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The nose normally acts as a filter and participates in
the immune response against viruses, bacteria and
fungi. Chemical substances produced in the nose,
such as nitric oxide and lysozyme, break down pathogens
such as bacteria, viruses and fungi in the nasal
and oral mucosa. Mouth breathing reduces the availability
of these substances, thus compromising the
child’s immune defence system. A major disadvantage
of mouth breathing is that the air passes into the lungs
and upper airway without undergoing the purification,
humidification and warming that normally occurs
when it passes through the nasal route. The result of
this is oral dysbiosis, increased dental caries and gum
disease and increased upper respiratory infection.
Oral dysbiosis or growth of abnormal bacteria in the
mouth and throat is a well-known cause of increased
tooth decay and gum disease and probably also
contributes to ongoing enlargement of adenoids and
tonsils and to ear infections. It may also contribute to
abnormal gut flora. Many parents report that when
their child stops mouth breathing not only do they
have fewer colds and upper respiratory tract infections
but also their enlarged lymph glands become smaller.
Parents also report that their children have fewer ear
infections, and this is supported by research showing
that otitis media is aggravated by habitual mouth
breathing and associated habits such as atypical swallowing
patterns and chronic sniffing.
Mouth breathing has also been shown to aggravate
airway related conditions such as asthma and sleep 

apnoea. Oral breathing causes a decrease in lung function
in mild asthmatic subjects at rest and during exercise
and is thought to play a role in the pathogenesis of
acute asthma exacerbations. Some research has shown
that improving nasal breathing can reduce the severity
of asthma.
Nasal breathing plays a major role in the regulation of
respiration in sleep. The effect of mouth breathing on
the patency of the pharyngeal airway is a major contributing
factor to sleep apnoea. Some researchers stress
that collapse of the pharyngeal airway triggered by
the switch to oral breathing is the key step in onset of
sleep-disordered breathing.