So, welcome to everybody who's joined us so far. I'm Dr. Trish Braga, but I'm stepping in right now for Dr. Fashid Areez, who is your moderator for this evening's webinar on comorbid insomnia and sleep apnea. And I'm joined with our speaker, Dr. Miguel Mary Cruz. If you're able to see and hear me right now, that means you've successfully logged into the meeting. All participants' audio has been muted to ensure that everyone can hear us clearly. If you're unable to see me, please try refreshing your browser. It's possible you may need to refresh your browser a couple of times. If refreshing your browser does not resolve the issue, click the link below the video that reads, connect directly to the webinar platform. And this will connect you to the webinar via Zoom. However, you will need to return to the conference's IO platform if you would like to use the Q&A feature for tonight's presentation. The platform we are using for this webinar allows you to submit questions anonymously. 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In instances where evidence is lacking, speakers have been asked to verbally disclose that their presentation is case-based or based on clinical experiences so that you can use independent clinical judgment to make decisions for your practice and your patients. And so now I'll turn it over to Dr. Miguel Meric Cruz. Thank you, Dr. Cruz. Thank you so much, Trish. It's really an honor. Good evening, all. I'm sharing the... I am already sharing the screen. I don't see that you are sharing. Okay. Yeah, so you want to go down to the green arrow at the bottom bar? No. There we go. Okay. Just... You got it. I'm trying to put in the first slide. I'm sorry. Okay, so thank you so much for your presentation, Trish. Good evening to all. It is really, really a great pleasure to be here with you today to present some of my evidence-based feelings about this amazing field of sleep medicine and its odontostomatological spectrum. I have no conflicts of interest regarding the topic I will present today, at least no other than to be convinced by the results obtained from my research that Kamiza is not a new condition, but it's really, meaning it's far away from being defined. And at the end, I expect you can have those feelings also as better understand what is Kamiza and its major implications on medicine, on sleep medicine field and dental sleep medicine to better associate insomnia phenotypes to sleep-related respiratory disturbances in adults and in children and improve their diagnostic and management-related skills regarding comorbid conditions often associated with Kamiza. And I thought it was interesting to start with a real case scenario involving a colleague of 48 years old exceeding his weight, but nothing which should alert us at first. She came to me because of her insomnia symptoms described as sleep onset and maintenance-related complaints. She also complained about snoring and some sleep-related respiratory distress, which was corroborated by her partner, which also told me about some pauses that happens during the night. She had hypertension for which is relatively controlled with medications and no other relevant clinical findings. Regarding habits, she was a smoker with 10 cigarettes per day, no history of regular exercise practice. And she confessed to be a little bit stressed during the day and to drink one or two glasses of wine socially. While her APOR sleepiness scale advocates a mild sleepiness, her husband tells us that she's frequently dozing. And I must tell you that even though I often give sleep consultations, this colleague come to my dental office and this story and her first complaint is in the context of this consultation and was snoring too much and because she wanted me to give her an oral appliance. So I ask you to honestly think about that and think if we usually really look for the whole picture during our daily interventions. Even though we often argue that each patient is different and that we treat patients and not actually disorders, I think you agree this is common. We commonly overlook for many of those things that I've stated here and maybe because some of this information can be difficult to integrate and interpret with the general background of dental practitioners. And do we really know why sleep apnea is important in the dental field? Do you agree that dentists could be critically important in other fields that only that related to respiratory spectrum of sleep medicine? And why? There are certainly many other reasons, but one major reason is on the bottom of our heart. Sleep is critical on cardiometabolic regulation and sleep loss imposes general risks on health, but greatly negatively impact cardiometabolic functions leading to cardiovascular and associated metabolic diseases. And those are the number one cause of death worldwide. And not only sleep apnea account for such risk, you know. Okay. That's true. But why should dentists care about that? The main reason may actually be because they can avoid such burden. They can help to avoid that. They can protect people from dying early or from developing several disabilities directly related with such cardiometabolic disturbances. Dentists may well be efficient cardiovascular screeners since they act as primary care practitioners and they have frequent access to the patient. And this is not only theory. This is not only defended by myself, although I clearly agree. Look for this paper from Richard Singer and colleagues who in 2019 showed that dentists may critically concur for a better primary prevention strategies, but also may contribute to less complications for those who will not succeed in such primary prevention and will have also a great impact in terms of secondary prevention, therefore avoiding greater health deterioration in many and many deaths. And it's apparently easy. It's just a question of wanting to do. Look how a simple method of proactive screening, the same is saying questioning patients on symptoms and demographics may improve early detection of under-recognized cardiovascular diseases in primary care settings. Exactly where we are, where dentists are. Because if we don't ask, we will never know about it. That's what's happened with Kamiza. And I will show you a little bit more. But before I go forward, I would like to define, even though some of you are very well knowledgeable on that concept, I would like to define some key concepts that are important. The first refers to normal sleep as a reference for any deviation from normality. Normal sleep is thus a circle rhythm with individual characteristics necessary for the daily restoration of homeostasis at different levels of body organization. And yet characterize it by a certain duration and quality that rise with age with certain limit. But all the three relevant concepts that should be defined for this presentation are insomnia, sleep disorder, breathing, and of course, Kamiza. Insomnia is thus defined as a persistent difficulty in initiation, duration, consolidation, or quality of sleep that occur despite adequate opportunities and circumstances for sleep and results in daytime impairments. And according to the ESST-3, insomnia is divided into two main nosological groups, chronic and short-term insomnia, and a third group that includes other unspecified insomnia. All of these conditions should be treated by considering individual symptoms, of course, such as excessive time in bed and short sleeper profile. I think we are listening here. Are you listening well? Because I feel a noise here. No? Well, going on with definitions, sleep-related breathing disorders, which describe respiratory abnormalities during sleep, can be divided into five main types, with obstructive sleep apnea being the main focus of the present work. OSA disorders are defined as repeated episodes of complete or partial apnea during sleep and results in a decrease in oxygen saturation, usually terminated by brief arousals. An OSA can occur in both adults and children with other diseases, but with different characteristics and diagnostic requirements. In addition, snoring as an isolated symptom is often persistent and frequently involved in the pathophysiological mechanism of OSA. And to stay with the definitions, COMISA, the acronym for comorbid insomnia and sleep apnea, is the umbrella term for the coincidence of the different types of insomnia and sleep apnea, which are controversial as a defined clinical entity because of the confounding mechanisms and different clinical phenotypes, of course. And another important concept for our presentation is that of cardiometabolic dysfunction, which is related to cardiovascular disease and associated metabolic disorders. Hypertension and diabetes are two of the most common examples. And, in fact, cardiovascular disease remains one of the living causes of death worldwide. And despite advances in treatment, risk factors such as obesity and diabetes remain widespread and contribute to the development of cardiovascular disease. And there is a link between sleep and cardiometabolic dysfunction, reinforced by the fact that one third of the adult population suffers from shortened sleep. In addition, up to 50 percent of adults suffer from sleep-related breathing disorders and 10 to 30 percent of them from OSA. And both insomnia and sleep-related breathing disorders are independently associated with increased cardiovascular risk. And that's a good reason why we should care about. As for the particular relationship between insomnia and cardiometabolic dysfunction, leading to established disorders, there are a number of mechanisms related to hormonal homeostasis, for example, cortisol, but also to autonomic control, as it's generally believed that autonomic dysregulation may play a role in this association in relationship with both inflammation, oxidative stress, and neuroimmune changes. And as for the epidemiological aspect, several papers have shown that insomnia is independently associated with higher cardiometabolic levels. And also some meta-analytic data corroborates such findings. It's interesting with regard to the plausibility of a cause-effect relationship, the finding that prolonging sleep has a restorative effect on some cardiometabolic risk. To a certain degree, we know that when we increase the sleep after sleep deprivation, we have a restorative effect on this, not only on insomnia, but also on cardiometabolic risk associated to that. And this is important. And this also important negative correlation between sleep and cardiometabolic disease seems to exist not only in sleep duration, but also in sleep quality, as it is shown by this paper. And as for the link between obstructive sleep apnea and cardiovascular risk, several mechanisms are known. Autonomic dysregulation and oxidative stress are two important factors. But in this context, there is also a persistent inflammatory condition and the neuroimmune implications in relationship with intermittent hypoxia and sleep fragmentation typical on these conditions. Interestingly, the American Heart Association have recently added to the algorithm of risk calculation sleep itself as the eighth life essential, as it is well recognized that shortened sleep is a predictor of cardiovascular and related metabolic impairments. And when I thought to study the insomnia and sleep-related breathing disorders interaction, I thought that it should be important to contribute to a clear definition and characterization of the confounding term COMISA and to clarify the prognostic value of COMISA or COMISAs, since they are maybe more than one kind, for the development and maintenance of cardiovascular and related metabolic disorders. And to accomplish with that, myself, together with my colleagues, my collaborators, have clinically characterized COMISA patients, both in adult and pediatric age, in a pilot multicenter populational study. We have defined some pathophysiological contributors and possible mechanisms linking COMISA to higher cardiometabolic risk. We therefore proposed phenotype-guided treatment option for COMISA patients, and we developed integrated tools to facilitate the screening and early diagnosis of COMISA and associated cardiometabolic risks. As not all the parts of this project are already finished, I will present some of the preliminary but rather important findings, which we already have. With the aim of defining and characterizing COMISA in the adult population, we conducted a retrospective multicenter populational study involving approximately 1,200 adult patients of both sexes referred to sleep laboratory. We collected demographic data as well as parameters related to sleep habits and patterns. And in addition, sleepiness, insomnia severity, and OSO risk were assessed using the Epworth scale, the Insomnia Severity Index, and the Stop Bank questionnaires. Patients with a low risk of sleep disorder breathing, according to Stop Bank, were excluded. And for the present work, insomnia was assumed to be present either by an easy, above 8, or by a positive response to the questions about difficulty falling asleep or staying asleep. We defined the period of insomnia as occurring at the beginning, middle, or end of the night and the persistence of symptoms. It was also required for this work that the presence of at least one daytime episode was confirmed. OSO was defined by three or more positive responses in the Stop Bank questionnaire, or if polysonography was available, by the ICSD3 criteria for diagnosis. And COMISA was accepted if cumulative criteria for insomnia and obstructive sleep apnea were present. In one of those groups, in one subgroup, we objectively measured arterial blood pressure and in another subgroup, we followed up OSO patients over 10 years to determine mortality rates. And we applied the same methodological criteria described before to the pediatric population in our work. And the same retrospective multicentric study design was applied to nearly 800 patients enrolled in this pediatric sample. And I will give you some of those results. And, well, this slide reflects the initial studies on 685 adult patients from Salvador Bahia, and we have found a prevalence of 26% of COMISA and a similar rate of insomnia and about a half of OSO in this sample. We also found that hypertension and diabetes were more prevalent in the COMISA group than in groups with isolated conditions. And another interesting finding was that the midpoint of sleep was significantly different in the COMISA group compared to the isolated groups. And one, when I talk about this midpoint, I actually refer and I will develop further thereafter about the clocks, how can we see the clocks and the chronotype function. And as I mentioned earlier, our aim was to objectively analyze arterial pressure in a subgroup of our total sample. And in these 158 patients, not only did we find that the Comisa group had the highest systolic and diastolic blood pressure, but also that some polysomnographic parameters were distinct in Comisa group compared to the isolated insomnia or sleep apnea groups. And this was the case for the sleep latency, total sleep time, sleep efficiency, N2, N3, and some respiratory indications, as you can see. In the 10-year follow-up study of a subgroup of nearly 400 patients with insomnia, of sleep apnea or Comisa, we found that the higher mortality rates were observed in the Comisa patients. Although these were not statistically significant, there is a trend and compared with other studies that tends to show the same trend, we actually believe that the Comisa patients have higher risks of mortality compared with isolated conditions. And in a final analysis of the adult population sample, we divided 179 patients with Comisa into different age groups, namely 11, 18 to 29 years, 30 to 49 years, 50 to 64 years, and over 65 years. And this division showed that phenotypic differences exist in different age groups of adulthood. Nevertheless, alcohol consumption and smoking habits, as well as a lack of physical activity and caffeine intake were the cardiometabolic risk factors most frequently observed between 30 and 64 years of age, in older ages. On the other side, for this first pediatric study on the topic, and as a novel, a very novel relevant finding, Comisa was detected in symptomatic children and adolescents being referred to a sleep clinic and accounted for 60 to 80% of all cases. Significant higher proportions of children with Comisa showed symptoms such as difficulty falling asleep and staying asleep, tiredness on waking and even on daytime, and showed daytime sleepiness as an important characteristic also. And in a subgroup of 329 patients from Israel, we investigated the association between a specific type of pediatric insomnia. As you know, behavioral insomnia of childhood is the most typical insomnia type in the early childhood. And we have therefore investigated the association between this type of insomnia and ulcer. However, the current results do not support the link between behavioral insomnia of childhood and obstructive sleep apnea in children. What was reasonably expected? To examine the impacts of Comisa and associated cardiometabolic risk across the lifespan, we studied different age groups. Now we have included children and older patients. And according to our findings, the greater prevalence of Comisa is found in adults with hypertension and cardiovascular disease affecting three quarters of these patients. While BMI appears to be an important factor in the cardiometabolic risk of Comisa in these patients, other factors also appear to play a role, namely physical activity or the absence of this, smoking and especially alcohol consumption. And those are important psychosocial stress-related factors that we should be aware of. And summarizing our results on the contributing to define and characterize Comisa, we have found that compared with insomnia or ulcer alone, about one fourth of adult patients affected by Comisa. And this was similar to insomnia and one in two regarding to ulcer. On the other hand, Comisa prevailed in males until the fifth decade of life, whereas in women's were more affected after the third decade of life. Patients with Comisa had a higher BMI and smoking habits, lower sleep duration and later sleep time. Adult patient with Comisa had the highest rates of hypertension and diabetes, therefore meaning cardiometabolic risk, with hypertension prevailing on the early ages and diabetes prevailing on advanced ages over the 65 years old. And Comisa had also an important prevalence in the pediatric age, about 60 to 80%, as I told you before, and increased BMI and poor physical activity were prevalent cardiometabolic risk factors since Comisa among pediatric ages also. So in initial pediatric assessments support the possibility that the concurrent presence of insomnia and sleep disorder breathing may further aggravate the phenotype and could potentially translate into more deleterious consequences if left undiagnosed and untreated. Because there are many potential contributors for the association between Comisa and cardiometabolic risk, we've tried to focus our attention on three possible factors with plausible common pathways. This involved the impairments of autonomic function and exacerbated stress. Therefore, we first sought to investigate Comisa in adult patients with sleep paroxysm. The same inclusion and exclusion criteria as in adult population were used and identical criteria for insomnia and obstructive sleep apnea were assumed. It's a pity that although data from this study have yet to be analyzed and therefore is not present here, but I can tell you that preliminary results show the higher rate of arousals in Comisa compared with insomnia and obstructive sleep apnea in Bruxelles. But we look for another physiological challenge, pregnancy as a possible factor in facilitating cardiometabolic and associated dysfunction in Comisa. Therefore, in a retrospective population-based study involving 214 high-risk pregnant women with up to 31 weeks gestation, we applied similar methodological standards as explained in adult population before. And we found that 28.5% from those women were diagnosed with Comisa because they had a cumulative insomnia severity index score above eight indicating clinical insomnia and a stock bank score with three or more positive responses indicating high risk for obstructive sleep apnea. And the prevalence of Comisa was higher in diabetics than in hypertensive patients and exceeded the sum of the isolated prevalences observed from insomnia and sleep-breathing disorders in each population. Another important finding is that Comisa prevalence was positively related with hypertension and diabetes since it was favored when both hypertension and diabetes were present in the same patients. In a third study within this section on the putative mediators between Comisa and cardiometabolic risk, we look for patients complaining of persistent or of facial pain. Since this is also a trigger for cardiometabolic risk factors through psychosocial stress. And therefore we calculated the prevalence rates of Comisa insomnia and obstructive sleep apnea in approximately 1,200 adult patients who saw treatment in university-based or a facial pain unit using the same methods, similarly the same methods we have explained before. And we already knew the relevance of psychosocial stress in this type of population. And it is really important for continuity and severity of pain, but also for sleep disturbance and for associated cardiometabolic burden. As so in this next study, we looked for psychosocial stressors such as anxiety and depression as a surrogates for cardiometabolic risk in this particular population. And in our sample, 31% of patients tested positive for insomnia. 25% had either persistent snoring or sleep apnea and 11.5% suffered from Comisa. The body mass index of patients with Comisa was higher than that of patients with insomnia and sleep disordered breathing. Smoking was also more common in Comisa group. And interestingly, psychometric tests assessing stress and anxiety, depression, pain, catastrophizing and stress were significantly higher in patients with Comisa than any other isolated condition. We can summarize our findings from this section on the possible mediators. And we noted that Comisa patients appear to have the highest rate of sleep-related bruxism arousals compared to insomnia and ozone alone. And I'm sorry that I could not provide this data to you in the next slide. I'm sorry that I could not provide this data since I don't have all data treated already. But in the another sample of the among the high-risk pregnant woman, those with Comisa had more cardiovascular and related metabolic disorders. And among patients complaining of persistent pain within the orofacial pain or facial region, psychosocial stress is higher in patients with Comisa also. And this seems to be, of course, important findings that was overlooked until now. And in the absence of an optimal model for appropriate management of Comisa patients, in the next set of studies, we've tried to examine whether the three main therapeutic standards for the isolated components of Comisa are also applicable to comorbid conditions. So we sought to start with retrospective pilot clinical study of adult obstructive sleep apnea patients referred for CPAP treatment. And in this case, insomnia was defined by a polysomnograph derived sleep latency of more than 30 minutes. And although the results of this study are also not yet completed, preliminary results suggest that patients with Comisa have lower adherence compared to other patients. And this is not new. Of course, you all know that it's intuitive, but it's also evidence-based now that CPAP is difficult to tolerate for those patients with obstructive sleep apnea, but even worse for those patients with obstructive sleep apnea and insomnia, of course. But in a second study, we wanted to find whether mandibular advancement devices would benefit Comisa patients. And we then included 78 patients, 35 with obstructive sleep apnea and 31 with Comisa. The same standards of a latency to fall asleep for more than 30 minutes was used to define insomnia within the polysomnographic exam, regardless of whether obstructive sleep apnea was still classified according to the ICSD-3 concepts. And compared to OSA patients, residual respiratory events as measured by HI were slightly higher in Comisa patients, although the required clinical improvement was achieved. While no changes in sleep latency were seen in OSA patients, significant improvement was seen in Comisa patients leading to resolution of insomnia. And that's quite amazing for us because not only improving, sort of it's clearly resolved insomnia. And in addition, we investigated the effect of mandibular advancement devices on heart rate variability as a surrogate for cardiac autonomic function in Comisa patients. And found that patients improved regard after therapy, possibly this imply there was a reduction in cardiometabolic risk. And if you see the lower CPAP rate but the higher parasympathetic tonus observed in this analysis indicates so. And in last study that I couldn't take for you also because it's not ready just to take some tips from this. The last study on potential treatment option for Comisa patients, we also investigated the effects of cognitive behavioral therapy on these patients in a prospective case control study involving adult patients referred to CPAP treatments. And we don't have yet the final results, but preliminary findings suggest that CBTI may actually improve both Comisa and associated psychological and social related stress as a surrogate for cardiometabolic risk. And I would like to make a parenthesis here because it's important that dentists be aware that cognitive behavioral therapy, or at least some strategies of cognitive behavioral therapy are prone to be used by dentists. So it's an important finding also for dentists of course. So compared with insomnia or obstructive sleep apnea, patients with Comisa seem to have poor adherence to CPAP therapy compared to those with single ulcer that was already shown. On the other hand, medieval advancement devices were effective in patients with Comisa both respecting to therapeutic adherence and improving AHI and sleep latency with clinical resolution of both aspects. And moreover, CBTI seemed to be effective on improving complaints about Comisa patients as well as psychometric dimensions of stress acting as cardiometabolic risk factors. Another step forward and given the lack of effective models for successful treatment of Comisa, we sought to contribute for screening and early detection of Comisa by developing an integrative patient management solution. And following the development of a web-based interdisciplinary symptom assessment tool for sleep disorders and Comisa, the Y-Sleep tool, that actually is the same tool we have already used to study those population with orofacial pain, but integrating questions regarding insomnia and questions regarding obstructive sleep apnea and factors associated to those, to both. And we integrated some data derived from Comisa characterization results together with a novel oximetric assessment mobile. And we aim to facilitate screening and early diagnosis of Comisa in these patients. And I really expect to present these results later this year. And with those achievements, we have published until now 11 journal publications, three oral presentations and congresses and 11 posters, which helped colleagues to understand better that insomnia plus sleep apnea is probably more than one plus one. But we must be aware that times change and we are through a challenging era from where we must to accept, we still not know too much. For instance, the so-called COVID insomnias have probably installed phenotypic features. We will must to face from now and on. And those include also insomnia and sleep apnea, but also changes on the clocks. Those which are tick tacking inside our brains and our bodies. And we should know well, because they integrate some pathophysiological pathways of insomnia and also of sleep apnea. We also must wait to see the repercussion of COVID and mainly the COVID long syndrome in cardiovascular disorders and associated metabolic dysfunctions and disturbances. And again, about the clock, when a minute seems like hours, that's exactly what a mobile that we've tried to study of the daylight changing time, tell us about the relevance of the highly assertive temporal regulation. Those are some results we have showed about the importance of changing time to cut a metabolic risk, even if only one hour during the daylight saving change era. I know that in United States, it's, there are many States that there are no change anymore, but unfortunately in Portugal, in Spain, in many countries in Europe persist with this chronodisruptor factor that have a lot to teach us also regarding sleep apnea and insomnia interaction. And that's why we have published this consensus, alerting for avoiding to neglect the power of our internal time. But look, this is non-published data. We know that the effects of bright light in our organism is impactant and is impactant in many ways, but is highly impactant, negatively impactant for insomnia. And see that in an experiment with, and this is a preliminary report, non-published data, in 12 women with clinical insomnia, and not only by easy, but also for actigraphic measures, we did four appointments in a blind study and we divide six experimental patients and six control. Those six experimental patients were directly affected by lights of the dental office, of the dental equipment, with more or less than 10,000 lux to their eyes. And the other group, we used an inverted light of less, which resulted in less than 2,500 lux. After one week and four appointments of that protocol, with that protocol, we have the results that experimental sleep latency was higher in 50% among the experimental group than the control group. This meaning that insomnia worse just with the use of dental office lights directly to the eyes of patients. And the quality, the sleep quality also got worse in those people that were directly affected by light. So imagine a simple experiment showing that actually when we work with patients and particularly with patients with sleep disorder or sleep complaints, we should be aware that many of our skills or many of our treatments may impact negatively in those patients, either in insomnia or in circadian rhythm disturbance that I didn't talk, but it may occur together. And we also know that sleep paroxysm was told early on to be or to plausibly play a role on the cardiovascular dysfunction. And we have argued recently together with a group from Poland that it may actually contribute because of the pathways involved on sleep paroxysm or at least in some kinds of sleep paroxysm, it may actually act not only for sleep disturbances that we already know, but also for the cardiometabolic related risk associated to that sleep disturbance. And when we talk about sleep paroxysm, we usually divide sleep paroxysm telling that there is a division in a chronobiological profile between sleep-related paroxysm and awake paroxysm. But this is not actually a chronobiologic division. This is a sleep-dependent division. When we say sleep-related paroxysm is during sleep, not during the night, even though he could not be sleeping, the patient. And same for awake, of course. But when we ask for patients, of course, it's a self-report and there are several limitations on that, but when we ask to patients, tell us what are the moment of the day that mostly perceive their paroxysm, you will find that there is a very symmetric distribution, at least in these patients, in these students. Of course, these were otherwise healthy students. With no cardiovascular risk factors. But interestingly, we thought that when we see in several moments of the day, the importance of paroxysm on the arterial pressure variation, it's not similar for every moment. And this teached another thing, is the relevance of the circadian profile of paroxysm manifestations in sleep disturbances. Because of course, this is not evidence-based, this is just a construction of my, this is a suggestion myself. But when we have a paroxysm that is mostly prevalent in the night, but not during sleep, we should have more negative impact on insomnia. For example, you will mostly agree. And of course, we care a lot in our dental offices about pain, about chronic pain, mostly chronic musculoskeletal pain. And there's some evidence also that pain and this kind of pain may have something to do with cardiovascular and metabolic increased risk. And insomnia was suggested to be a mediator. And insomnia is in a high percentage of our patients as we showed in this paper of patients with orofacial pain complaints. And we must also be care about the use of medications, or at least we should be able to screen about some medication that patients commonly use and that may be included in the risk factors for insomnia and the risk factors for cardiometabolic dysfunction also. And well, at the end, I would like to be somehow provocative. And since we have a novel definition, a new definition of dental sleep medicine, I think maybe it's time for adding something else. And maybe we should add in the future and assume that as primary care practitioners, specialized and sleep medicine certified dentists should be able to apply the general sleep medicine concepts and tools to their daily practice, therefore preventing, screening, diagnosing, and treating prevalent and potentially threatening condition causally related to increased rates of morbidity and mortality, namely cardiovascular and associated metabolic disorder, just because these are the number one cause of deaths around the world. And if dentists rule, or if dentists play a role in sleep medicine, well, I've discussed that with Mayra and with Edward Staville, that is a famous pediatric sleep specialist in Spain. And of course we have no doubts. And yes, also for insomnia. And I would say also for circadian rhythms and also maybe for more, and also because of the heart. And widening the scope through education, because we must remember that we only ask about what we know that exists. Training, experience also helps a lot. And dental sleep medicine should not be confounded with oral appliances. And I certainly know that you are all aware of this, but it's easy to forget sometimes. So thank you so much for your attentions. And there is no doubt also that COMISA must be continued because there's a lot to be done yet. Thank you. Thank you, Dr. Miracruz. I'm waiting for Dr. Ariz to come on. Yes. Okay, he's here. That's great. Good, good. Thank you. Sorry for being a little late to the party, but beautiful presentation. I know you have a beautiful publication and we all enjoy that presentation, but let me just go quickly to a couple of questions that are coming up. And if you'd be kind enough to answer those, and if you're running a little bit late, and we can still entertain those questions. So the first question is, are dentists allowed to make direct referral for congenital behavioral therapy for insomnia or write a prescription for pharmaceutical grade melatonin? Or does everything has to go through a sleep physician? It's difficult. It's difficult to discuss this with... I defend what I suggest is that yes, dentists should, of course, dentists who have training, who are educated, who have proof education on that, and sufficient experience should be able to do so. At least some part of CVTI aspects. Of course, I don't want that psychologists be mad with me. I'm not trying to take out psychologists from this role. What I mean is that we know that some part, some important part of the CVTI strategies are teaching. Are providing what we should provide always to make patients understand what they have, exactly what's happens in his body, and try to, from that, that they could be aware of some behavioral strategies and behavioral strategies that could improve his status. Either those related to alcohol consumption, cigarette consumption, eating too much before going to bed, some strategies regarding to even cognitive issues, because patients have so many wrong beliefs that could play a negative impact in our treatment. So I think, yes, of course, I'm a little bit afraid of being judged because of that. But, and I'm sorry, I don't want to go in contrary of... Go in contrary of, I think it depends. Well, of course, legally, it depends from where we are working. Of course, because there are different laws and different medical legal aspects in different countries. But I think we should be aware that as critical players in a scenario where we can actually protect patients from dying, we can actually protect patients that would not be seen by other professional many times from getting worse from several issues. Of course, when we can, we should refer, we should adequately refer and we should be aware of that. But there are some limits on which we could have some important rules and that maybe are not explored because of politics rather than public health issues. Sure, beautiful. So we have a few more questions. So if we can quickly answer all those, that would be great. So next question has two part. Do you recommend any special forms or ideal questionnaires in the dental office to ask about insomnia for our patients? And second part, this is also, it's important to know about OSA and insomnia. Lots of patients come to our offices regarding insomnia, but they actually suffer from OSA. Yeah, I think it's easy. It's easy. It's easy, easy, easy. The Insomnia Severe Index is a very easy tool to apply and it actually is validated. It's, and it tell us about the intensity of insomnia as a symptom, of course. We can have some questions regarding what, how is your sleep, how is your sleep time? How is your sleep quality? And to look for further, but again, this may be a problem for some countries because of the medical legal issues. But I think we should be obligated to that since we are practicing in a field that derives one third of our life functions. And one is sleeping well, not only breathing well, sleeping well and sleeping well regarding the time of sleeping, the duration and the temporal disposition of such function. And I think we should be aware of that. So I think we should apply systematically a tool, for example, the ISEE, the PSKI, Pittsburgh Sleep Quality Index or a visual analog scale regarding some issues. Of course, again, we must be trained to do so because it requires adequate interpretation. Even saw that for reference, but we only can refer adequately if we could interpretate and we could interpretate when we ask the right answers and we ask the right answers when we know about the field. Okay, beautiful. Next question is, what do you think about combination of the B-complex with 100 milligram fentanyl acid and vitamin D for insomnia? And have there been any studies that you're aware of regarding the relationship of this combination and its effect on insomnia or improved quality and quantity of the sleep? I'm very sorry, but I have not any experience on that. I'm sorry. Okay, so let's move on to the next question. Regarding your study with heart rate availability and commissural patients, were there a comparison to patients with OSA alone? What? Sorry, I didn't understand. The question is regarding the heart rate availability study and in commissural patients, was there a comparison to patients with OSA alone? So I guess they're trying to find out if there's any differences between the OSA patients with heart rate availability in relationship to commissure. Ah, yes, yes, yes. There was a, yes, there was a higher, if there was a difference between obstructive sepiablen and commissure. Yes. Yes, yes. I've showed that there was a, ah, but I did not show the results. Sorry. No, no, no. In what I presented, I did not show the results, but yes, commissure patients, commissure patients has differences, significant differences in the heart rate availability. But actually, one interesting question, and that's, again, refers to the, to why I think it's commissure to be continued. And as I told you, there's probably many kinds of commissure. When we see obstructive sepiaplenia together with insomnia, we see mostly a sympathetic tonus activation. But when we see not obstructive events, but when we see rareness or flow limitations, we see that mostly we have a parasympathetic activation. Well, in the other side, when we treat patients, we have a decrease in sympathetic activation. And in the patients with rareness or flow limitations, we have an increase in parasympathetic tonus. And that it's quite important because probably the mechanism by which autonomic function response is different. Okay. Finally, last questions for tonight is how many congenital behavioral therapy for insomnia usually is needed to be seen any improvements? Ah, usually, well, it depends. But if we talk only for insomnia, about six, eight, 10, it depends. It depends. But for commissure patients, probably different because commissure patients, it's not for insomnia only. We must many times to provide cognitive behavioral therapy also for the use of the appliances, either for CPAP or for medieval advanced devices, depends of what is indicated. Or also for some behavioral changes that will not only improve insomnia, but is importantly, and is differentially important for obstructive sleep apnea. So it is quite more complex, but I think we don't have any study on that. But about between eight to 12 sessions, I think it's mostly acceptable. All right, beautiful. Well, that's all the time we have for this evening. I'd like to thank our speaker, Dr. Miguel Miracruz for their participation. We all appreciate your generosity in participating in tonight's webinar. And thank you to all our attendees to joining us. We hope to see you in our annual session in Philadelphia. Annual session in Philadelphia. Have a good night, everyone.

comorbid insomnia

sleep apnea

prevalence

cardiovascular dysfunction

metabolic dysfunction

assessment tools

CPAP

mandibular advancement devices

cognitive behavioral therapy

dentists