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A lot is missing: the Orcade study
Sleep Medicine 19 (2016) 126–127
Contents lists available at ScienceDirect
Sleep Medicine j o u r n a l h o m e p a g e : w w w. e l s e v i e r. c o m / l o c a t e / s l e e p
Editorial
A lot is missing: the Orcade study
The authors report on short-term follow-up of dental device usage in obstructive sleep apnea (OSA) patients [1]. In this day and age, with data and studies accumulated over the past 20 years, it is surprising that this study has such a limited protocol: (1) Based on investigation of baseline sleep-disordered breathing (SDB) and follow-up of patients, functional magnetic resonance imaging (fMRI) and psychometric studies [2–5] demonstrate that the major impact of obstructive sleep apnea syndrome (OSAS) is on the brain and brain functioning, while its cardiovascular impact is much less severe and body mass index has as much an impact as the abnormal breathing during sleep [6]. The foremost difficulty is the sleep disturbance and the amount of arousal during sleep. Studies have shown that the lack of inclusion of the “hypopnea arousal” in the investigation offers a very limited and inaccurate view of sleep-disordered breathing. Official scoring manuals indicate the need to include the “hypopnea arousals” in their report [7], which is one of the foremost difficulties when an ambulatory study without recording of the electroencephalography (EEG) is performed as inaccurate results are obtained. Usage of this device may be considered in a clinical setting but would be absolutely unacceptable in a research study where potential public health decisions are made. As there is no notion of how data were obtained in the report, one could hope for the best, but “hypopnea arousals” should be reported systematically. (2) Another scoring problem is the absence of measurement of “flow limitation” [8]. The International Classification of Sleep Disorders–third edition (ICSD-3), and other classifications have included “upper airway resistance syndrome” as part of the “SDB–OSA spectrum,” and at present there are numerous publications in the world literature to affirm that, such pattern has a chronic negative impact on brain functioning and persistence of long-term poor sleep [9,10]. One clear problem with dental devices is that they have little impact on the maxillary component of the abnormal breathing problem, and they also often lead to mouth breathing, a very negative issue in long-term studies [11,12]. No notion of such evaluation and scoring is presented here. (3) During the past 15 years, the involvement of orthodontists, maxillomandibular specialists, and myofunctional therapists [13] has reminded us that craniofacial bones remodel from applied force on the bones or the teeth. This is the basis of orthodontic tooth movement, and usage of rapid- or slowmaxillary- or bi-maxillary expansion, myofunctional therapies http://dx.doi.org/10.1016/j.sleep.2015.10.008 1389-9457/© 2015 Elsevier B.V. All rights reserved.
(active or passive) have been used on children and adults in the treatment of OSA. Adult pulmonary specialists have demonstrated the importance of orofacial muscle activity in the treatment of OSAS [14,15]. The major goal of these approaches in both children and adults is to lead to nasal breathing and eliminate mouth breathing during sleep [11,12]. Long-term mouth breathing leads to progressive worsening of the orofacial anatomic factors and the associated SDB syndrome. (4) Another problem is the lack of information on the anatomic orofacial structures at entry and absence of systematic evaluation at follow-up evaluation. Tsuda et al. [16] have shown well that within two years, adult OSA treated with nasal continuous positive airway pressure (CPAP) develop significant changes involving the mandible and maxilla related to the nightly usage of a CPAP mask, as demonstrated on cephalometric X-rays, and to date three-dimensional computed tomography (3D-CT). Commercial ventures dealing with CPAP have since made important efforts to develop masks with little or no contact with the maxilla and mandible. In addition, the recommendation of using a “chin” strap has been very much de-emphasized as it can lead to a retraction of the mandible and act on mandibular condyle in a growing patient. The absence of any follow-up imaging data when following up patients placed on any dental device, particularly in a research investigation, is absolutely unacceptable, especially given that the patient’s age at entry included 18-year-old patients who may still have residual craniofacial growth. In clinical practice, at certain places around the world, the absence of documentation of maxillomandibular impact of dental devices at regular intervals is considered poor practice. It is important to know when to interrupt treatment and understand the real risks of such treatment. Recent studies have tried to counteract the negative effects of any dental device on the maxillomandibular complex and on the bite by implementing daily myofunctional exercises. As this study was performed in a country where myofunctional therapy was developed over 50 years ago [17], it is surprising that such countermeasures were not included in the protocol. If it was, it was not mentioned. (5) In terms of the amount and type of advancement, it is indicated that “the traction-based triangle and connector articulations enable mandibular advancement in parallel to the occlusion plane. This vector of advancement reduces stress on muscles and temporomandibular joint contact force [18], and may be a possible explanation for the good tolerance of
Editorial / Sleep Medicine 19 (2016) 126–127
127
References
Fig. 1. Bite change after usage of a “bi-block” “push” oral device for OSA: Note the posterior movement of the maxilla and posterior tilting of upper teeth, and forward placement of mandible with forward tilting of lower teeth, all consequences of oraldevice usage.
minimal residual disease (MRD) in the present cohort.” The connector articulations on any type of MRD will not allow parallel advancement to the occlusal plane if the patient’s malocclusion cannot support it. The direction of the lower jaw advancement is a reflection of the patient’s overbite and the incline of the glenoid fossa. Understanding these jaw mechanics may be lost at the 3–6-month assessment because the patients did not see the dental sleep specialist along with the sleep physician. This can affect the success and efficacy of the appliance if a physician or medical device company is asked to evaluate for the dental side effects. It is precisely the dentoalveolar side effects that limit the compliance and longterm success of MRD therapy. In conclusion, the protocol presented in this study may have been acceptable 20 years ago, but the protocol reported here does not bring information on a key issue: the risks associated with the studied treatment and impact on maxillary–mandibular bones (Fig. 1). Conflict of interest The ICMJE Uniform Disclosure Form for Potential Conflicts of Interest associated with this article can be viewed by clicking on the following link: http://dx.doi.org/10.1016/j.sleep.2015.10.008.
[1] Vecchierini MF, Attali A, Collet JM, et al. A custom-made mandibular repositioning device for obstructive sleep apnea-hypopnoea syndrome: the Orcades study. Sleep Med 2015. pii: S1389-9457(15)00827-8. doi:10.3402/ meo.v15i0.5063. [2] Diomedi M, Placidi F, Cupini LM, et al. Cerebral hemodynamic changes in sleep apnea syndrome and effect of continuous positive airway pressure treatment. Neurology 1998;51:1051–6. [3] Ferini-Strambi L, Baietto C, Di Gioia MR, et al. Cognitive dysfunction in patients with obstructive sleep apnea (OSA): partial reversibility after continuous positive airway pressure (CPAP). Brain Res Bull 2003;61:87–92. [4] Reichmuth KJ, Dopp JM, Barczi SR, et al. Impaired vascular regulation in patients with obstructive sleep apnea: effects of continuous positive airway pressure treatment. Am J Respir Crit Care Med 2009;180:1143–50. [5] Morgan BJ, Reichmuth KJ, Peppard PE, et al. Effects of sleep-disordered breathing on cerebrovascular regulation: a population-based study. Am J Respir Crit Care Med 2010;182:1445–52. [6] Chirinos JA, Guru bhagavatula I, Teff K, et al. CPAP, weight loss, or both for obstructive sleep apnea. N Engl J Med 2014;370:2265–75. [7] Guilleminault C, Hagen CC, Hunyh NT. Comparison of hypopnea definitions in lean patients with known obstructive sleep apnea hypopnea syndrome (OSAHS). Sleep Breath 2009;13(4):341–7. [8] Palombini L, Tufik S, Rapoport D, et al. Inspiratory flow limitation in a normal population of adults in Sao Paolo, Brazil. Sleep 2013;36:1663–8. [9] Bao G, Guilleminault C. Upper Airway Resistance Syndrome 1 decade later. Curr Opin Pulm Med 2004;10:461–7. [10] Tantrakul V, Guilleminault C. Sleep complaints in pre-menopausal women and its association with sleep-disordered breathing. Lung 2009;187:82–92. [11] Guilleminault C, Sullivan SS. Toward restauration of continuous nasal breathing as the ultimate treatment goal in pediatric obstructive sleep apnea. Enliven Pediatr Neonatol Biol 2014;1:1–7. [12] Lee SY, Guilleminaul C, Chiu HY, et al. Mouth breathing, “nasal dis-use” and pediatric sleep-disordered-breathing. Sleep Breath 2015;in press. [13] Chauvois A, Fournier M, Girardin F. Reeducation des fonctions dans la therapeutique orthodontiques. Paris: S.I.D; 1991. p. 1–231. [14] Guimarães KC, Drager LF, Genta PR, et al. Effects of oropharyngeal exercises on patients with moderate obstructive sleep apnea syndrome. Am J Respir Crit Care Med 2009;179(10):962–6. [15] Camacho M, Certal V, Abdullatif J, et al. Myofunctional therapy to treat obstructive sleep apnea: a systematic review and meta-analysis. Sleep 2015;38(5):669–75. [16] Tsuda H, Almeida RF, Tsuda T, et al. Cranio-facial changes after 2 years of nasal-continuous-positive-airway-pressure use in patients with obstructivesleep-apnea. Chest 2010;138:870–4. [17] Andrews JM, Guilleminault C, Holdaway RA. Use of a mandibular positioning device in obstructive sleep apnea: a case report. Bull Eur Physiopath Resp (Clin Resp Physiol) 1983;19:61. [18] Cheze L. Navailles B impact on temporomandibular joint of two oral appliances for sleep-apnoea treatment. ITBM-RBM 2006;27:233–7.
Stacey Quo Dental School Orthodontics Division, University of California, California USA Christian Guilleminault * Division of Sleep Medicine, Stanford University, California USA * Tel.: +1 6507236601. E-mail address: [email protected] Available online 5 November 2015
Contents lists available at ScienceDirect
Sleep Medicine j o u r n a l h o m e p a g e : w w w. e l s e v i e r. c o m / l o c a t e / s l e e p
Editorial
A lot is missing: the Orcade study
The authors report on short-term follow-up of dental device usage in obstructive sleep apnea (OSA) patients [1]. In this day and age, with data and studies accumulated over the past 20 years, it is surprising that this study has such a limited protocol: (1) Based on investigation of baseline sleep-disordered breathing (SDB) and follow-up of patients, functional magnetic resonance imaging (fMRI) and psychometric studies [2–5] demonstrate that the major impact of obstructive sleep apnea syndrome (OSAS) is on the brain and brain functioning, while its cardiovascular impact is much less severe and body mass index has as much an impact as the abnormal breathing during sleep [6]. The foremost difficulty is the sleep disturbance and the amount of arousal during sleep. Studies have shown that the lack of inclusion of the “hypopnea arousal” in the investigation offers a very limited and inaccurate view of sleep-disordered breathing. Official scoring manuals indicate the need to include the “hypopnea arousals” in their report [7], which is one of the foremost difficulties when an ambulatory study without recording of the electroencephalography (EEG) is performed as inaccurate results are obtained. Usage of this device may be considered in a clinical setting but would be absolutely unacceptable in a research study where potential public health decisions are made. As there is no notion of how data were obtained in the report, one could hope for the best, but “hypopnea arousals” should be reported systematically. (2) Another scoring problem is the absence of measurement of “flow limitation” [8]. The International Classification of Sleep Disorders–third edition (ICSD-3), and other classifications have included “upper airway resistance syndrome” as part of the “SDB–OSA spectrum,” and at present there are numerous publications in the world literature to affirm that, such pattern has a chronic negative impact on brain functioning and persistence of long-term poor sleep [9,10]. One clear problem with dental devices is that they have little impact on the maxillary component of the abnormal breathing problem, and they also often lead to mouth breathing, a very negative issue in long-term studies [11,12]. No notion of such evaluation and scoring is presented here. (3) During the past 15 years, the involvement of orthodontists, maxillomandibular specialists, and myofunctional therapists [13] has reminded us that craniofacial bones remodel from applied force on the bones or the teeth. This is the basis of orthodontic tooth movement, and usage of rapid- or slowmaxillary- or bi-maxillary expansion, myofunctional therapies http://dx.doi.org/10.1016/j.sleep.2015.10.008 1389-9457/© 2015 Elsevier B.V. All rights reserved.
(active or passive) have been used on children and adults in the treatment of OSA. Adult pulmonary specialists have demonstrated the importance of orofacial muscle activity in the treatment of OSAS [14,15]. The major goal of these approaches in both children and adults is to lead to nasal breathing and eliminate mouth breathing during sleep [11,12]. Long-term mouth breathing leads to progressive worsening of the orofacial anatomic factors and the associated SDB syndrome. (4) Another problem is the lack of information on the anatomic orofacial structures at entry and absence of systematic evaluation at follow-up evaluation. Tsuda et al. [16] have shown well that within two years, adult OSA treated with nasal continuous positive airway pressure (CPAP) develop significant changes involving the mandible and maxilla related to the nightly usage of a CPAP mask, as demonstrated on cephalometric X-rays, and to date three-dimensional computed tomography (3D-CT). Commercial ventures dealing with CPAP have since made important efforts to develop masks with little or no contact with the maxilla and mandible. In addition, the recommendation of using a “chin” strap has been very much de-emphasized as it can lead to a retraction of the mandible and act on mandibular condyle in a growing patient. The absence of any follow-up imaging data when following up patients placed on any dental device, particularly in a research investigation, is absolutely unacceptable, especially given that the patient’s age at entry included 18-year-old patients who may still have residual craniofacial growth. In clinical practice, at certain places around the world, the absence of documentation of maxillomandibular impact of dental devices at regular intervals is considered poor practice. It is important to know when to interrupt treatment and understand the real risks of such treatment. Recent studies have tried to counteract the negative effects of any dental device on the maxillomandibular complex and on the bite by implementing daily myofunctional exercises. As this study was performed in a country where myofunctional therapy was developed over 50 years ago [17], it is surprising that such countermeasures were not included in the protocol. If it was, it was not mentioned. (5) In terms of the amount and type of advancement, it is indicated that “the traction-based triangle and connector articulations enable mandibular advancement in parallel to the occlusion plane. This vector of advancement reduces stress on muscles and temporomandibular joint contact force [18], and may be a possible explanation for the good tolerance of
Editorial / Sleep Medicine 19 (2016) 126–127
127
References
Fig. 1. Bite change after usage of a “bi-block” “push” oral device for OSA: Note the posterior movement of the maxilla and posterior tilting of upper teeth, and forward placement of mandible with forward tilting of lower teeth, all consequences of oraldevice usage.
minimal residual disease (MRD) in the present cohort.” The connector articulations on any type of MRD will not allow parallel advancement to the occlusal plane if the patient’s malocclusion cannot support it. The direction of the lower jaw advancement is a reflection of the patient’s overbite and the incline of the glenoid fossa. Understanding these jaw mechanics may be lost at the 3–6-month assessment because the patients did not see the dental sleep specialist along with the sleep physician. This can affect the success and efficacy of the appliance if a physician or medical device company is asked to evaluate for the dental side effects. It is precisely the dentoalveolar side effects that limit the compliance and longterm success of MRD therapy. In conclusion, the protocol presented in this study may have been acceptable 20 years ago, but the protocol reported here does not bring information on a key issue: the risks associated with the studied treatment and impact on maxillary–mandibular bones (Fig. 1). Conflict of interest The ICMJE Uniform Disclosure Form for Potential Conflicts of Interest associated with this article can be viewed by clicking on the following link: http://dx.doi.org/10.1016/j.sleep.2015.10.008.
[1] Vecchierini MF, Attali A, Collet JM, et al. A custom-made mandibular repositioning device for obstructive sleep apnea-hypopnoea syndrome: the Orcades study. Sleep Med 2015. pii: S1389-9457(15)00827-8. doi:10.3402/ meo.v15i0.5063. [2] Diomedi M, Placidi F, Cupini LM, et al. Cerebral hemodynamic changes in sleep apnea syndrome and effect of continuous positive airway pressure treatment. Neurology 1998;51:1051–6. [3] Ferini-Strambi L, Baietto C, Di Gioia MR, et al. Cognitive dysfunction in patients with obstructive sleep apnea (OSA): partial reversibility after continuous positive airway pressure (CPAP). Brain Res Bull 2003;61:87–92. [4] Reichmuth KJ, Dopp JM, Barczi SR, et al. Impaired vascular regulation in patients with obstructive sleep apnea: effects of continuous positive airway pressure treatment. Am J Respir Crit Care Med 2009;180:1143–50. [5] Morgan BJ, Reichmuth KJ, Peppard PE, et al. Effects of sleep-disordered breathing on cerebrovascular regulation: a population-based study. Am J Respir Crit Care Med 2010;182:1445–52. [6] Chirinos JA, Guru bhagavatula I, Teff K, et al. CPAP, weight loss, or both for obstructive sleep apnea. N Engl J Med 2014;370:2265–75. [7] Guilleminault C, Hagen CC, Hunyh NT. Comparison of hypopnea definitions in lean patients with known obstructive sleep apnea hypopnea syndrome (OSAHS). Sleep Breath 2009;13(4):341–7. [8] Palombini L, Tufik S, Rapoport D, et al. Inspiratory flow limitation in a normal population of adults in Sao Paolo, Brazil. Sleep 2013;36:1663–8. [9] Bao G, Guilleminault C. Upper Airway Resistance Syndrome 1 decade later. Curr Opin Pulm Med 2004;10:461–7. [10] Tantrakul V, Guilleminault C. Sleep complaints in pre-menopausal women and its association with sleep-disordered breathing. Lung 2009;187:82–92. [11] Guilleminault C, Sullivan SS. Toward restauration of continuous nasal breathing as the ultimate treatment goal in pediatric obstructive sleep apnea. Enliven Pediatr Neonatol Biol 2014;1:1–7. [12] Lee SY, Guilleminaul C, Chiu HY, et al. Mouth breathing, “nasal dis-use” and pediatric sleep-disordered-breathing. Sleep Breath 2015;in press. [13] Chauvois A, Fournier M, Girardin F. Reeducation des fonctions dans la therapeutique orthodontiques. Paris: S.I.D; 1991. p. 1–231. [14] Guimarães KC, Drager LF, Genta PR, et al. Effects of oropharyngeal exercises on patients with moderate obstructive sleep apnea syndrome. Am J Respir Crit Care Med 2009;179(10):962–6. [15] Camacho M, Certal V, Abdullatif J, et al. Myofunctional therapy to treat obstructive sleep apnea: a systematic review and meta-analysis. Sleep 2015;38(5):669–75. [16] Tsuda H, Almeida RF, Tsuda T, et al. Cranio-facial changes after 2 years of nasal-continuous-positive-airway-pressure use in patients with obstructivesleep-apnea. Chest 2010;138:870–4. [17] Andrews JM, Guilleminault C, Holdaway RA. Use of a mandibular positioning device in obstructive sleep apnea: a case report. Bull Eur Physiopath Resp (Clin Resp Physiol) 1983;19:61. [18] Cheze L. Navailles B impact on temporomandibular joint of two oral appliances for sleep-apnoea treatment. ITBM-RBM 2006;27:233–7.
Stacey Quo Dental School Orthodontics Division, University of California, California USA Christian Guilleminault * Division of Sleep Medicine, Stanford University, California USA * Tel.: +1 6507236601. E-mail address: [email protected] Available online 5 November 2015