Читать книгу 6Ways to Design a Face - Paul Coceancig - Страница 9
ОглавлениеWHY OBSTRUCTIVE SLEEP APNEA OCCURS
The baby with Pierre Robin syndrome born with a small jaw. The Class II adolescent with braces and impacted third molars (Fig 2-1). The middle-aged overweight person with sleep-disordered breathing (SDB) and a new diagnosis of obstructive sleep apnea (OSA) supported by a high apnea-hypopnea index (AHI) score. These are all the same person but at different stages of life.
FIG 2-1 Before and after photographs (taken 6 weeks apart) of a 12-year-old adolescent girl with severe mandibular hypoplasia (caused by Melnick-Needles syndrome; see Fig 8-1) associated with snoring and sleep-disordered breathing (SDB). Weighing only 51 pounds, this patient’s small size reflects the scientific evidence that SDB has significant negative effects on growth hormone (GH) assay and associated growth retardation. Early adolescent treatment by modern jaw surgery correction methods such as intermolar mandibular distraction osteogenesis (IMDO) have clear benefit.
I am 52 years old as I write this, and behind me lies a professional lifetime of treating small jaws, treating the effects of small jaws, and avoiding the effects of small jaws. As a maxillofacial surgeon, I offer a perspective that is not as a sleep dentist offering a mandibular advancement device (MAD), a throat surgeon offering uvulopalatopharyngoplasty (UPPP), an otolaryngologist prescribing tonsillectomy, a craniofacial surgeon treating a neonate with jaw distraction, an orthodontist offering braces, an oral surgeon recommending tooth extraction, a psychiatrist prescribing amphetamines to a sleepy schoolchild, or a respiratory physician offering a sleep study and a continuous positive airway pressure (CPAP) device.
As a maxillofacial surgeon, my training is as a dentist, an oral surgeon, a bite specialist, a general medical doctor, and as a primary medical-surgical specialist in corrective jaw surgery.
I can stretch a small jaw, and with it I stretch out the tongue behind it, the face in front of it, and the spaces between the crowded teeth as well. I have particular insight into these issues because I suffer from the same diseases that I treat. But how do my surgical therapies also medically treat my patients? What are my overall therapeutic aims?
MY JOURNEY WITH OSA
I was innately skinny as a young adult and adolescent. Until I was 28 years old I weighed only 150 pounds and had a body mass index (BMI) of 21, with only about 5% body fat. I always had mildly small jaws (see Introduction), but I never snored. I was just a mouth breather drooling silently into my pillow.
As my active young adult life increasingly became settled, my children were born, and work started to dominate my life, I sat more, exercised less, socialized with more dinners, traveled in planes, and lived in more hotels. So I started putting on weight. My new external environment eventually gained a new equilibrium, and internally my equilibrium changed to suit. I put on more muscle. I was physically stronger. But I was also putting on much more fat too.
By the time I was 34 years old, I was up to 174 pounds with a BMI of 25. When I hit 42, I weighed 209 pounds and my BMI was 30. By 51, I was almost 245 pounds, and my BMI was a shocking 35. My fasting blood glucose, which should have been below 5.5, was now 6.0. My fasting insulin, which should have been 8.0 at most, was now 11. My knees and ankles hurt when I walked. I was grumpy. After plane trips my ankles swelled. My wardrobe was a museum of thin to fat.
In the 8 years previous, I had successfully tried four diets, each of which lasted a year and brought me down to 165 pounds, but something always stopped the momentum, and my weight would return to a newer and bigger number. And if I plotted these new weights (y) on an age (x) scale, they fell on the one straight line.
What was happening was that I could not change my environment, and I could not permanently keep a low weight to suit that environment. I still worked at the same job. I still had the same social world, the same town that surrounded me. The same kids, the same food, the same supermarket, the same kitchen, the same subtle pressures. So when you combined everything into one big ball of different-colored strings, it all really meant I just lived in the same inflexible universe of modern human life.
My weight was essentially an end-point expression of my internal balance point. My internal equilibrium was always reverting back to the same point that was defined by the static equilibrium that surrounded me. And I was aging. And everything was getting unnoticeably and slowly worse. It was all so subtle. But what really woke me up was when I started snoring. Literally.
It’s a horrible feeling. The choking. And it would force me to suddenly sit up, trying to catch my breath. And I’d stay propped up with pillows scared to fall asleep again. I put on a home monitor, and it gave me an AHI score around 5. Not much. My phone had an app that recorded how well I slept. It wasn’t good. Another app recorded my snoring sounds. It sounded like a freight train. More frightening was when I fully obstructed, and I wasn’t breathing at all.
I woke up tired. My thoughts were muddled. I spontaneously fell asleep. Everywhere. In movies. Watching TV. Lying in the grass under a tree. My mood changed too. I was less patient. Maybe I was more curmudgeonly. So I had bariatric surgery, and had almost 90% of a very large stomach permanently removed. It is called a “gastric sleeve.” The weight loss was dramatic and relentless and permanent. By 212 pounds my snoring had stopped, and my old shirts started fitting around my neck. At 198 pounds my blood glucose and fasting insulin levels were completely normal. My blood pressure returned to 120/70. By 165 pounds I was completely healthy again. I wasn’t hungry at all, and I easily maintained small meals. My ankles were normal. My knees worked normally. And of course I was sleeping fully, my dreams returned, my emotional balance was regained, and my thinking restored.
I couldn’t change the equilibrium of my external world, so I forced permanent change on my own internal equilibrium. Even as surgeons, we are all dependent consumers on our own craft and colleagues.
SNORING AND DENTISTRY
Snoring has an enormous impact on people and society. Sleeping partners are the first affected, and eventually our bodies too start telling us that something’s wrong (Fig 2-2). The health effects of poor sleep, including poor rapid eye movement (REM) cycles, chronic hypoxia, hypocognition, cardiovascular hypertension, and of course obesity, bleed into our personal lives, and this has become a real problem for society at large. When seen across a lifetime, the individual and economic effects of SDB make snoring a major health crisis that has real effects across the world economy.
FIG 2-2 The symptom of snoring coupled with an AHI score from a sleep study ignores completely the anatomical reasons underlying why the patient has recurrent apnea episodes during sleep. Our faces are so much a part of the consideration of personal identity that we forget that faces are functional objects. A person born with a small mandible relative to the rest of their body will always have that disproportion as their body ages. Overbites, camouflage orthodontics, big tonsils, and eventually OSA are all part of the same life journey that many of us travel.
Snoring causes lethargy. Poor sleep translates into reduced cognition and reduced physical activity. Snoring has a direct effect on every facet of the way each of us performs, lives, and remains healthy. While we can see the direct day-to-day effects of a poor night’s sleep, in the long term, snoring’s effects are cumulative—and relentless.
In 1923, Pierre Robin was the first person in the world to relate dentistry to snoring. While we associate Pierre Robin syndrome (and the micromandible) to his name, what he actually described were three things. First, Robin recognized that at least 40% of all Europeans (he was a Parisian dentist) had small mandibles. He called this condition mandibular hypoplasia. Second, Robin observed that all people with a small mandible snored. He saw the effect of a collapsed tongue on the back of the throat and gave the condition a name—glossoptosis. Third, Robin developed a jaw splint to hold the mandible forward, and with it the back of the tongue. The use of the device was life-changing for patients who suffered from breathing difficulty at night. Pierre Robin called this invention the Monobloc. It lives on today, with little recognition of his profound ideas, in the form of modern orthodontic MADs.
Today, the management of SDB represents an enormous worldwide medical economy. We know that snoring, upper airway resistance syndrome (UARS), and its end-expression of OSA is a major contributor to the development of obesity, diabetes, and cardiovascular disease in the forms of hypertension, stroke, and heart attack risk. We also know that OSA, UARS, and SDB have primary effects related to childhood cognitive performance and physical growth (see Fig 2-1) and adult-related risk of traffic accidents or workplace injury.
The Australian government, along with the Royal Australasian College of General Practitioners, has dedicated enormous economic and medical resources to the endeavor of surveillance, diagnosis, and management of SDB. Australia has led the way with developing treatments for snoring. Both the CPAP machine and at least one major dental (MAD) device company, SomnoMed, began their lives in backyard Australian garages. For almost 100 years, the dentist has been front and center of the war against snoring, and Australian dentists have helped lead the way for the past 20 years.
Most of us really don’t know what causes UARS. And people may not know the small mandible is a major primary cause of snoring. Physicians find this difficult to see, because a fat neck and obesity and aging often mask the small chin. In older kids, dentists recognize the Class II malocclusion associated with the small mandible relatively easily. But in adults, this dental sign of the small mandible can be obscured by the camouflage orthodontics the patient had during adolescence.
By identifying the small mandible and recognizing glossoptosis, the dental practitioner is the primary means of identifying the risk of snoring. Whether it is in the child presenting with a big dental overbite or in the adult presenting in the late stages of full-blown OSA, the dentist is front and center in the ability to offer definitive help.
By working with the orthodontic practitioner, sleep physician, or maxillofacial surgeon, the dentist becomes much more than someone giving fillings, extracting teeth, or applying splints. They become a frontline oral physician, applying their expertise of head and neck anatomy and clinical diagnosis for the cure of a first-world medical disease.
OBSTRUCTIVE SLEEP APNEA
The stories that many older people offer when discussing why they are on a CPAP machine often start with the terrifying discovery of their unconscious apneic states (Fig 2-3). What started as innocent weight gain, or complaints of daytime tiredness or general mental fogginess, or a sleeping partner’s complaint of relentless snoring, eventually becomes a cry of an unbearable, life-dependent, and desperate need for medical help.
FIG 2-3 (a) The person with increased UARS will obstruct their upper airway between their soft palate and upper epiglottis at approximately the level of the 2nd and 3rd cervical vertebrae (inset). This is called a closed torus or horn torus. The author anatomically calls this C3ERPO, or 3rd cervical, upper epiglottic, retropharyngeal obstruction. (b) Using increased air pressure will drive air via the nose and push open the collapsed airway (torus) through the collapsed C3ERPO column (large inset). Increasing nasal air pressure through the CPAP can be titrated against the upper airway resistance, pneumatically opening the collapsed torus, until airway passage occurs through the C3ERPO region. The temporomandibular joint (TMJ) remains in its normal position (small inset). (c) Pulling the mandible forward through use of a MAD will directly pull the lower part of the C3ERPO column forward and hold the mouth partially open, allowing mouth breathing to occur (large inset). The forward position of the mandible moves the TMJ out of its fossa (small inset), which can lead to the development of TMJ pathology. The splint itself can orthodontically retrude the maxillary teeth and procline the mandibular teeth, eventually leading to development of a chronic malocclusion.
Diagnosing OSA
The general medical practitioner’s referral to a sleep specialist can be a frustrating one for their patient. Linked up to machines and monitors through wires and stickers—and in a hospital bed with technicians and soft lights, strange sheets, and different pillows—is not a true replication of your own bedroom and your own natural state. In this anxious environment, many people find it hard to fall asleep. Or they wake up early and often.
And the test, unless it is repeated regularly and averaged, is not truly a reflection of how well or poorly a patient naturally sleeps at home and over many months. For many people who snore and who take part in a sleep study, they may still come away without a positive test outcome to confirm that they have OSA. Without a critical AHI score barrier (> 5 apnea or hypopnea episodes an hour), the offer of relief through CPAP may be frustratingly denied; or, at best, a repeat sleep study, with all the attendant inconveniences of that, is all that may be offered.
AHI SCORE
Usually, an admission to the hospital provides a sleep technician who will monitor a range of physiologic activities during sleep. Restlessness, blood-oxygen saturation, brain wave activity, nasal air movement, blood pressure, heart rate, and breathing effort are all measured. In the morning, the sleep physician will then analyze the data in a way that will give a number. This number is called the apnea-hypopnea index or AHI. It is a reflection of the number of sleep-wake cycles and low oxygen periods—or choking attacks—a person may or may not have per hour and averaged over the sleeping period. It is scored as mild (5–14), moderate (15–29), or severe OSA (30+).
While snoring, poor sleep, or daytime tiredness is often part and parcel of why people attend a sleep study, for the sleep physician the important medical question is to confirm whether a person is suffocating in their sleep or not. Having apnea literally means you are not breathing. And without breathing your blood-oxygen levels can fall low enough that you may simply not wake up. Ever.
Having a high AHI number (> 5 in adults), along with other measurement parameters, will help confirm a diagnosis of OSA. Being diagnosed with OSA is important to know, because the condition is linked to developing high blood pressure as well as myriad irreversible problems such as arterial wall thickening, stroke risk, heart disease, kidney disease, and diabetes. Most importantly, OSA is associated with a real association of reduced life span, which is a product of developing diseases that directly arise from having chronically low blood-oxygen levels.
Even though it may be the reason why a person first went for a sleep study, a complaint of snoring fundamentally does not primarily support a diagnosis for OSA, and there are no physical signs, other than the AHI score, that a doctor can search for that will positively support a diagnosis of OSA. Some patients who snore are not actually measurably choking in the night. Hospital-based studies exist to assess whether the patient has a critical number of apnea or hypopnea episodes; they are not designed to determine whether that patient has the risk factors that may or may not meet the criteria for OSA in the future. Nevertheless, the diagnosis of OSA is one that belongs to the sleep physician. For an AHI score above 5, CPAP is the remedial treatment of choice by the sleep physician to reduce the AHI score.
Treating OSA
Unfortunately, the medical profession is less interested in “why” or “how” a patient is obstructing their airway than whether or not they are actually suffocating in their sleep. We know that medically treating airway collapse during sleep, regardless of the reason, is relatively accessible. And as long as you haven’t reached a physical end-point, for most people there is at least a limited promise of potential relief.
All a person needs is two things. The first is a mask and a machine that can deliver continuous positive airway pressure via the nose and mouth (Fig 2-4). This is called a CPAP device.
FIG 2-4 (a) Lying awake, the tongue has enough tone to resist gravity, and the retroglossal airway is patent. (b) With deepening sleep, there is a loss of tongue tone, and under gravity the retroglossal airway collapses—producing airway obstruction—and apnea occurs. (c) A positive increase in airway pressure using CPAP can partially overcome retroglossal airway collapse for most (but not all) people. Mathematically, CPAP works best up to the horn torus, but not past the horn torus.
The second thing is personal tolerance. Without tolerance, a person with OSA will not be able to use a CPAP machine for 8 hours a night, every night, for the rest of their life.
CPAP THERAPY
The effectiveness of CPAP therapy is measured by the AHI score through repeat sleep studies. The practical effective goal of CPAP is to reduce the AHI score by reducing the average number of apnea or hypopnea episodes per hour a person suffers while they are asleep.
However, CPAP does NOT reverse hypertension, diabetes, obesity, heart disease, or stroke risk. And, more importantly, CPAP does not cure a person of OSA. CPAP will never give anyone a permanent AHI of 0 because, fundamentally, a sleep study does not acknowledge or eliminate the reasons why OSA is happening in the first place.
CPAP does NOT reverse hypertension, diabetes, obesity, heart disease, or stroke risk. And, more importantly, CPAP does not cure a person of OSA.
SYMPTOMS AND COMPLAINTS OF OSA
Ironically, the very same complaints that often bring the patient to the clinic for testing are not measurable or primary goals of CPAP therapy—things like getting a better night’s sleep or feeling better during the day.
A person’s set of symptoms and complaints may be wide, and they may even seem oddly disconnected to OSA or to each other. They can include insomnia in bed—they may be having an arousal as they fall asleep lying on their back—while somehow easily falling asleep at their desk with their head forward over a book. General anxiety and depression is commonly reported, as is poor concentration or poor work or scholastic performance. There may be specific complaints, seemingly unrelated to each other, such as muscle soreness, neck problems, recurrent headaches, or teeth grinding or jaw clenching or TMJ problems. People can complain of general fatigue, poor sports participation, general unfitness, and maybe even more general problems such as vague stomachache, irritable bowels, general muscle pain, restless legs, or chronic tiredness. And they may complain of ongoing weight gain that is almost impossible to control, slow down, or reverse.
All of these personal concerns are not measured or reported in a sleep study. And these complaints are not reflected in an AHI score either. Even though they may be considered effects or associations of OSA, whether they go away or not using CPAP is unpredictable and unmeasurable.
MAD THERAPY
Another treatment option for OSA offered by sleep dentists is the MAD, or mandibular advancement device (Fig 2-5). The MAD helps to hold the mandible and back of the tongue forward and may help with breathing at night (Fig 2-6). Like CPAP, the effect of the MAD can be measured by an AHI score, and the sleep physician may suggest a MAD if CPAP does not seem to be tolerable for their patient.
FIG 2-5 For some patients, the CPAP can be intolerable. Also, with extensive obstruction, CPAP pressures may not be enough to overcome airway collapse. The only other device that has been shown to provide a known and objective (nonsurgical) improvement to the AHI score, and possibly also to other symptoms, is the MAD. These dental splints are given a range of different proprietary names and are marketed on a broad range of therapeutic claims or comfort levels. But all of them are variations of Pierre Robin’s original Monobloc invention. The one main advantage of the MAD is that by activating the wedge and screw in the top appliance, it can incrementally extend the mandible forward. In achieving symptomatic relief, and a reduction of AHI score, it is possible to ascertain the distance that jaw surgery may need to permanently overcome to open the collapsed nighttime airway.
FIG 2-6 (a) Lying awake, the tongue has enough tone to resist gravity, and the retroglossal airway is patent. (b) With deepening sleep, there is a loss of tongue tone, and under gravity the retroglossal airway collapses—producing airway obstruction—and apnea occurs. (c) Opening the mouth and advancing the mandible pulls the hyoid and epiglottis forward (the lower part of the C3ERPO column), but only allows for oral breathing to occur. The MAD is far more effective at opening the closed torus surrounding the obstructed airway than the CPAP device. Unlike CPAP, the MAD does not allow for nasal airflow to occur. Successful use of a MAD to relieve someone of OSA absolutely confirms the presence of glossoptosis.
Just like CPAP, the MAD is also not a permanent cure for OSA, and it may or may not assist in addressing daytime symptoms and complaints. Unlike CPAP, however, a MAD can only enable oral breathing, not nasal breathing. And, unlike CPAP use, which really does not have any secondary side effects apart from intolerance, the MAD can lead to significant TMJ issues such as pain, joint clicking, and jaw muscle discomfort. Because the MAD holds the whole bite and mandible forward, chronically it can also lead to permanent negative effects on a person’s bite and normal chewing patterns.
How body fat aggravates OSA
Obesity is seen so often with snoring and OSA that it is casually seen as causative. We also see OSA occurring in people who have thick muscular necks, such as weight lifters. This common association of obesity, thick necks, increased intra-abdominal fat, and older age—and the simple fact that we see OSA so rarely in people who have thin necks and who are generally skinny—means we assume that being fat is the cause of snoring and OSA.
However, these co-observations of obesity and OSA reflect more of an association, or at best an aggravation. The association between the two is not true causation. There are many people who are fundamentally skinny, and young, and who still have upper airway collapse. What really causes OSA is far more fundamental and detailed than a simple blame upon obesity. That being said, it is absolutely true that weight reduction can eliminate OSA, but only where weight gain caused and fueled and aggravated the full end-point expression of OSA to finally occur.
When considering how obesity aggravates OSA, it is helpful to imagine the neck as essentially a donut (Fig 2-7). As fat is deposited under the skin and around the intestines, so too does fat thicken the neck and constrict the soft flabby tissues that surround the upper airway. As the donut gets bigger, the hole in the middle gets smaller. If the hole was already small to begin with, the donut doesn’t need to get much bigger before the inside hole doesn’t exist anymore. When the hole just pinches, this is called a horn torus. As neck thickening advances, the inner hole closes more and more, until the donut achieves the shape of a sphere. A patent torus can be given a value > 1, meaning airway passage is absolute. A horn torus, where the inner hourglass airway has just pinched, has a value of 1. A perfect sphere has a value of 0. Between 1 and 0 is the mathematic chance that a CPAP or MAD has the ability to regain the inner hole and regain nighttime airflow.
FIG 2-7 A radial neck and inner airway can be teratologically represented and topologically considered as a simple toroid (T). (a) A thin neck has a wide hole and allows for normal laminar noiseless airflow (T > 1). (b) A thickening neck, induced by increasing muscle mass or inner fat, makes the hole smaller (T → 1). The passage of air thins and increasingly becomes turbulent and noisy. Air resistance increases. The venturi of increased inner airflow, particularly with aerobic exercise, induces further collapse. (c) Eventually the neck can be so wide, and the inner airway so small, that we approach a horn torus (T = 1). Increasing airflow pressure through CPAP can overcome this near-complete toroidal collapse, but barely. (d) Once the toroid has collapsed, only increasing air pressure can reliably recreate an already closed airway (0 < T < 1). The greater the toroidal collapse, the more the torus approaches the shape of a sphere (T = 0), where air pressures to regain an airway approaches infinity. Therapeutically creating an incollapsible airway occurs only by making the toroid thinner—through weight loss—or by coring the inner walls through ablative ear, nose, and throat (ENT) surgery; physically stretching the toroid through a MAD; or permanently by advancing the jaw surgically. The toroid provides a physical mathematic model to explain why people become intolerant of CPAP, or are CPAP resistant, where AHI scores do not adequately reduce with CPAP therapy.
Weight control is a huge part of controlling OSA. Fat scans such as dual-energy x-ray absorptiometry (DEXA) can accurately see and monitor fat store loss through diet-selective high-protein, low-carbohydrate ketogenesis. Very low–calorie or food volume–restrictive diets (portion control) can be enhanced by use of intragastric balloons inserted by a gastroenterologist. Weight loss can be more permanently obtained through surgery such as gastric sleeve or gastric bypass procedures performed by an upper GI surgeon.
Surgical treatment of OSA
ENT SURGERY
The common surgical referral given for a person who is unable to control their OSA or snoring—either with CPAP or with a MAD—is ear, nose, and throat (ENT) surgery. ENT surgery traditionally looks at the nasal septum, nasal turbinates, nasal valves, adenoids, tonsils, soft palate, and back of the tongue.
For the nasal septum, the ENT surgeon will resect, carve, and straighten it. This is called a functional septoplasty. ENT surgeons can also open the doorways and remove the walls between the sinuses. This is called fine endoscopic sinus surgery or FESS.
For the turbinates, the ENT surgeon can reduce them. This is called a turbinectomy. For the nasal valves (nostrils), grafts can be placed to widen them. These are called nasal alae, nasal tip lifts, or nostril battens or overall may be called a functional rhinoplasty.
For enlarged or encroaching adenoids behind the soft palate, the ENT surgeon can scrape them away. This is called an adenoidectomy. For enlarged tonsils that seem to fill the back of the mouth behind the tongue, the ENT surgeon can remove them. This is called a tonsillectomy.
For a vibrating soft palate, the ENT surgeon can tighten and scar it using radiofrequencies or surgery and also remove your uvula, especially if it is long. This is called a uvulopalatopharyngoplasty or UPPP. If the back of the tongue is considered too large for the throat, the ENT surgeon can surgically partially remove it. This is called a partial posterior wedge glossectomy.
I place corrective jaw surgery at the top because fundamentally it should correct the absolute “why” behind choking in your sleep in the first place.
The aim of all of these procedures is to reduce the encroachments of the walls and sides and roof and passages of the sinuses, nose, and back of the throat into the airway. In the small rooms and corridors of the upper airways, the ENT surgeon is removing the furniture and inner walls, scouring the paint, and opening the doorways. If, after all this surgery, the patient is still snoring, the ultimate ENT option is to bypass the whole house and create a direct and permanent breathing tube in your trachea. This is called a tracheostomy.
CORRECTIVE JAW SURGERY
At the bottom of the OSA treatment list is corrective jaw surgery, or maxillomandibular advancement (MMA) as ENT surgeons call it. It runs dead last, and it is the only surgical procedure that is not performed by an ENT surgeon. It is also the least understood operation of them all.
For me, and for the reasons I explain in this book, an assessment toward corrective jaw surgery should be at the top of the medical pile. I place it at the top of the list not because it is the best at treating an AHI score. I place it at the top because it is the best at treating everything else that isn’t an AHI score. I place corrective jaw surgery at the top because fundamentally it should correct the absolute “why” behind choking in your sleep in the first place.
THE TRUE CAUSE OF SNORING AND OSA
The fundamental premise of this book is that upper airway obstruction, which leads eventually to apneic episodes during sleep, is caused by a collapsing tongue. This tongue obstruction is called glossoptosis, and it has been a known phenomenon since at least 1923 when it was first described by Pierre Robin in Paris. This tongue collapse occurs more easily when you lie on your back—and during a state of deep sleep—when the body and the tongue lose all tone.
The second fundamental premise of my book is that glossoptosis is inherently associated with people who have small jaws. Small jaws are very common in Western society. Small jaws lead to bad bites and crowded teeth in adolescents, which itself leads to adolescent orthodontic interventions. In older adults, especially as weight is naturally gained, this same small jaw, and the same glossoptosis, inherently leads to a reduced airway lumen, which, promoted by weight gain and the laxity of aging, evolves into the development of snoring and then OSA during deep sleep (Fig 2-8).
The fundamental premise of this book is that upper airway obstruction, which leads eventually to apneic episodes during sleep, is caused by a collapsing tongue.
FIG 2-8 Treating the older patient who had camouflage orthodontics as an adolescent through the process of remedial BIMAX is curative for the glossoptosis that is intrinsically linked to the small mandible. Corrective jaw surgery permanently holds the upper airway open (the C3ERPO column) and effectively resists the development of OSA. How that surgical process occurs, and the links that tie all the bits that make up a face together, is explained in the remainder of this book.
The third and most important premise I make is that there is a surgical remedy that can reverse the associated glossoptosis of the small jaw in adolescents as well as correct for the orthodontic consequences of the small jaw. The evolution of this philosophy is to recognize that variants of the same surgical jaw procedures can be used in older people who already have developed OSA in order to cure them of their glossoptosis and therefore reverse their tongue obstruction that is actually causing their OSA.
Remedial corrective jaw surgery
For me, the common reports of adolescent dental crowding, dental extractions, impacted teeth, and orthodontic problems such as a bad bite or prominent anterior teeth in younger years are just as indicative of the reasons underlying why a person has glossoptosis than a standalone consideration of AHI score, CPAP history, diet trials, BMI measure, or medical background. Orthodontics, oral surgery (by way of dental extractions), and ENT procedures (tonsil removal and nasal surgery) are common stories of childhood, and they are also common to many older people who snore or who have OSA.
A lot of what follows in this book is an explanation of how crowded teeth, bad bites, and big tonsils occur as a result of the general and common smallness of our jaws. Permanently making small jaws a normal size is a well-documented and scientifically supported fundamental and permanent cure for OSA. Corrective jaw surgery is designed to work whether you are in deep supine sleep or wide awake, breathing heavily and running on a treadmill. By curing people of breathing difficulties, such as snoring, or of the risk or presence of OSA, the jaw correction surgeon is also helping to prevent a range of other diseases that are very commonly associated with OSA.
Very fundamentally, maxillofacial surgeons are not sleep physicians. We are jaw correction surgeons. We are not here to treat an AHI score or to compete against CPAP or snoring splints or ENT surgeons wanting to remove tonsils. As jaw surgeons, we are not treating what the obstructions are causing. Instead we are treating what causes the obstructions We want to change the collective story. The summation of the airway anatomy, apneic episodes, snoring, daytime tiredness, and all the other potentialities of the problem.
As surgeons, we are not treating what the obstructions are causing. Instead we are treating what causes the obstructions.
Unlike sleep physicians, we do not have Band-Aid cures. And unlike ENT surgeons, we are not wanting to take bits and pieces away. We are not here to remove the furniture from the room. Everything we do is about making the room bigger to help patients keep all their anatomical furniture. And to keep patients living better and more healthily, and hopefully for a much longer period of time—free of the common diseases we usually associate with abnormal aging.
