The MEDQOR Podcast Network

Innovation is rampant in orthodontics—to the point that we’re seeing innovation within innovation. Take 3D printing, for example. The 3D printer alone—just the printer itself—has been revolutionary. It has allowed the orthodontic practice to take control and fabricate aligners in-office, on their own schedule. But it wasn’t the 3D printer alone that facilitated this. Along the way, additional innovations were needed—chief among them the thermoforming plastic material. And now, these materials are further evolving with a new material that allows for direct 3D-printed aligners. Orthodontic Products Chief Editor Alison Werner spoke to Ki Beom Kim, DDS, PhD, the Dr Lysle Johnston Endowed Chair in Orthodontics, and the program director in the orthodontic department at the Center for Advanced Dental Education at Saint Louis University, on a recent podcast episode about a new material that allows for direct 3D-printed aligners.
Kim and his colleagues have spent the last 3 years testing the Direct Aligner photopolymer material from the South Korean 3D printing material company Graphy. Their findings were recently published in Progress in Orthodontics. The team found that controlling material dimensions, structure, and properties of aligners directly—compared to thermoforming plastic sheets—has the potential to make the process of tooth movement faster, less wasteful, and more precise.

• “If you have a 3D printer, you can now directly print this aligner without having [a] model, without going through the thermoforming process,” said Kim, adding that, with this new FDA approved material, the in-office lab can skip several steps in the current manufacturing workflow, including cutting out the aligners and polishing before delivery to the patient.
• What’s more, according to Kim, with a direct printed aligner, the clinician can more precisely control the thickness and insert bumps as needed. Kim shared that he and his team found that when the orthodontist can control the thickness they can “control the geometric inside of the aligner.” That, and the ability to add bumps, creates a huge opportunity for the orthodontist because it helps reduce the need for attachments, he said.

For Kim, the shape memory polymer used to make the material is very interesting.

• He says it somewhat mimics the behavior of NiTi wire. The difference being that a NiTi wire can be exposed to cold temperature to become more flexible, while this Direct Aligner material becomes totally flexible when placed in warm/hot water. The advantage of this shape memory, according to Kim, is that the patient can maintain the shape—and thus the forces—of the aligner at home. Kim points out that patients remove their aligner up to 10 to 20 times a day to eat. “So think about the plastic deformation” every time they remove the aligner, said Kim. But with this material and some warm water, the shape can be restored. Kim uses the analogy of a deformed plastic Coke bottle. Once it’s deformed, it’s not going back to its original shape. But with this material, he can advise patients to put their aligner in warm water at the end of the day if they notice it’s not tight enough. “It will go back to the original shape so they can maintain [a better fit] every day,” he added.

Now when it comes to forces, Kim shares he has been able to apply bigger activations per aligner, thus saving time in treatment and decreasing the number of aligners over the course of treatment. With traditional thermoforming plastics, Kim points out, something like a .5 mm activation per aligner can create a force level that causes the patient too much discomfort and even pain. But with this material, Kim can do that.

• “I’m constantly putting .5 mm activations and even 5° rotation per aligner, and then have patients wear [the aligner] just a little bit longer—maybe 2 weeks. Sometimes we go longer,” said Kim, adding that with a standard activation of .25 mm per aligner, to move 1 mm you need four aligners. “But if I can put .5 mm activation per aligner [and] have them wear [it] for 2 weeks, then I need only two aligners.”

In this episode, Kim also talks about the hardware requirements, including 3D printer compatibility with the material needed, and the need for a specific type of curing machine. He also talks about the staging software needed to plan cases using direct 3D-printed aligners. What’s more, he talks about retention and his plans to test an on-site retainer-bending machine from YOAT, a medical technology manufacturer based in Seattle. OP

While the pathophysiology of idiopathic hypersomnia is unknown, emerging science suggests that nighttime sleep dysfunction may contribute to daytime sleepiness in patients with idiopathic hypersomnia. A systematic review and meta-analysis that included 10 studies found that, on average, several sleep architecture hallmarks were different in patients with idiopathic hypersomnia relative to controls.

• Total sleep time and percent of REM sleep were increased in patients with idiopathic hypersomnia compared with controls.
• Sleep-onset latency and percent of slow-wave sleep were decreased in patients with idiopathic hypersomnia compared with controls.
• Sleep efficiency and REM latency were similar between patients with IH and controls.

In addition to nighttime sleep dysfunction, other physiological changes have been observed in some patients with idiopathic hypersomnia and theorized as possible contributors to its pathophysiology including:

• Dysfunction of the GABAergic system
• Autonomic system dysfunction
• Altered functional or regional connectivity in the brain
• Circadian system dysfunction
• Dysfunction of energy metabolism

This episode is produced by Sleep Review and is episode 5 of a 5-part series sponsored by Jazz Pharmaceuticals. Visit Jazzpharma.com and SleepCountsHCP.com for more information. In episode 5, listen as Sleep Review’s Sree Roy and neurologist-sleep specialist Isabelle Arnulf, MD, PhD, discuss:

• Science doesn’t fully understand the pathophysiology of idiopathic hypersomnia. Research has revealed potential clues, however. For example, idiopathic hypersomnia is associated with changes in sleep staging and architecture. What does emerging science suggest are differences in nighttime sleep?
• How might the arousal index differ in idiopathic hypersomnia versus in people without it, and why might that matter?
• In addition to nighttime sleep dysfunction, other physiological changes have been observed in some patients with idiopathic hypersomnia and theorized as possible contributors to its pathophysiology. What is the GABAergic system and its possible role?
• What are some emerging findings surrounding idiopathic hypersomnia and autonomic system dysfunction?
• What is the evidence that supports the idea of altered functional or regional connectivity in the brain in people with idiopathic hypersomnia?
• There were fascinating studies done on skin fibroblasts, suggesting that circadian period length may be different in people with idiopathic hypersomnia versus in people without it. What role might circadian rhythm dysfunction have in idiopathic hypersomnia?
• What has science discovered about the possible role of dysfunction of energy metabolism in idiopathic hypersomnia?
• What further research would you like to see conducted on the pathophysiology of idiopathic hypersomnia?

Listen to Episode 1: Symptoms of Idiopathic Hypersomnia

Listen to Episode 2: Diagnosis of Idiopathic Hypersomnia

Listen to Episode 3: Differential Diagnosis of Idiopathic Hypersomnia

Listen to Episode 4: Burden of Idiopathic Hypersomnia

People with idiopathic hypersomnia face a significant disease burden. Idiopathic hypersomnia is associated with challenges that impact daily living activities, such as limitations at school, work, interpersonal relationships, and social activities. Various impairments include 

• • Impacts on attention and cognition, which can be characterized as “brain fog”
  • The burden of memory problems and a feeling of the mind going blank or making a mistake in a habitual activity

Public health and safety are also impacted, as more severe causes of sleepiness can be cause for accidents. Management strategies may not address the underlying sleep dysfunction associated, resulting in suboptimal symptom management. Patient survey and registry data suggest patients continue to experience symptoms of idiopathic hypersomnia and residual disease burden. This episode is produced by Sleep Review and is episode 4 of a 5-part series sponsored by Jazz Pharmaceuticals. Visit Jazzpharma.com and SleepCountsHCP.com for more information. In episode 4, listen as Sleep Review’s Sree Roy and pulmonologist-sleep specialist Richard K. Bogan, MD, discuss: 

• • What are some limits that people with idiopathic hypersomnia can experience in their daily living activities?
  • How do people with idiopathic hypersomnia commonly describe "brain fog," and what are some of the real-life consequences it?
  • How does prolonged sleep inertia place a burden on the people with idiopathic hypersomnia who experience this symptom?
  • What do you see as the burden of idiopathic hypersomnia on public health and safety?
  • Beyond medications, how is idiopathic hypersomnia typically managed to control for symptoms as much as possible?
  • How do you determine when therapy for idiopathic hypersomnia has been optimized, and what symptoms may remain at this point?

• What exactly is mouth taping during sleep?
• How has the practice of mouth taping during sleep evolved in popularity over the years?
• Is there any evidence that mouth taping is useful for healthy sleepers, that is, people without any sleep disorders?
• Is there any evidence that mouth taping is useful for people with any sleep disorders, perhaps as an add-on to a device such as an oral appliance for sleep apnea?
• What dangers are associated with mouth taping during sleep?
• What is your advice to sleep techs for how to handle the situation of an in-lab sleep study patient who wants to use mouth taping during an in-lab sleep study?
• What is your evidence to sleep medicine professionals if their patients confide in them that they using mouth tape, either with or without their prescribed device, to treat a sleep disorder?

• • Sleep inertia: sleep inertia is common in patients with idiopathic hypersomnia but can also be reported by individuals with mood disorders

• • Patients with idiopathic hypersomnia often find naps to be long and unrefreshing, while patients with narcolepsy generally find short naps to be restorative

• • If a patient has prolonged nighttime sleep, long sleeper syndrome should be considered; in contrast to patients with idiopathic hypersomnia, long sleepers feel refreshed and do not have daytime sleepiness and difficulty awakening if they are allowed to sleep as long as they need

• • Cognitive complaints, often described as "brain fog" are common symptoms of idiopathic hypersomnia but also can occur in patients with various sleep-wake disorders (including narcolepsy type 1 and insufficient sleep syndrome)

• • Idiopathic hypersomnia can be particularly challenging to diagnose because of its lack of specific biomarkers, as well as its symptoms resembling those of other disorders. How do you differentiate idiopathic hypersomnia from hypersomnias of a specific cause, such as narcolepsy type 1 and type 2, insufficient sleep syndrome, or hypersomnia due to a neurodegenerative disease?

• • A minority of people simply need to sleep longer than most, even 10 hours or more, to feel refreshed. How do you determine if that applies to a given person, who may not have a sleep disorder at all?

• • How do you differentiate idiopathic hypersomnia from hypersomnia comorbid to psychiatric disorders, such as prolonged sleep time tied to depression?

• • At what point in ruling out other disorders should objective sleep testing, such as polysomnography and multiple sleep latency testing, be done?

• • Why is idiopathic hypersomnia sometimes confused with sleep-breathing disorders? When would you recommend a CPAP trial to address possible apneas, hypopneas, or respiratory-event related arousals?

• • How do you distinguish chronic fatigue syndrome from idiopathic hypersomnia?

• What is obstructive sleep apnea, also known as OSA for short?
• What do you think is the most troubling risk of not treating obstructive sleep apnea?
• How has treatment-resistant hypertension been linked to OSA?
• How can the impaired brain function linked to OSA manifest in patients?
• What evidence is out there that erectile dysfunction and female sexual dysfunction can be tied to OSA?
• How has obstructive sleep apnea been linked to diabetes?
• The worst link in my view is that obstructive sleep apnea has been linked to an earlier death. Why is that?
• Treatment of sleep apnea typically involves a device, such as a CPAP machine or an oral appliance, though surgery can be an option for some patients. Is there any evidence that treating OSA can alleviate some of sleep apnea morbidities or mortality?
• With all of this evidence in mind, what should healthcare providers do to help identify patients who are likely to have obstructive sleep apnea?
• What should any patients listening to this podcast do if they think they have symptoms of obstructive sleep apnea?