The Relationship of Temporomandibular Joint, Orofacial Pain, and Sleep Apnea

Author(s):  
Mayoor Patel ◽  
G. Gary Demerjian ◽  
Anthony B. Sims
1977 ◽  
Vol 3 (1) ◽  
pp. 11-26
Author(s):  
Brendan Stack ◽  
Lawerence Funt

Beginning with its founding at the start of this century by Edward H. Angle, the orthodontic profession's primary concern for its first forty years was the relationship of teeth. Orthodontists' efforts were directed towards how the teeth interdigitated. Since the early 1940's, due to the influence of Doctors Tweed, Brodie, Steiner, Margolis, etc., emphasis has been placed upon the effects of orthodontics on the patient's profile, and the profession was then concerned with both esthetics and tooth function. There are two final areas into which the bulk of the orthodontic profession has yet to move, and they are the areas of the temporomandibular joint myofunctional therapy. Orthodontists must now begin to incorporate TMJ function and the results of myofunctional therapy into their thinking and into their treatment plans and realize the effect they have upon improving the skeletal muscle, neurology and physiology of the patient's face as well as his facial esthetics and the cuspal interdigitation of his teeth. The dental profession as a whole must not only realize the role myofunctional therapy has in attaining these goals, but the role it plays in maintaining their subsequent stability.


2018 ◽  
Vol 22 (4) ◽  
pp. 955-961 ◽  
Author(s):  
Edward T. Chang ◽  
Grace Baik ◽  
Carlos Torre ◽  
Scott E. Brietzke ◽  
Macario Camacho

2020 ◽  
Vol 19 (3) ◽  
pp. 2405
Author(s):  
М. V. Agaltsov ◽  
O. M. Drapkina

The results of prospective studies, meta-analyzes and systematic reviews on the associations of obstructive sleep apnea (OSA) with various cardiovascular diseases (CVD) were analyzed. Currently, the mechanisms related to high prevalence of breathing-related sleep disorders among population of economically developed countries are clear, and an increase in the number of OSA patients has been shown. The relationship between OSA and CVD has been widely confirmed in large cohort studies. The first review part discusses the relationship of hypertension (HTN) and various heart arrhythmias (atrial fibrillation (AF), bradyarrhythmias, premature ventricular contraction, sudden death during sleep) with breathing-related sleep disorders. These groups of cardiovascular disorders currently show the most proven relationship with sleep apnea. In addition to cross-sectional studies indicating the high prevalence of OSA in patients with HTN and AF, some observational studies indicate an increase in the number of patients with HTN and paroxysmal AF with history of untreated sleep apnea. An analysis of the current issues of OSA phenotypes (in particular, REM-related OSA in hypertensive patients) as the most unfavorable cardiovascular factors is carried out.


Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Stefanie Aeschbacher ◽  
Matthias Bossard ◽  
Mirco von Rotz ◽  
Tobias Schoen ◽  
Anna Maseli ◽  
...  

Background: The influence of sleep related breathing disorders on heart rate variability (HRV), a measure of autonomic nervous function, is not well studied. We therefore assessed the relationship of the Apnea-Hypopnea Index (AHI) and the Oxygen Desaturation Index (ODI) with 24-hour HRV in a large population of young and healthy adults. Methods: Individuals aged between 25-41 years with a body mass index ≤35km/kg2 and without known sleep apnea syndrome (SAS) or cardiovascular disease were included in the population-based GAPP-study. A 24-hour electrocardiogram (ECG) was obtained in every participant, and systematic post-processing performed with a dedicated software. The standard deviation of all normal RR intervals (SDNN) was used as main HRV marker. AHI and ODI were obtained from nighttime pulsoxymetry with nasal airflow measurements. Sleep apnea (SA) was defined as either an AHI ≥5 or an ODI ≥5. Multivariable regression models were constructed to assess the relationship of SDNN with either AHI or ODI and to adjust for a large number of confounders. Results: We included 1266 participants (47% men) with a median age of 35 years. Mean SDNN among men and women was 162 and 148ms (p<0.0001), respectively. The proportion of participants with SA using an AHI- or ODI-based definition was 10 and 11%, respectively. Compared to individuals without SA, the beta coefficient (95% confidence interval (CI)) for SDNN was -7.48 (-14.75; -0.23, p=0.04) among those with an AHI-based SA definition, and was -11.45 (-18.39; -4.52, p=0.001) among those with an ODI-based SA definition. A highly significant inverse trend across different categories of AHI and ODI was observed, as shown in the Table. Conclusion: Early stages of sleep related breathing disorders are strongly associated with decreasing HRV in young and healthy adults, without evidence of a threshold. These findings suggest a tight link between sleep related breathing disorders and autonomic dysfunction.


2000 ◽  
Vol 88 (1) ◽  
pp. 257-264 ◽  
Author(s):  
Kenneth I. Berger ◽  
Indu Ayappa ◽  
I. Barry Sorkin ◽  
Robert G. Norman ◽  
David M. Rapoport ◽  
...  

The contribution of apnea to chronic hypercapnia in obstructive sleep apnea (OSA) has not been clarified. Using a model (D. M. Rapoport, R. G. Norman, and R. M. Goldring. J. Appl. Physiol. 75: 2302–2309, 1993), we previously illustrated failure of CO2 homeostasis during periodic breathing resulting from temporal dissociation between ventilation and perfusion (“temporal V˙/Q˙mismatch”). This study measures acute kinetics of CO2 during periodic breathing and addresses interapnea ventilatory compensation for maintenance of CO2 homeostasis in 11 patients with OSA during daytime sleep (37–171 min). Ventilation and expiratory CO2 and O2 fractions were measured on a breath-by-breath basis by means of a tight-fitting full facemask. Calculations included CO2excretion, metabolic CO2production, and CO2 balance (metabolic CO2 production − exhaled CO2). CO2 balance was tabulated for each apnea/hypopnea event-interevent cycle and as a cumulative value during sleep. Cumulative CO2 balance varied (−3,570 to +1,388 ml). Positive cumulative CO2 balance occurred in the absence of overall hypoventilation during sleep. For each cycle, positive CO2 balance occurred despite increased interevent ventilation to rates as high as 45 l/min. This failure of CO2 homeostasis was dependent on the event-to-interevent duration ratio. The results demonstrate that 1) periodic breathing provides a mechanism for acute hypercapnia in OSA, 2) acute hypercapnia during periodic breathing may occur without a decrease in average minute ventilation, supporting the presence of temporalV˙/Q˙ mismatch, as predicted from our model, and 3) compensation for CO2 accumulation during apnea/hypopnea may be limited by the duration of the interevent interval. The relationship of this acute hypercapnia to sustained chronic hypercapnia in OSA remains to be further explored.


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