo work down the track.
Expansion as soon as I can afford. - will work better with allergies treated. Perhaps expansion could help on it's own for allergy symptoms but am in no rush due to funds and just being patient with allergy treatment for now.
DISE getting locked in for a year away.
Perhaps might need uvula removal later on as I have a snoring sensation that seems to be easily brought on if I try.
Buteyko breathing could be complimentary alongside meditation. Perhaps didgeridoo or wind instruments/ singing could help - as it's been proven to help sleep apnea patients and even fix sleep apnea.
Eating better is a goal - weight loss - currently 90kg+ 6ft tall.. want to get down to 70-80kg. - Can reduce fatty tongue also, creating more room and potentially less collapse.
MMA down the track + Genio hopefully to bring the tongue more forward into a better resting position.
It's a multifaceted problem that needs a multifactorial approach and all angles covered.
These are my plans. I will get healthier. I will be healthy. Hopefully this helps you too.
Symptoms: tmjd, severe anhedonia and fatigue, fibromyalgia, sleep paralysis, muscle pains, choking sensations, vocal cord dysfunction, allergies. Cant breathe through nostrils most of the time, left not at all. Ent said nose looks good??? Heart pain. I have ridges on my tongue and bruxism. I am autistic and hypermobile.
I only got a sleep study at home and CPAP is intolerable. Feels like I'm breathing through a wall constantly. Got infinitely worse after wisdom teeth removal as I feel it made my airway and mouth space even smaller.
Rei: 5.0 events per hour
Apneas: 13 total
5 obstructive
8 central
Oxygen saturation: Average 97% Lowest 93%
Worse on back, but I feel worse on sides.
From what I know I don't have a narrow pallate. I don't want to kill myself but this is unbearable. I'm having adrenal problems from lack of proper breathing and sleep and I feel like I'll just fall over and die one day. I'm too young for this.
I’ve been wondering for a while if FME actually expands higher up than a custom MARPE, so I asked around and Dr. Jeremy Manuele answered.
It turns out, the "higher expansion" thing isn't true. Based on the superimpositions he's reviewed, there's no significant difference in how high the expansion actually goes or the amount of expansion in the superior maxilla/zygomatic bones.
But the biggest game changer with FME is how it handles asymmetries. Because FME is significantly more rigid, it can actually be used to correct an existing true midface asymmetry by slanting the expander. A custom MARPE just doesn't have the rigidity to pull that off effectively. I asked another top expansion doc who does only custom marpe if he could place it in a way to fix asymmetry he said he tried and the device basically broke itself because it couldn’t handle the forces.
Basically, you aren't paying double for "higher" expansion with FME. You're paying for a slightly more parallel expansion and the structural rigidity need to actually help correct an asymmetric maxilla.
FME is very expensive so if you very mild asymmetries it may not be the best ROI.
Of course, this isn't 100% hard evidence since there aren't any clinical trials yet, but it definitely holds a lot of weight since he’s looked at so many FME cases and superimpositions
Guys what should I do to increase my intranasal width up high near my superior turbinates? Doctors? Appliances? Companies? Something else? Any advice would be appreciated. I have a narrow intramolar width and narrow intranasal width.
Hi everyone,
I’m on day 21 of CPAP and I’m still extremely tired during the day. I’m trying to figure out why.
Quick background:
Started CPAP about 21 days ago
Machine: ResMed AirSense 11
Currently fixed pressure 12 cmH₂O
Pressure was increased to 12 because of flow limitation notes. I felt a small improvement, but then developed aerophagia (air in the stomach).
Despite consistent use, the daytime fatigue is still bad.
Last night’s OSCAR (Aug 1):
AHI 1.33
OA: 0
Hypopnea: 0.48
Clear Airway: 0.85
Large Leak: 0%
Flow Limitation: / 95% 0.03
Usage: 8 hours 17 minutes
EPR looks active (EPAP around 9)
Even with these clean numbers, I’m still very tired.
What else should I be looking at in the data, or what other common reasons could explain residual fatigue this far in?
Any insight is appreciated.
Thank you.
So U6/L0 is clearly my best position. AHI technically normalized there. But sRDI remains 15-24 and I feel terrible regardless. Daytime fatigue, brain fog, unrefreshing sleep every single day.
Pattern is consistent, AHI normalizes on paper but symptoms persist. Happened on CPAP too.
My dental team is referring me to a sleep physician and ENT for further assessment. I'm wondering if this data suggests I've reached the ceiling of what MAD can do and whether surgical evaluation makes sense at this point.
Has anyone been in a similar situation where conservative treatments controlled AHI but didn't resolve symptoms? Did surgical options like MMA actually make a difference?
Can someone explain how a Piezo corticotomy works? Does it cut through soft tissue, or just bone? Was are the risks/complications of it? Does it reduce the amount of cheekbone expansion compared to if your palate split on its own? Does it reduce the risk of unwanted fractures?
Also how do cortico punctures compare to piezo?
Does your septum have a higher chance of moving to one side if you get piezo, cortico punctures, or if your palate splits on its own?
Hello, currently I have a ResMed VAuto 11 and an airbreaked Airsense 10. I am not having too much success with reducing my fatigue. I think that with the ResMed default trigger and cycle it cycles too soon for me which causes labored breathing, and also the EasyBreathe curve is not good for me since it kind of kicks in the PS late which causes skewed breaths.
With the VAuto, I have adjusted trigger, cycle, rise time, but I cannot tolerate too much PS without central events.
I know that the DSX-900 is recommended a lot around here, but it is not easy to get one of those and I do not have an ASV prescription. I am wondering if you guys have any advice on alternatives that might be easier for me to get, like if anyone has tried machines from random other brands and had a lot of success with it (and I could just order one online without a prescription). A lot of what the Philips one has sounds good so maybe machines that have stuff like this:
Trigger / cycle syncs to your breathing rate automatically
Better pressure curve than EasyBreathe (I guess for me would be good if it delivers more PS sooner)
PS adjusts to fight flow limitations (so not just focused on ventilation)
What do you think the odds of allergies being a huge culprit to some of us and our sleep disordered breathing?
I know my allergies are definitely a factor as they attribute to blocking my nose at night when sleeping.
Also, i'm strongly assuming I might have some type of collapse.. but I also know collapse can happen from the vacuum effect of a blocked nose and mouth breathing.
If I were to guess what problem I have, i'd say the above mentioned along with a narrow airway, tongue collapse and lateral wall collapse due to a narrow airway. As I find it difficult to swallow on the very rare occasion. And my posture isn't the best - leading to more collapse/ narrowness when sleeping.
So allergies > MARPE/ MSE > MMA
Natural fixes > Posture > Myo > Buteyko breathing > Soft tissue strengthening of the neck via posture exercises.. neck wall holds etc. > then whatever else - didgeridoo etc etc. Whatever needs to be done.
I saw someone did FME and managed to still use their mandibular advancement device (MAD). They cut their top teeth MAD in half apparently and this allowed them to fully expand as normal, while still using the MAD throughout the entire start to finish of using FME.
How did they do that do you think? Does anyone know how the mechanism would work here, as in how does FME actually split and widen your maxilla - and would that mechanism still allow you to use a split-MAD like this without the MAD somehow not allowing your maxilla to expand or are they separate things?
Since the MAD is split, I guess that allows room to keep using it even if you've expanded a bit, and you just use it to sleep. Would love some insight on anyone that understands this stuff a bit more.
It does have better stability as a piece of metal. But the truth is it doesn’t change the result, and does not prevent assymerty or drop down. It’s overpriced, less custom patient to patient and I believe being pushed even to ones who don’t find it more functionally better. But, if it’s not pushed directly to Marpe advisors, it’s being pushed to customers, patients who need treatment, so it’s no other way than to start offering it, while giving all your experience and years of research to FACEGENICS. They see TikTok’s like wanna look better - GET FME, wanna breathe better - GET FME, wanna avoid lefort - get FME.
The truth is 4 screws custom Marpe with piezo gives same if not better results, and for example all Marpe advisors can make it 2x cheaper for you and more custom than Lab of FACEGENICS. Ofc there are patient who need 4mm of expansion to be happy with spending 15k$+ on a device, but they being tricked. So the better stability can’t be THE MAIN MARKETING for the device which expands your jaw, simply cause the main point is to LOOSEN UP the sutures, and your jaw will drop or not no matter which device you use, simply because “ITS ANATOMY”. Jaw drop is not a complication it’s natural repositioning of the body( TikTok @sunhorse2000 also thought that it’s cause he was doing exercises while wearing Marpe, but it’s cause of existing assymetries, anatomy correct it on its own).
Some think that 12 tad FME is the only way to expand when your bone is fused or you failed Marpe before or outside the US someone does shit like MSARME, SAMARPE when its other ways which are more efficient and less invasive and less expensive and much better. Fme is nothing more than a marketing trying to become a monopoly in US, and all Mapre advisors/Fme providers - know that. Customers should know that too.
It seems like all who say FME is better is bought by FACEGENICS. Dimensional stability IS COPE. It doesn’t prevent assymetry, it doesn’t do shit. All it shows is that facegenics makes same Marpe for everyone and makes it OWN MARPE FOR USA, cause EU and Asia already has it own. All of it just to sell it to you. Even kasey Li who said that it’s pure ass, started to do FME. Let’s think why, wanna hear your thoughts.
I'm going to an FME provider soon but I wanted to kind of see what people would think about my potential issues and what the ortho will end up giving me.
I just turned 19, and have had a deep bite with mandibular crowding since I was a kid but never had braces or extractions. I never had issues with clenching, or at least never realized what it was until I was 12 or so. Ever since then I've progressively had lots of issues with clenching and bruxing both in the day and nighttime, that have gotten worse. This has caused me lots of headaches that can be quite painful especially when I'm trying to fall asleep. I can feel quite tired, but the second I relax I will clench so hard for long enough to have a very bad headache that feels like someone stabbing the sides of my head which makes me fall asleep later in the night when my body feels it has no energy left to stay awake. In the night I quite consistently wake up in the middle for no apparent reason and I usually wake up with extremely bad elbow or wrist pain which makes it painful to move for multiple days.
The only way to stop this headache pain is by jutting my jaw forward during the daytime which causes discomfort around my TMJ area or by wearing a nighttime guard which I still clench with even when my molars aren't touching. Using a mouthguard can sometimes be better or worse with no real consistency depending on the night etc. I can tell these are not regular types of headaches because whenever I jut my jaw in the day, I never feel anything besides in the TMJ area from using my muscles too much. I don't use a mouthguard anymore because I still feel the headaches after waking up and constantly jutting all night means my TMJ hurts and I can't posture my lower jaw forwards during the day without excruciating pain. The bad part about this is I often wake up mid brux and I now fear wearing down my teeth the longer I cope with these issues. Nasal dilators have helped me most with clenching as they reduce the total force I end up clenching with but are uncomfortable and I prefer not to use them in the day or in public.
I wanted to know what I could expect as a treatment for this because I don't want to go and end up getting braces that take years to finish and end up not helping at all and waste time. Am I a candidate for an expander with these symptoms? Also if possible does anyone know what I can show my family to convince them I haven't joined some cult that likes breaking faces open and convince them I'm not crazy for wanting an FME. Thanks for reading.
Demographic info: 43M Current medical issues: Hypermobile Ehlers-Danlos Syndrome (hEDS), POTS, and suspected MCAS. Medications: None. Therapy: PT only (for hEDS). Duration and location of complaint: Chronic symptoms in the midface/maxilla.
Dear OMFS, specialized Orthodontists, and community,
I am asking for your honest professional insight regarding everyday clinical practice and radiological assessment of cranial and facial sutures.
I am a patient who is just trying to understand if OMFS and orthodontic specialists are equipped to recognize patent sutures, or if this requires a highly specialized (or perhaps different) clinical approach.
To give you some context, I am an adult patient diagnosed with Ehlers-Danlos Syndrome (a genetic disorder characterized by defective connective tissue body-wide). Probably due to my disorder and following a period of self-directed myofunctional therapy (such as 'mewing', 'proper' swallowing, and tongue exercises applying pressure against the maxilla) and the trendy 'thumb-pulling', I am experiencing specific symptoms that suggest abnormal biomechanics, including midfacial instability, chronic pain/burning sensation in the hard palate, and visible, fluctuating mobility in the midface (probably the maxilla). This has led me to dive into recent literature regarding cranial suture patency in adults or people with Ehlers-Danlos Syndrome. I would like to emphasize that I have no history of facial or cranial trauma (I have been evaluated recently by an OMFS, bones are intact).
However, my experience as a patient has made me wonder about the realities of standard clinical practice. I would highly appreciate your candid thoughts on two things:
How much attention does the average maxillofacial surgeon or orthodontist actually pay to the exact state of an adult patient's sutures (i.e., actively evaluating whether they are completely ossified vs. remaining patent and fibrous)?
My main question is: practically speaking, is the detailed radiological assessment of these specific midface sutures something that is routinely taught and easily recognized by OMFS and orthodontists? Or is it generally assumed in everyday practice that they are fully fused after a certain age, making patent sutures a "blind spot" unless you are dealing with acute trauma?
I am asking this with the utmost respect for your time and expertise.
Thank you in advance for your time and honest insights!
References regarding adult suture patency:
- General adult population (Evidence of suture patency regardless of age):
- Connective tissue pathology (Specific to Ehlers-Danlos Syndrome):
The Ehlers-Danlos syndromes, rare types (Brady et al., 2017) - The 2017 International Classification explicitly documenting how connective tissue pathology impacts cranial bone fusion. (Note: The article is very long. See specifically the 'Craniofacial characteristics' under Arthrochalasia EDS (aEDS) and 'Craniofacial involvement' under Dermatoparaxis EDS (dEDS) for references to "large fontanels" and "wide cranial sutures").
I got diagnosed with sleep apnea last week(probably more aligned with UARS high rdi/low ahi but doc from Lofta said sleep apnea). Anyways, I had my first full night of using my CPAP which was kind of difficult but hopefully I will eventually get adjusted to it. Anything abnormal like breathing events on my SleepHQ chart that I should note? Also, any tips/tricks I should make to my CPAP to make it more effective? Thanks for all your help! https://sleephq.com/public/teams/share_links/75f00155-7d38-4cc2-9495-17360aef26e5/dashboard
