The influence of nasal respiratory function on the growth and development of craniofacial structures was first generated over a century ago by anecdotal reports describing the effects of “mouth breathing” on dental and facial morphology.

In 1872, Tomes (1872) described the dentofacial changes associated with chronic nasal airway obstruction, citing the lips-apart posture as the cause for decreased pressure on the incisors and proclined anterior teeth. He also coined the term “adenoid faces” to describe the associated facial changes.

In 1925, Dr. Edward H. Angle reprinted a book by George Catlin entitled “The Breath of Life (All Life on Earth is Breath, All Else on Earth is Death).” This book by Catlin advocated the superiority of nasal breathing over mouth breathing in sleep and described the consequences of habitual mouth breathing on teeth and facial features (Goldsmith and Stool 1994). Dr. Angle (1900) was also a firm believer in these concepts and stated in his textbook:

When there is normal nasal respiration and normal relations of the dental arches, the teeth, and the muscles, the conditions are such as to perfectly maintain the equilibrium and the mutual support necessary to the normal development of the teeth and jaws. Should nasal obstruction occur in the developing child, inducing habitual mouth-breathing, immediately the equilibrium is disturbed, the lips and muscles are placed on a different tension, and pressure upon the arches, instead of being equal, is localized, being greater than normal at some points and less at others. No matter how strenuously it may be denied, malocclusion of the teeth and abnormalities in the formation of the bones of the jaws naturally follow. The undeveloped nose and adjacent region of the face, the vacant look, the short upper lip, the open mouth, and irregular teeth of the mouth-breather are common sights familiar to all.

Later other reports reiterated the relationship between altered dentofacial form and mouth breathing. Chronic nasal allergies were suggested to cause paranasal depression, V-shaped palate, and proclination of the maxillary incisors (Duke 1930; Balyeat and Bowen 1934). Cohen (1937) attributed mouth breathing due to allergies to high-arched and narrow palates, a flat and narrow face, and some type of orthodontic deformity (although he did not classify which type). Subtelny (1954) theorized that enlarged adenoids will cause a separation of the lips, downward and forward movement of the tongue away from the soft palate, depression in the position of the mandible, constriction of the maxillary arch, and a Class II division 1 type of malocclusion due to procumbent maxillary anterior teeth. Paul and Nanda (1973) also found a tendency toward Class II malocclusion with an increase in overbite and overjet in mouth-breathing subjects when compared to nasal breathers.

Different theories were proposed to explain the relationship between respiratory mode and possible dentofacial changes. Morrison (1931) suggested that the oral airstream in mouth-breathing individuals caused the negative pressure between the tongue and palate to be lost hindering normal downward palatal descent. James and Hastings (1932) proposed that the loss of the normal pressure in the mouth due to an impairment of the airway is associated with impaired action of the tongue, lips, cheeks, and other forces acting on the jaws. They considered the impaired and misdirected action of these forces as the reason for the deformities of the jaws. A clearer understanding of these effects was possible when Moss (1962) developed the “functional matrix theory.” This theory was based on the principle that the skeletal unit in the functional craniofacial component provides protection and mechanical support for its specific functional matrix and grows in response to the functional demands of surrounding tissues and structures. According to Moss’s theory nasal breathing allowed proper growth and development of craniofacial and dentofacial complex (Moss 1969). Later, Solow and Tallgren (1976) found an association between the posture of the head and cervical column and craniofacial alterations seen in mouth-breathing patients. These results led to an alternative explanation known as “Soft Tissue Stretching Hypothesis” (Solow and Kreiberg 1977). This theory suggested that nasal obstruction caused extension of the head and that this postural change causes soft tissue stretching causing differential forces to act on skeleton causing morphological changes. Hence, the existence of a relationship between respiratory mode and dentofacial growth changes was widely accepted, and early treatment of allergies and removal of adenoid tissue before the eruption of permanent teeth were suggested to prevent the alterations in dental arches (Subtelny 1954; Marks 1965).

However, there were others who were skeptical of such wide acceptance of a possible relationship between oral respiration and growth changes. Kingsley (1889) considered the deep and narrow palate a congenital morphological trait rather than the results of a muscle imbalance due to mouth breathing. Gwynne-Evans and Ballard (1959) observed the relationship between jaw form, soft tissue morphology, and upper respiratory conditions for more than 15 years and concluded that mouth breathing does not result in deformities of the jaws, malocclusion, or adenoidal facies. Other authors reported that more than 50 % of the patients who were characterized as mouth breathers had Class I occlusions and no specific malocclusion pattern was correlated with mouth breathing (Howard 1932; Leech 1958; Huber and Reynolds 1946).

Since then, investigators have attempted to look more critically at the issue through experimental models and clinical research with objectively defined criteria for mouth breathing. Harvold (1968) used the rhesus monkey, Macaca mulatta, as a model in his experiments to test the connection between neuromuscular activity and skeletal morphogenesis. He anchored a piece of plastic in the palatal vault between the molars and found that the mandible moved lower and the tongue moved forward resulting in an anterior open bite. This study was followed by another one in which the animals were induced to lower their mandibles by fitting an acrylic block in the palatal vault (Harvold et al. 1972). After 6 months there was a significant increase in face height in experimental groups. They concluded that any factor, such as mouth breathing, that lowers the postural position of the mandible could also increase the face height. They tested their hypothesis by blocking nasal inhalation with silicone nose plugs in growing monkeys (Harvold et al. 1973, 1981). Radiographic, electromyographic, and dental cast measurements showed increased face height, decreased maxillary and mandibular intercanine distance, decreased maxillary dental arch length, steeper mandibular plane, larger gonial angle, altered muscle activity, and changes in the morphology of the tongue in the experimental group. The pattern of maintaining an airway differed between monkeys. Those that kept their mouths constantly open by lowering the mandible and protruding their tongues developed more severe malocclusions than those that rhythmically opened and closed their mouths with respiration.

The altered muscle activity in the rhesus monkeys due to forced oral breathing was further explored in other studies (Miller et al. 1982; 1984; Vargervik et al. 1984). These experiments documented changes in neuromuscular recruitment patterns resulting in changed function and posture of the mandible, tongue, and upper lip with considerable variation among the animals and concluded that nasal obstruction can induce neuromuscular changes which extend beyond the period of obstruction and remain even after nasal breathing is established.

More recent animal studies also found that nasopharyngeal respiratory obstruction was associated with downward and backward rotation of the mandible, upward and backward growth of the condyle, divergent gonial angle, anterior open bite, spaced dental arch in the lower anterior region, and a reduction in the height of the maxilla (Yamada et al. 1997; Scarano et al. 1998).

These experimental findings corroborated the previous data on the relationship between mouth breathing and an increase in facial height. However, it should be kept in mind that the results of these animal studies cannot be readily extrapolated to humans. Total nasal obstruction, as induced by researchers in these experiments, is extremely rare in humans. The oropharyngeal structures also differ between the species. Thus, the postural changes that occur in animals due to forced oral breathing may not be the same in humans.

Early clinical studies on humans generally used lateral cephalograms to evaluate dentofacial changes and the upper airway. Linder-Aronson (1970) studied 162 children aged 6–12 years. Half of these children were determined to need adenoidectomies, while the other half were controls. The patients were examined with respect to nasal airflow, breathing pattern, and dentofacial morphologic variables. He reported a significant relationship between enlarged adenoids determined by cephalometric x-rays and certain craniofacial changes, including low tongue position, mouth breathing, narrow maxillary arch, crossbite, and retroclined maxillary and mandibular incisors. In 1974, he examined a group of Swedish children before and after adenoidectomies and compared them to controls with respect to changes in cephalometric measurements. He reported that the patients in adenoidectomy group had increased anterior facial height, maxillary constriction, and retroclined incisors compared to controls. After their adenoidectomies, upper airway obstruction was resolved in these patients and their growth pattern became horizontal (Linder-Aronson 1974).

Hannuksela (1981) compared allergic and nonallergic children and reported a tendency toward clockwise rotation of the mandible and retroclined mandibular incisors. However, further evaluation of this population revealed no significant differences in the occlusion between groups (Hannuksela 1983). Other cephalometric studies also failed to show a relationship between the airway space or adenoid size and malocclusion (Sosa et al. 1982; Mergen and Jacobs 1970).

Lateral cephalograms were readily available to orthodontists and valuable in determining dentofacial changes. They were also recommended for assessing adenoid size (Shapiro and Shapiro 1984). However, since lateral cephalograms are two dimensional and unable to provide volumetric data, their reliability in determining airway size and adenoids have been criticized (Vig and Hall 1980; Maw et al. 1981).

With the development of respirometric techniques, a more objective classification of respiratory patterns became possible. Vig et al. (1981) reported higher nasal resistance in increased facial height groups compared with controls, but they found no significant differences in the nasal volume flow rate between groups. Fields et al. (1991) also concluded that subjects with long faces had a significantly smaller component of nasal airflow. Warren and Spalding (1991) suggested that high airway resistance due to nasal impairment may cause an exaggerated postural response if there is a low drape to the velum, the pillars form a posterior curtain, the tonsils are enlarged, or the posterior portion of the tongue is carried high.

The early clinical studies that used lateral cephalograms and/or other respirometric techniques showed that the relationship between dentofacial growth and development and respiratory mode is variable and multifactorial.

Heredity and environmental factors are both effective in the development of dental arches and postnatal determination of craniofacial features. One of the most important environmental factors is the predominant respiratory pattern. Nasal breathing is associated with normal posture of the tongue and lips and normal muscle activity. If there is nasal obstruction, this would likely affect the muscle forces acting on the dentofacial region. This change in muscular action may cause abnormal facial growth and development. It has been shown that during oral breathing masseter muscle activity is inhibited (Ono et al. 1998). Increased airway resistance also stimulates mechanoreceptors in the upper airway and increases the activities of the genioglossus and mylohyoid muscles due to forward positioning of the tongue and opening of the mouth to maintain the airway (Song and Pae 2001).

Today, it is accepted that growth occurs under the control of both genetic and environmental factors. Genetics act on cartilages and the bones respond to the changes in these cartilaginous structures. The growth and needs of the soft tissue matrix also cause reactive changes in both the bone and the cartilage.

Long-term mouth breathing seems to affect the occlusion and facial morphology during periods of rapid growth. However, not every patient has the same growth changes due to oral breathing. The heritable characteristics of anatomical structures also seem to play a role in determining which patients will be most affected. In some patients a slight opening of the lips may be enough to provide the necessary airway, while in others a more exaggerated postural response of the mandible, tongue, and head will be necessary. Children with narrow facial patterns also may be more susceptible to growth changes due to mouth breathing than children with broad facial features. It is also possible for patients with a vertical facial growth pattern to be more likely to be mouth breathers. The severity of the obstruction will also determine if the child is a chronic mouth breather or a partial one. If the obstruction is severe, the changed postural responses will be in place longer causing more extensive growth changes in dentofacial structures.

The most common cause of oral breathing in children is enlarged pharyngeal lymphoid tissue. The enlargement of these tissues may adversely affect pharyngeal patency (Gross and Harrison 2000). Normally, the size of the adenoid tissue is dependent on the associated skeletal structures. However, abnormal growth of this tissue may predispose the patient to upper airway obstruction causing oral respiration. As a matter of fact, any reason that causes nasal resistance to increase for long periods of time, such as allergies or nasal septal deformity, has the potential to cause chronic oral respiration.