Snoring: is this noisy behavior just an embarrassing situation or is it a sign of an underlying problem? Why obstructive sleep apnoea will almost always leads to loud and frequent snoring, while snoring does not always indicate sleep apnoea? If you suffer of any of these two conditions, it is better that you understand where snoring and sleep apnoea originates because your health is at risk!
While obstructive sleep apnoea is taken more seriously, snoring is usually considered as a simple harmless embarrassing condition. The reality is that both have the same underlying cause that should not be ignored: a poor craniofacial development.
Posture and activity of oral and facial muscles (tongue, masseter, buccinator and others), together with forces coming from the teeth, determine the direction of growth of the maxilla (Figure 1) [1,2]. Open-mouth posture is one of the most common disturbances of oral posture, always present in mouth breather. However, open-mouth habits do not necessarily coincide with mouth breathing [3].
Figure 1 – Direction of growth of the maxilla depends from the forces coming from teeth, tongue and other orofacial muscles. (From [34])As also confirmed by experiments on primates [4], when the tongue posture is low and teeth are not in contact (at rest and when swallowing), the maxilla drops down and back. This reduces the eye support, flattens the cheekbones, narrows the nasal airway, lengthens the mid facial third, and lowers the palate, which narrows and create malocclusion [5]. Also, a vertical growth of the maxilla forces the mandible to swing back, restricting the pharynx (Figure 2). As a compensatory mechanism, a retruded mandible causes the head to tilt forward in a forward head posture, freeing in this way the airways in the erect posture [6,7].
Figure 2 – Two patients from study [8]: subject HB003 shows vertical growth of maxilla, with facial retrognathism and large mandibular inclination. Notice the forward head posture and the reduced airways’ space. Subject HB092 shows forward growth of maxilla, with facial prognathism and small mandibular inclination. Notice the head posture aligned with the cervical column and the bigger space for the airways.
Restriction of the upper respiratory tract, including narrowing of both nasal cavity and pharinx, is a key element in the development of snoring and obstructive sleep apnoea [9,10,11]. In adults, the site of airway occlusion during apnoeic episodes is usually located in the oropharyngeal region. As Figure 3 shows, individuals with a vertical growth of the maxilla have a lower palate, the tongue is in a low posture nearer to the airways and the posterior pharyngeal wall is restricted [12,13,14]. When sleeping lied down, the tongue, the soft palate and the mandible fall into the airways, obstructing the air flow.
Figure 3 – Individuals with a low tongue posture have a vertical growth of the maxilla, with a lower palate and a retruded mandible. When sleeping lied down, the tongue, the soft palate and the mandible fall into the airways, obstructing the air flow. (From [35])
When airways obstruction is only partial, the air can still flow, but it encounters more resistance, inducing the typical noise of snoring. Instead, when the obstruction is total, the air cannot flows and apnoeic episodes arises, as Figure 4 suggests. As we can seen, the principle is the same for both snoring and apnoea, as well as the underlying cause (a vertical growth of the maxilla).
Figure 4 – Partial obstruction of the airways leads to snoring, while total obstruction causes sleep apnoea. (From [36])Obstructive apnoeas may induce severe intermittent hypoxemia (low level of oxygen in the blood) and carbon dioxide (CO2) retention during sleep, disrupting the normal physiologic interactions between sleep and the cardiovascular system. Hypoxia (deficiency in the amount of oxygen reaching the tissues) and hypercapnia (abnormally elevated carbon dioxide levels in the blood) stimulate ventilatory effort and ultimately arousal from sleep to terminate the apnoeic event. Toward the end of apnoeic episodes, blood pressure can reach levels as high as 240/130 mm Hg (normal blood pressure while awake is between 120/80 and 140/90). For these reasons obstructive sleep apnea is considered a risk factor and possible cause of cardiovascular diseases [15,16,17], but the mechanisms behind the link are unclear.
Hypoxemia caused by sleep apnoea and poor quality of sleep are also linked with attention and memory deficits, resulting as a risk factor for dementia and Alzhaimer’s disease later in life [18,19]. However, also in this case, mechanisms behind this link are not clear.
Snoring and sleep apnoea are also associated with higher incidence of stroke and death [20,21,22], together with hypertension (high blood pressure) [23,24]. Hypertension in mid-life is linked to development of dementia and Alzhaimer’s disease later in life [25,26,27,28]. Link’s origins are unknown in this case too.
So, it looks like there is a clear link between snoring, sleep apnoea, hypertension, cardiovascular diseases, dementia, Alzheimer, stroke and death. Current medicine cannot explain the reasons behind these connections, but the most careful reader should have some doubts.
A poor craniofacial development leads to body’s compensations (e.g. forward head posture, kyphosis, lordosis, scoliosis). Muscle chains of the body are in continue tension since out of balance, the spine has excessive curvatures and vertebrae are out of alignment. All of this can cause compression of blood vessels, with consequent hypoxemia, hypoxia, as in the case of hair loss, and hypertension. Interestingly, many studies have associated baldness with higher risk of coronary heart disease, of which hypertension is a risk factor [29,30,31,32,33]. So, knowing the common underlying cause of both baldness and obstructive sleep apnea, could craniofacial development be the responsible of all these unclear links?
TMD - Occlusion 