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 Table of Contents  
Year : 2022  |  Volume : 13  |  Issue : 4  |  Page : 154-157

Could Mouth Breathing Lead to Adenoid Hypertrophy?

1 Department of Research, Beijing Aipulisi Health Technology Co., Ltd., China
2 Beijing Beimei Pediatric Dental Clinic, China

Date of Submission27-Oct-2022
Date of Decision08-Nov-2022
Date of Acceptance10-Nov-2022
Date of Web Publication12-Dec-2022

Correspondence Address:
Qingyu Wang
Zhangyang Road, Pudong New Area, Shanghai
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/denthyp.denthyp_132_22

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Introduction: Adenoid hypertrophy (AH), an immune response of the body against infections, is common in children and has adverse effects on their physical and mental health. The hypothesis: We hypothesized that mouth breathing (MB) may induce AH, and that they interact with each other. Evaluation of The Hypothesis: AH may cause upper airway obstruction, which can induce the patient to switch from nasal breathing to mouth breathing (MB). However, MB does not involve the processes of warming, humidifying, and cleaning the inhaled air, which leads to changes in the oral environment and increases the risk of inflammation of the upper respiratory tract. This study discussed the relationship between MB and AH. The importance of this hypothesis is that attention should be paid to the status of MB or AH while treating them in order to block the interaction and thus improve the efficiency of treatment.

Keywords: Adenoid hypertrophy, children, mouth breathing

How to cite this article:
Ma XK, Wang Q. Could Mouth Breathing Lead to Adenoid Hypertrophy?. Dent Hypotheses 2022;13:154-7

How to cite this URL:
Ma XK, Wang Q. Could Mouth Breathing Lead to Adenoid Hypertrophy?. Dent Hypotheses [serial online] 2022 [cited 2023 Feb 5];13:154-7. Available from:

  Introduction Top

Adenoids are a large mass of lymphoid tissue located in the posterior wall of the nasopharynx, and they enlarge shortly after birth through puberty when they generally regress.[1] Adenoid hypertrophy (AH) is a natural response to increased immunologic activity in early life.[2] Pereira et al.[3] reported that the prevalence of AH was 34.5% in a random representative pediatric population, but the prevalence ranged from 42% to 70% in convenience samples. Accumulated studies have indicated that AH could cause series of local and systemic symptoms, such as nasal obstruction, snoring, mouth breathing (MB), and obstructive sleep apnea.[4],[5] Several studies have reported that the prevalence of MB ranges from 4.3% to 56.8%, and the broad range may probably be due to the difference in region, age, and form of diagnosing the breathing pattern.[6],[7] Moreover, studies have shown that MB has adverse effects on facial growth, occlusion, and quality of life of children.[6],[8]

Linder-Aronson[9] reported that nasopharyngeal obstruction, whether due to AH or any other etiology, increased the resistance to nasal airflow such that children were forced to perform MB. Adenotonsillar hypertrophy was a reported leading factor causing partial or total obstruction of upper airways in childhood.[10],[11] The prevailing view is that AH causes MB, but is their relationship only unidirectional?

Existing studies have found that compared with nasal breathing, MB changes the oral environment and increases the stimulation of the upper airway due to the lack of the processes of warming, humidifying, and cleaning the inhaled air.[11],[12],[13],[14] Furthermore, the upper respiratory tract-associated lymphoid tissues, comprising the adenoids and palatine tonsils are the body’s first line of immune defense, and they are exposed to antigens from both the outside air (allergens and pathogens) and the alimentary tract.[15],[16] Weakened or absent nasal defense mechanisms may increase the risk of upper respiratory tract infections in children.[16] Therefore, according to the above research evidence, MB may also be a risk factor for AH, affecting the process of the adenoidal inflammatory response.

  The Hypothesis Top

It is well known that AH can cause MB. Here, we propose the hypothesis that MB is likely to cause AH, and that their effects may be reciprocal.

Evaluation of The Hypothesis

The adenoids are an aggregate of lymphatic tissue located in the posterior nasopharyngeal airway. They usually appear in early childhood between 6 and 10 years and then disappear at 16 years.[5] Local immunity and immune surveillance are considered to be the two major immune functions of the tonsils and adenoids.[1] AH is a common disorder in children, which has many adverse effects on children’s physical and mental health and growth and development.[17],[18],[19] It may be physiological (and reversible whenever a pathological agent has ceased to function), or pathological in which case the condition remains constant.[18] Infection is the main cause of AH, which is clinically expressed as nightly snoring, nasal obstruction, MB, recurrent sinusitis, auditory tube dysfunction, otitis media, reduced ability to smell and taste, speech problems, changes in facial growth and behavioral development, and/or more serious problems, such as obstructive sleep apnea syndrome.[16] Adenoids are mainly composed of lymphoid T cells, and the location and function of effector T cells are critical for generating an effective immune response.[16] In particular, CD81 T lymphocytes can mobilize via the following two main mechanisms: cytolysis; and production of cytokines, chemokines, and microbicidal molecules.[20] Studies have shown that microbial stimulation and external stimuli, such as cigarette smoke, are associated with AH.[21] In allergic children, allergic rhinitis (AR), positive reactivity to molds, and possibly, to some seasonal allergens have been reported to be risk factors for AH.[17] The effect of AH on MB has been generally confirmed, and the inflammatory response of adenoids to external stimuli also indirectly supports our hypothesis that MB may stimulate adenoidal inflammatory responses.

The nose includes the following three parts: the external nose, the nasal cavity, and the sinuses. It is the first part of the respiratory tract and an important entry point for pathogenic factors to invade the body. In addition to olfactory and sensory functions, the nose also performs the function of cleaning, warming, and humidifying the inhaled air, making it suitable for use in the lungs and reducing irritation.[22] Moreover, the nose also performs local immune function. A large amount of immunoglobulin A (IgA) in nasal secretions is synthesized locally, and it exists on the surface of the nasal mucosa and in secretions in the form of secretory IgA (sIgA), which can neutralize foreign invading antigenic substances to protect the respiratory tract.[23],[24]

Nasal breathing is the first physiological function that develops at birth.[25] MB is an unnatural act that occurs when the primary airway is blocked by oversized tonsils and adenoids, nasal septal deviation, sinusitis, turbinate hypertrophy, and nasal polyp[11]; and it is characterized by mixed breathing or mouth-assisted breathing instead of simple nasal breathing in children, and has adverse effects on physical and mental health and academic performance of children and adolescents.[26] Studies have reported that MB does not involve the processing of inhaled air, thereby having adverse effects on respiratory organs and causing varying degrees of inflammatory responses.[6],[13],[27] Increased evaporation of saliva due to MB reduces the cleaning effect of saliva, leading to dry mouth, accumulation of food debris and dental plaque, and increased risk of tooth decay, inflammation, and halitosis.[11] The study by Araújo et al.[28] showed that asthmatic individuals had a higher proportion of MB than non-asthmatic individuals, and that there was an association between MB and asthma in children and adolescents. The above studies demonstrate the adverse effects of MB on the immune response of the body, and they also show the possibility that MB may affect the normal structure and function of adenoids, which provides support for our hypothesis that MB probably plays a dual role in the relationship—MB may not only be the result of enlarged adenoids, but may also be a cause of enlarged adenoids.

Implications of the hypothesis

AH is common in children and adolescents.[3] Current treatments for AH include adenoidectomy and pharmaceutical therapy.[17] Adenoidectomy is one of the most common surgical procedures performed in pediatric populations worldwide.[29] In 2006, more than half a million of outpatient adenoidectomy procedures were performed in children in the United States.[30] Adenoidectomy is associated with some complications, such as postoperative hemorrhage and infection[17],[31]; in addition, previous studies have indicated that the early removal of adenoidal tissue may have a negative impact on immune function.[32],[33] Moreover, Ing et al.[34] reported that children who undergo minor surgery requiring anesthesia under age 5 have a small but statistically significant increased risk of mental disorder diagnoses and developmental delay and attention deficit hyperactivity disorder diagnoses.

According to our hypothesis, attention should be paid to correcting MB while treating AH to improve the therapeutic effect. The combination of pharmaceutical therapy and correction of MB can reduce the stimulation of adenoids, and considering the physiological atrophy of adenoids simultaneously, adenoidectomy and its adverse effects can be avoided. However, in children with only MB symptoms, attention should be paid to the physiological condition of adenoids, tonsils, and other immune tissues to prevent the development of inflammatory reactions and reduce the risk and adverse effects of adenotonsillar hypertrophy. In China, adenoidectomy in children is also common, considered as the first-line method,[35] and used extremely frequently in some areas. This study discusses the relationship between MB and AH, and proposes treatment recommendations in order to reduce the occurrence of adenoidectomy. If the hypothesis of this study can be generalized, it will be of great help to the treatment of related diseases in children and adolescents in China.In addition, nitric oxide (NO) is a reactive oxygen species that is continually produced by epithelial cells of the paranasal sinuses and nasopharynx via NO synthase enzymes.[36] Studies indicate that NO may also help to reduce respiratory tract infection by inactivating viruses and inhibiting their replication in epithelial cells.[37] Winchester et al.[38] found that the treatment with nitric oxide nasal spray in their trial was effective in reducing the viral load in patients with mild, symptomatic COVID-19 infection. Promoting nasal breathing and inhibiting MB may have potential benefits against coronavirus infection.[37] Thus, it is important to clarify the relationship between MB and AH and to take effective treatment to prevent COVID-19 in children.

The interaction between MB and AH suggests that attention should be paid to the changes in both entities during the treatment process, and corresponding treatments should be given simultaneously when conditions allow promotion of the curative effect and avoidance of the vicious circle between MB and AH.

Financial support and sponsorship


Conflicts of interest

The authors report no conflicts of interest.

  References Top

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