The Etiology of Orthodontic Problems

Disturbances in Embryologic Development

Defects in embryologic development usually result in death of the embryo. As many as 20% of early pregnancies terminate because of lethal embryologic defects, often so early that the mother is not even aware of conception. Although most defects in embryos are of genetic origin, effects from the environment also are important. Chemical and other agents capable of producing embryologic defects if given at the critical time are called teratogens. Most drugs do not interfere with normal development or, at high doses, kill the embryo without producing defects, and therefore are not teratogenic. Teratogens typically cause specific defects if present at low levels but if given in higher doses, do have lethal effects. Teratogens known to produce orthodontic problems are listed in Table 5-1.

There are five principal stages in craniofacial development (Table 5-2), and effects on the developing face and jaws can arise during each stage:

The best example of a problem that can be traced to the very early first and second stages is the characteristic facies of fetal alcohol syndrome (FAS; Figure 5-2). This is due to deficiencies of midline tissue of the neural plate very early in embryonic development caused by exposure to very high levels of ethanol. Although such blood levels can be reached only in extreme intoxication in chronic alcoholics, the resulting facial deformity and developmental delay occur frequently enough to be implicated in many cases of midface deficiency.¹ In these unfortunate children, the delay in dental development matches the skeletal delay.²

Many of the problems that result in craniofacial anomalies arise in the third stage of development and are related to neural crest cell origin and migration. Since most structures of the face are ultimately derived from migrating neural crest cells (Figure 5-3), it is not surprising that interferences with this migration produce facial deformities. At the completion of the migration of the neural crest cells in the fourth week of human embryonic life, they form practically all of the loose mesenchymal tissue in the facial region that lies between the surface ectoderm and the underlying forebrain and eye and most of the mesenchyme in the mandibular arch. Most of the neural crest cells in the facial area later differentiate into skeletal and connective tissues, including the bones of the jaw and the teeth.

The importance of neural crest migration and the possibility of drug-induced impairment of the migration have been demonstrated clearly by unfortunate experience. In the 1960s and 1970s, exposure to thalidomide caused major congenital defects, including facial anomalies in thousands of children. In the 1980s, severe facial malformations related to the anti-acne drug isotretinoin (Accutane) were reported. The similarities in the defects make it likely that both these drugs affect neural crest cells. Retinoic acid plays a crucial role in the ontogenesis of the midface, and recent work suggests that loss of retinoic acid receptor genes affects postmigratory activity of crest cells, clarifying the timing of Accutane effects.³ The danger with isotretinoin is that it affects a developing embryo before the mother knows she is pregnant.

Altered development of cells derived from the neural crest also has been implicated in Treacher Collins syndrome (Figure 5-4), which is characterized by a generalized lack of mesenchymal tissue and now known to be due (at least in some instances) to mutations in a specific gene (TCOF1) that lead to loss of a specific exon.⁴

Craniofacial microsomia (formerly called hemifacial microsomia) is characterized by a lack of development in lateral facial areas. Typically, the external ear is deformed and both the ramus of the mandible and associated soft tissues (muscle, fascia) are deficient or missing (Figure 5-5). Although facial asymmetry is always seen (thus the former name), cranial as well as facial structures are affected. The cause is loss of neural crest cells (for an unknown reason) during migration. Neural crest cells with the longest migration path, those taking a circuitous route to the lateral and lower areas of the face, are most affected, whereas those going to the central face tend to complete their migratory movement, so midline facial defects, including clefts, rarely are part of the syndrome.⁵

Neural crest cells migrating to lower regions are important in the formation of the great vessels (aorta, pulmonary artery, aortic arch), and they also are likely to be affected by problems in crest cell migration. For this reason, defects in the great vessels (as in the tetralogy of Fallot) are common in children with craniofacial malformations.

The most common congenital defect involving the face and jaws, second only to clubfoot in the entire spectrum of congenital deformities, is clefting of the lip, palate, or (less commonly) other facial structures. Clefts arise during the fourth developmental stage. Exactly where they appear is determined by the locations at which fusion of the various facial processes failed to occur (Figures 5-6 and 5-7), and this in turn is influenced by the time in embryologic life when some interference with development occurred.

Clefting of the lip occurs because of a failure of fusion between the median and lateral nasal processes and the maxillary prominence, which normally occurs in humans during the sixth week of development. At least theoretically, a midline cleft of the upper lip could develop because of a split within the median nasal process, but this almost never occurs. Instead, clefts of the lip occur lateral to the midline on either or both sides (Figure 5-8). Since the fusion of these processes during primary palate formation creates not only the lip but the area of the alveolar ridge containing the central and lateral incisors, it is likely that a notch in the alveolar process will accompany a cleft lip even if there is no cleft of the secondary palate.

Closure of the secondary palate by elevation of the palatal shelves (Figures 5-9 and 5-10) follows that of the primary palate by nearly 2 weeks, which means that an interference with lip closure that still is present can also affect the palate. About 60% of individuals with a cleft lip also have a palatal cleft (Figure 5-11). An isolated cleft of the secondary palate is the result of a problem that arose after lip closure was completed. Incomplete fusion of the secondary palate produces a notch in its posterior extent (sometimes only a bifid uvula). This indicates a very late-appearing interference with fusion.

The width of the mouth is determined by fusion of the maxillary and mandibular processes at their lateral extent, so a failure of fusion in this area could produce an exceptionally wide mouth, or macrostomia. Failure of fusion between the maxillary and lateral processes could produce an obliquely directed cleft of the face. Other patterns of facial clefts are possible, based on the details of fusion, and were classified by Tessier.⁶ Fortunately, these conditions are rare.

Morphogenetic movements of the tissues are a prominent part of the fourth stage of facial development. As these have become better understood, the way in which clefts of the lip and palate develop has been clarified. For example, it is known now that cigarette smoking by the mother is an etiologic factor in the development of cleft lip and palate,⁷ and even passive smoke increases the risk of cleft palate.⁸ An important initial step in development of the primary palate is a forward movement of the lateral nasal process, which positions it so that contact with the median nasal process is possible. The hypoxia associated with smoking probably interferes with this movement.

Another major group of craniofacial malformations arise considerably later than the ones discussed so far, during the final stage of facial development and in the early fetal rather than the embryologic period of prenatal life. These are the craniosynostosis syndromes, which result from early closure of the sutures between the cranial and facial bones. In fetal life, normal cranial and facial development depends on growth adjustments at the sutures in response to growth of the brain and facial soft tissues. Early closure of a suture, called synostosis, leads to characteristic distortions, depending on the location of the early fusion.⁹

Crouzon’s syndrome is the most frequently occurring member of this group. It is characterized by underdevelopment of the midface and eyes that seem to bulge from their sockets (Figure 5-12). This syndrome arises because of prenatal fusion of the superior and posterior sutures of the maxilla along the wall of the orbit. The premature fusion frequently extends posteriorly into the cranium, producing distortions of the cranial vault as well. If fusion in the orbital area prevents the maxilla from translating downward and forward, the result is severe underdevelopment of the middle third of the face. The characteristic protrusion of the eyes is largely an illusion—the eyes appear to bulge outward because the area beneath them is underdeveloped. There may be a component of true extrusion of the eyes, however, because when cranial sutures become synostosed, intracranial pressure increases.

Although the characteristic deformity is recognized at birth, the situation worsens as growth disturbances caused by the fused sutures continue postnatally. Surgery to release the sutures is necessary at an early age.

Growth Disturbances in the Fetal and Perinatal Period

Progressive Deformities in Childhood

A progressive deformity is one that steadily becomes worse, which, of course, indicates early treatment. These problems, fortunately, arise much less frequently than the severe but stable deformities that comprise most of the jaw problems encountered in children.

Disturbances Arising in Adolescence or Early Adult Life

Occasionally, unilateral excessive growth of the mandible occurs in individuals who seem metabolically normal. Why this occurs is entirely unknown. It is most likely in girls between the ages of 15 and 20 but may occur as early as age 10 or as late as the early 30s in either sex. The condition formerly was called condylar hyperplasia, and proliferation of the condylar cartilage is a prominent aspect; however, because the body of the mandible also is affected (Figure 5-20), hemimandibular hypertrophy now is considered a more accurate descriptive term.¹³ The excessive growth may stop spontaneously, but in severe cases removal of the affected condyle and reconstruction of the area are necessary.

In acromegaly, which is caused by an anterior pituitary tumor that secretes excessive amounts of growth hormone, excessive growth of the mandible may occur, creating a skeletal Class III malocclusion in adult life (Figure 5-21). Often (but not always—sometimes the mandible is unaffected while hands and/or feet grow), mandibular growth accelerates again to the levels seen in the adolescent growth spurt, years after adolescent growth was completed.¹⁴ The condylar cartilage proliferates, but it is difficult to be sure whether this is the cause of the mandibular growth or merely accompanies it. Although the excessive growth stops when the tumor is removed or irradiated, the skeletal deformity persists and orthognathic surgery to reposition the mandible is likely to be necessary (see Chapter 19).

Disturbances of Dental Development

Most disturbances of dental development are contributors to isolated Class I malocclusion, and these conditions (such as drift of permanent teeth after early loss of primary teeth) are discussed in Chapter 11. Dental problems that are related to larger congenital or health problems include:

Equilibrium Considerations

The laws of physics state that an object subjected to unequal forces will be accelerated and thereby will move to a different position in space. It follows that if any object is subjected to a set of forces but remains in the same position, any forces must be in balance or equilibrium. From this perspective, the dentition is obviously in equilibrium, since the teeth are subjected to a variety of forces but do not move to a new location under usual circumstances.

The effectiveness of orthodontic treatment is itself a demonstration that forces on the dentition are normally in equilibrium. Teeth normally experience forces from masticatory effort, swallowing, and speaking but do not move. If a tooth is subjected to a continuous force from an orthodontic appliance, it does move, so the force applied by the orthodontist has altered the previous equilibrium. The nature of the forces necessary for tooth movement is discussed in detail in Chapter 8, but at this point, we must briefly preview what is known about force magnitude and force duration in producing changes in tooth position.

A key consideration is that the supporting structures of the dentition (periodontal ligament [PDL] and alveolar bone) are constructed to withstand heavy forces of short duration such as those from mastication. During mastication, the fluid in the PDL space acts as a shock absorber, so that the soft tissues in the PDL are not compressed although bending of alveolar bone occurs. Only if pressure is maintained long enough to squeeze out the fluid (a few seconds) is there an impact on the soft tissues. Then, since that hurts, the pressure is released and the fluid returns before the next chewing stroke. The result is that only light force of long duration (6 hours or so per day) is important in determining whether there is enough of an imbalance of forces to lead to tooth movement, which means if the balance between tongue versus lip/cheek pressure changes, tooth movement would be expected.

It is easy to demonstrate that this is indeed the case. For example, if an injury to the soft tissue of the lip results in scarring and contracture, the incisors in this vicinity will be moved lingually as the lip tightens against them (Figure 5-29). On the other hand, if restraining pressure by the lip or cheek is removed, the teeth move outward in response to unopposed pressure from the tongue (Figure 5-30, A). Pressure from the tongue, whether from an enlargement of the tongue from a tumor or other source or because its posture has changed, will result in labial displacement of the teeth even though the lips and cheeks are intact because the equilibrium is altered (Figure 5-30, B).

These observations make it plain that, in contrast to forces from mastication, light sustained pressures from lips, cheeks, and tongue at rest are important determinants of tooth position. It seems unlikely, however, that the intermittent short-duration pressures created when the tongue and lips contact the teeth during swallowing or speaking would have any significant impact on tooth position. As with masticatory forces, the pressure magnitudes would be great enough to move a tooth, but the duration is inadequate (Table 5-3).

Equilibrium considerations also apply to the skeleton, including the facial skeleton. Skeletal alterations occur all the time in response to functional demands and are magnified under unusual experimental situations. As discussed in Chapter 2, the bony processes to which muscles attach are especially influenced by the muscles and the location of the attachments. The form of the mandible, because it is largely dictated by the shape of its functional processes, is particularly prone to alteration. The density of the facial bones, like the skeleton as a whole, increases when heavy work is done and decreases in its absence.

Let us now consider the role of function in the etiology of malocclusion and dentofacial deformity from this perspective.

Masticatory Function

The pressures generated by chewing activity potentially could affect dentofacial development in two ways: (1) greater use of the jaws, with higher and/or more prolonged biting force, could increase the dimensions of the jaws and dental arches or (2) less use of the jaws might lead to underdeveloped dental arches and crowded and irregular teeth and the resulting decreased biting force could affect how much the teeth erupt, thereby affecting lower face height and overbite/open bite relationships.

Sucking and Other Habits

Almost all normal children engage in non-nutritive sucking of a thumb or pacifier, and as a general rule, sucking habits during the primary dentition years have little if any long-term effect. If these habits persist beyond the time that the permanent teeth begin to erupt, however, malocclusion characterized by flared and spaced maxillary incisors, lingually positioned lower incisors, anterior open bite, and a narrow upper arch is the likely result (Figure 5-34). The characteristic malocclusion associated with sucking arises from a combination of direct pressure on the teeth and an alteration in the pattern of resting cheek and lip pressures.

When a child places a thumb or finger between the teeth, it is usually positioned at an angle so that it presses lingually against the lower incisors and labially against the upper incisors (Figure 5-35). There can be considerable variation in which teeth are affected and how much. From equilibrium theory, one would expect that how much the teeth are displaced would correlate better with the number of hours per day of sucking than with the magnitude of the pressure. Children who suck vigorously but intermittently may not displace the incisors much if at all, whereas others, particularly those who sleep with a thumb or finger between the teeth all night, can cause a significant malocclusion.

The anterior open bite associated with thumbsucking arises by a combination of interference with normal eruption of incisors and excessive eruption of posterior teeth. When a thumb or finger is placed between the anterior teeth, the mandible must be positioned downward to accommodate it. The interposed thumb directly impedes incisor eruption. At the same time, the separation of the jaws alters the vertical equilibrium on the posterior teeth, and as a result, there is more eruption of posterior teeth than might otherwise have occurred. Because of the geometry of the jaws, 1 mm of elongation posteriorly opens the bite about 2 mm anteriorly, so this can be a powerful contributor to the development of anterior open bite (Figure 5-36).

Although negative pressure is created within the mouth during sucking, there is no reason to believe that this is responsible for the constriction of the maxillary arch that usually accompanies sucking habits. Instead, arch form is affected by an alteration in the balance between cheek and tongue pressures. If the thumb is placed between the teeth, the tongue must be lowered, which decreases pressure by the tongue against the lingual of upper posterior teeth. At the same time, cheek pressure against these teeth is increased as the buccinator muscle contracts during sucking (Figure 5-37). Cheek pressures are greatest at the corners of the mouth, and this probably explains why the maxillary arch tends to become V-shaped, with more constriction across the canines than the molars. A child who sucks vigorously is more likely to have a narrow upper arch than one who just places the thumb between the teeth.

Mild displacement of the primary incisor teeth is often noted in a 3- or 4-year-old thumbsucker, but if sucking stops at this stage, normal lip and cheek pressures soon restore the teeth to their usual positions. If the habit persists after the permanent incisors begin to erupt, orthodontic treatment may be necessary to overcome the resulting tooth displacements. The constricted maxillary arch is the aspect of the malocclusion least likely to correct spontaneously. In many children with a history of thumbsucking, if the maxillary arch is expanded transversely, both the incisor protrusion and anterior open bite will improve spontaneously (see Chapter 12). There is no point in beginning orthodontic therapy, of course, until the habit has stopped.

Whether a habit can serve in the same way as an orthodontic appliance to change the position of the teeth has been the subject of controversy since at least the first century AD, when Celsus recommended that a child with a crooked tooth be instructed to apply finger pressure against it to move it to its proper position. From our present understanding of equilibrium, we would expect that this might work, but only if the child kept finger pressure against the tooth for 6 hours or more per day.

This concept also makes it easier to understand how playing a musical instrument might relate to the development of a malocclusion. In the past, many clinicians have suspected that playing a wind instrument might affect the position of the anterior teeth, and some have prescribed musical instruments as part of orthodontic therapy. Playing a clarinet, for instance, might lead to increased overjet because of the way the reeds are placed between the incisors, and this instrument could be considered both a potential cause of a Class II malocclusion and a therapeutic device for treatment of Class III. String instruments like the violin and viola require a specific head and jaw posture that affects tongue versus lip/cheek pressures and could produce asymmetries in arch form. Although the expected types of displacement of teeth are seen in professional musicians,³¹ even in this group the effects are not dramatic, and little or no effect is observed in most children.³² It seems quite likely that the duration of tongue and lip pressures associated with playing the instrument is too short to make any difference, except in the most devoted musician.

Can habits affect development of the jaws? In Edward Angle’s era, a “sleeping habit” in which the weight of the head rested on the chin once was thought to be a major cause of Class II malocclusion. Facial asymmetries have been attributed to always sleeping on one side of the face or even to “leaning habits,” as when an inattentive child leans the side of his face against one hand to doze without falling out of the classroom chair. It is not nearly as easy to distort the facial skeleton as these views implied. Sucking habits often exceed the time threshold necessary to produce an effect on the teeth, but even prolonged sucking has little impact on the underlying form of the jaws. On close analysis, most other habits have such a short duration that dental effects, much less skeletal effects, are unlikely.

Tongue Thrusting

Much attention has been paid at various times to the tongue and tongue habits as possible etiologic factors in malocclusion. The possible deleterious effects of “tongue thrust swallowing” (Figure 5-38), defined as placement of the tongue tip forward between the incisors during swallowing, received particular emphasis in the 1950s and 1960s.

Laboratory studies indicate that individuals who place the tongue tip forward when they swallow usually do not have more tongue force against the teeth than those who keep the tongue tip back; in fact, tongue pressure may be lower.³³ The term tongue thrust is therefore something of a misnomer because it implies that the tongue is forcefully thrust forward. Swallowing is not a learned behavior but is integrated and controlled physiologically at subconscious levels, so whatever the pattern of swallow, it cannot be considered a habit in the usual sense. It is true, however, that individuals with an anterior open bite malocclusion place the tongue between the anterior teeth when they swallow, while those who have a normal incisor relationship usually do not, and it is tempting to blame the open bite on this pattern of tongue activity.

As discussed in detail in Chapter 2, the mature or adult swallow pattern appears in some normal children as early as age 3 but is not present in the majority until about age 6 and is never achieved in 10% to 15% of a typical population. Tongue thrust swallowing in older patients superficially resembles the infantile swallow (described in Chapter 3), and sometimes children or adults who place the tongue between the anterior teeth are spoken of as having a retained infantile swallow. This is clearly incorrect. Only brain-damaged children retain a truly infantile swallow in which the posterior part of the tongue has little or no role.

Since coordinated movements of the posterior tongue and elevation of the mandible tend to develop before protrusion of the tongue tip between the incisor teeth disappears, what is called “tongue thrusting” in young children is often a normal transitional stage in swallowing. During the transition from an infantile to a mature swallow, a child can be expected to pass through a stage in which the swallow is characterized by muscular activity to bring the lips together, separation of the posterior teeth, and forward protrusion of the tongue between the teeth. This is also a description of the classic tongue thrust swallow. A delay in the normal swallow transition can be expected when a child has a sucking habit.

When there is an anterior open bite and/or upper incisor protrusion, as often occurs from sucking habits, it is more difficult to seal off the front of the mouth during swallowing to prevent food or liquids from escaping. Bringing the lips together and placing the tongue between the separated anterior teeth is a successful maneuver to close off the front of the mouth and form an anterior seal. In other words, a tongue thrust swallow is a useful physiologic adaptation if you have an open bite, which is why an individual with an open bite also has a tongue thrust swallow. The reverse is not true—protruding the tongue between the anterior teeth during swallowing is often present in children with good anterior occlusion. After a sucking habit stops, the anterior open bite tends to close spontaneously, but the position of the tongue between the anterior teeth persists for a while as the open bite closes. Until the open bite disappears, an anterior seal by the tongue tip remains necessary.

The modern viewpoint is, in short, that tongue thrust swallowing is seen primarily in two circumstances: in younger children with reasonably normal occlusion, in whom it represents only a transitional stage in normal physiologic maturation; and in individuals of any age with displaced incisors, in whom it is an adaptation to the space between the teeth. The presence of a large overjet (often) and anterior open bite (nearly always) conditions a child or adult to place the tongue between the anterior teeth. A tongue thrust swallow therefore is more likely to be the result of displaced incisors, not the cause. It follows, of course, that correcting the tooth position should cause a change in swallow pattern, and this usually happens. It is neither necessary nor desirable to try to teach the patient to swallow differently before beginning orthodontic treatment.

This is not to say that the tongue has no etiologic role in the development of open bite malocclusion. From equilibrium theory, light but sustained pressure by the tongue against the teeth would be expected to have significant effects. Tongue thrust swallowing simply has too short a duration to have an impact on tooth position. Pressure by the tongue against the teeth during a typical swallow lasts for approximately 1 second. A typical individual swallows about 800 times per day while awake but has only a few swallows per hour while asleep. The total per day therefore is usually under 1000. One thousand seconds of pressure, of course, totals only a few minutes, not nearly enough to affect the equilibrium.

On the other hand, if a patient has a forward resting posture of the tongue, the duration of this light pressure could affect tooth position, vertically or horizontally. Tongue tip protrusion during swallowing is sometimes associated with a forward tongue posture. If the position from which tongue movements start is different from normal, so that the pattern of resting pressures is different, there is likely to be an effect on the teeth, whereas if the postural position is normal, the tongue thrust swallow has no clinical significance.

Perhaps this point can best be put in perspective by comparing the number of children who have an anterior open bite malocclusion with the number of children of the same age reported to have a tongue thrust swallow. As Figure 5-39 shows, at every age above 6, the number of children reported to have a tongue thrust swallow is about 10 times greater than the number reported to have an anterior open bite. Thus there is no reason to believe that a tongue thrust swallow always implies an altered rest position and will lead to malocclusion. In a child who has an open bite, tongue posture may be a factor, but the swallow itself is not.

Respiratory Pattern

Respiratory needs are the primary determinant of the posture of the jaws and tongue (and of the head itself, to a lesser extent). Therefore it seems entirely reasonable that an altered respiratory pattern, such as breathing through the mouth rather than the nose, could change the posture of the head, jaw, and tongue. This in turn could alter the equilibrium of pressures on the jaws and teeth and affect both jaw growth and tooth position. In order to breathe through the mouth, it is necessary to lower the mandible and tongue, and extend (tip back) the head. If these postural changes were maintained, face height would increase, and posterior teeth would super-erupt; unless there was unusual vertical growth of the ramus, the mandible would rotate down and back, opening the bite anteriorly and increasing overjet; and increased pressure from the stretched cheeks might cause a narrower maxillary dental arch.

Exactly this type of malocclusion often is associated with mouth breathing (note its similarity to the pattern also blamed on sucking habits and tongue thrust swallow). The association has been noted for many years: the descriptive term adenoid facies has appeared in the English literature for at least a century, probably longer (Figure 5-40). Unfortunately, the relationship between mouth breathing, altered posture, and the development of malocclusion is not so clear-cut as the theoretical outcome of shifting to oral respiration might appear at first glance.³⁴ Recent experimental studies have only partially clarified the situation.

In analyzing this, it is important to understand first that although humans are primarily nasal breathers, everyone breathes partially through the mouth under certain physiologic conditions, the most prominent being an increased need for air during exercise. For the average individual, there is a transition to partial oral breathing when ventilatory exchange rates above 40 to 45 L/min are reached. At maximum effort, 80 or more L/min of air are needed, about half of which is obtained through the mouth. At rest, minimum airflow is 20 to 25 L/min, but heavy mental concentration or even normal conversation lead to increased airflow and a transition to partial mouth breathing.

During resting conditions, greater effort is required to breathe through the nose than through the mouth—the tortuous nasal passages introduce an element of resistance to airflow as they perform their function of warming and humidifying the inspired air. The increased work for nasal respiration is physiologically acceptable up to a point, and indeed respiration is most efficient with modest resistance present in the system. If the nose is partially obstructed, the work associated with nasal breathing increases, and at a certain level of resistance to nasal airflow, the individual switches to partial mouth breathing. This crossover point varies among individuals but is usually reached at resistance levels of about 3.5 to 4 cm H₂O/L/min.³⁵ The swelling of the nasal mucosa accompanying a common cold occasionally converts all of us to mouth breathing at rest by this mechanism.

Chronic respiratory obstruction can be produced by prolonged inflammation of the nasal mucosa associated with allergies or chronic infection. It can also be produced by mechanical obstruction anywhere within the nasorespiratory system, from the nares to the posterior nasal choanae. Under normal conditions, the size of the nostril is the limiting factor in nasal airflow. The pharyngeal tonsils or adenoids normally are large in children, and partial obstruction from this source may contribute to mouth breathing in children. Individuals who have had chronic nasal obstruction may continue to breathe partially through the mouth even after the obstruction has been relieved. In this sense, mouth breathing can sometimes be considered a habit.

If respiration had an effect on the jaws and teeth, it should do so by causing a change in posture that secondarily altered long-duration pressures from the soft tissues. Experiments with human subjects have shown that a change in posture does accompany nasal obstruction. For instance, when the nose is completely blocked, usually there is an immediate change of about 5 degrees in the craniovertebral angle (Figure 5-41). The jaws move apart, as much by elevation of the maxilla because the head tips back, as by depression of the mandible. When the nasal obstruction is removed, the original posture immediately returns. This physiologic response occurs to the same extent, however, in individuals who already have some nasal obstruction, which indicates that it may not totally result from respiratory demands.

Harvold’s classic experiments with growing monkeys showed that totally obstructing the nostrils for a prolonged period in this species leads to the development of malocclusion, but not the type commonly associated with mouth breathing in humans.³⁶ Instead, the monkeys tend to develop some degree of mandibular prognathism, although their response shows considerable variety. In evaluating these experiments, it must be kept in mind that mouth breathing of any extent is completely unnatural for monkeys, who will die if the nasal passages are obstructed abruptly. To carry out the experiments, it was necessary to gradually obstruct their noses, giving the animals a chance to learn how to survive as mouth breathers. The variety of responses in the monkeys suggests that the type of malocclusion is determined by the individual animal’s pattern of adaptation.

Total nasal obstruction is extremely rare in humans. There are only a few well-documented cases of facial growth in children with long-term total nasal obstruction, but it appears that under these circumstances the growth pattern is altered in the way one would predict (Figure 5-42). Because total nasal obstruction in humans is so rare, the important clinical question is whether partial nasal obstruction, of the type that occurs occasionally for a short time in everyone and chronically in some children, can lead to malocclusion; or more precisely, how close to total obstruction does partial obstruction have to come before it is clinically significant?

The question is difficult to answer, primarily because it is difficult to know what the pattern of respiration really is at any given time in humans. Observers tend to equate lip separation at rest with mouth breathing (see Figure 5-40), but this is simply not correct. It is perfectly possible for an individual to breathe through the nose while the lips are apart. To do this, it is only necessary to seal off the mouth by placing the tongue against the palate. Since some lip separation at rest (lip incompetence) is normal in children, many children who appear to be mouth breathers may not be.

Simple clinical tests for mouth breathing can also be misleading. The highly vascular nasal mucosa undergoes cycles of engorgement with blood and shrinkage. The cycles alternate between the two nostrils: when one is clear, the other is usually somewhat obstructed. For this reason, clinical tests to determine whether the patient can breathe freely through both nostrils nearly always show that one is at least partially blocked. One partially obstructed nostril should not be interpreted as a problem with normal nasal breathing.

The only reliable way to quantify the extent of mouth breathing is to establish how much of the total airflow goes through the nose and how much through the mouth, which requires special instrumentation to simultaneously measure nasal and oral airflow. This allows the percentage of nasal or oral respiration (nasal/oral ratio) to be calculated for the length of time the subject can tolerate being continuously monitored. It seems obvious that a certain percentage of oral respiration maintained for a certain percentage of the time should be the definition of significant mouth breathing, but despite years of effort such a definition has not been produced.

The best experimental data for the relationship between malocclusion and mouth breathing are derived from studies of the nasal/oral ratio in normal versus long-face children.³⁷ The relationship is not nearly as clear-cut as theory might predict. It is useful to represent the data as in Figure 5-43, which shows that both normal and long-face children are likely to be predominantly nasal breathers under laboratory conditions. A minority of the long-face children had less than 40% nasal breathing, while none of the normal children had such low nasal percentages. When adult long-face patients are examined, the findings are similar: the number with evidence of nasal obstruction is increased in comparison to a normal population, but the majority are not mouth breathers in the sense of predominantly oral respiration.

It seems reasonable to presume that children who require adenoidectomy and/or tonsillectomy for medical purposes, or those diagnosed as having chronic nasal allergies, would have some degree of nasal obstruction. Studies of Swedish children who underwent adenoidectomy showed that on the average, children in the adenoidectomy group had a significantly longer anterior face height than control children (Figure 5-44). They also had a tendency toward maxillary constriction and more upright incisors.³⁸ Furthermore, when children in the adenoidectomy group were followed after their treatment, they tended to return toward the mean of the control group, though the differences persisted (Figure 5-45). Similar differences from normal control groups were seen in other groups requiring adenoidectomy and/or tonsillectomy.³⁹

Although the differences between normal children and those in the allergy or adenoidectomy groups were statistically significant and undoubtedly real, they were not large. Face height on the average was about 3 mm greater in the adenoidectomy group. It appears therefore that research to this point on respiration has established two opposing principles, leaving a large gray area between them: (1) total nasal obstruction is highly likely to alter the pattern of growth and lead to malocclusion in experimental animals and humans, and individuals with a high percentage of oral respiration are overrepresented in the long-face population; but (2) the majority of individuals with the long-face pattern of deformity have no evidence of nasal obstruction and must therefore have some other etiologic factor as the principal cause. Perhaps the alterations in posture associated with partial nasal obstruction and moderate increases in the percentage of oral respiration are not great enough by themselves to create a severe malocclusion. Mouth breathing, in short, may contribute to the development of orthodontic problems but is difficult to indict as a frequent etiologic agent.

It is interesting to consider the other side of this relationship: can malocclusion sometimes cause respiratory obstruction? Sleep apnea has been recognized recently as a more frequent problem than had been appreciated, and it is apparent that mandibular deficiency can contribute to its development (see Chapter 18). Its etiology, however, is by no means determined just by orofacial morphology—obesity, age/gender, and cephalometric characteristics seem to be important, in that order.⁴⁰

1. Moore, ES, Ward, RE, Jamison, PL, et al. New perspectives on the face in fetal alcohol syndrome: what anthropometry tells us. Am J Med Genet. 2002;109:249–260.

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