Chapter 376. Dental Occlusion and Its Management

Dental occlusion is the term used to describe the relationship of the maxillary and mandibular teeth to each other when in contact and the relationship of the teeth to one another within each jaw. The American Academy of Pediatric Dentistry “recognizes the importance of managing the developing dentition and occlusion and its effect on the well-being of children, adolescents, and adults.” Such management requires the appropriate and timely diagnosis of any developing malocclusion and the ability to either provide the proper treatment or to refer the patient to the appropriate specialist for treatment, with the ultimate goal of obtaining a stable, functional, and esthetically pleasing occlusion in the permanent dentition.1

In order to establish a definitive diagnosis and formulate a comprehensive plan to treat the presenting malocclusion, preliminary information must be acquired from a clinical exam, radiographs, dental casts, and photographs. However, the pediatrician is uniquely positioned to clinically detect many malocclusions in the course of his or her routine medical practice. This chapter covers the stages of dental development and normal occlusion and provides basic knowledge regarding the most common types of malocclusions seen in children. A more detailed description of relevant oral and dental anatomy is provided on the textbook DVD and in eFigure 376.1. The information contained herein is essential if the clinician wishes to recognize malocclusions that may benefit from treatment and to evaluate the effectiveness of any treatment rendered.

Hard Tissues

Tooth tissues grow in a similar manner to skeletal bones. Each tooth has a very specific, genetically determined shape and location (Fig. 376-1). Normal structural development requires that the tissues calcify in a manner somewhat similar to the formation of skeletal bones (eFig. 376.1). Three forms of an organic matrix calcify to varying degrees to form different components of the tooth. The tooth above the gingival margin, known as the crown, is covered by enamel, which is an organic matrix closely resembling hydroxyapatite in bone. When mature, enamel is very hard and is approximately 96% inorganic in an organic matrix. Dentin is the calcified tissue that makes up the bulk of the crown and root of the tooth. It is only 20% organic by weight. Collagen fibers make up about 18% of this weight, and the remaining inorganic portion is in the form of hydroxyapatite crystallites. Cementum is the dental tissue covering the anatomic root of the tooth, from the point at which the enamel layer ends to the apex of the root. The point where the enamel ends and the cementum starts is the cervix of the tooth or the cementoenamel junction (CEJ). The density of cementum is less than that of dentin and is about 50% inorganic. Connective tissue fibers from the periodontal ligament or membrane become embedded in the forming cementum to provide the attachment of the root to the surrounding bone.

Soft Tissues

The dental pulp is a specialized form of connective tissue filling the tooth’s internal cavity, with the pulp chamber decreasing in size with advancing age through the slow, continuous deposition of dentin. This tissue also contains nerves and vessels, which provide both sensory and nutritive functions for the tooth. Pulp can become inflamed by trauma or excessive thermal change and can become infected from the carious process. The periodontal ligament is comprised primarily of white collagenous fibers that surround the root and function as a suspensory ligament between the root surface and the alveolar bone.

The oral cavity is lined with varying types of mucosa in different locations. The gingivae cover an area limited to the outer surfaces of the jaws to a line termed the mucogingival junction, where it meets the alveolar mucosa. Gingival mucosa is pink and is adapted to sustaining the stresses of mastication by being keratinized and bound to the underlying periosteum. The mucosa covering the alveolar bone of the maxilla and mandible contain numerous small vessels close to the surface, resulting in a red coloration. The hard palate is covered with pink, thick mucosa that is highly keratinized and very tightly bound to the periosteum covering the bone. The dorsum of the tongue is covered by specialized mucosa to accommodate its sensory function of taste. The remaining areas of the oral cavity—lips, cheeks, soft palate, vestibular fornix, and floor of the mouth—are lined with relatively thin, elastic, nonkeratinized vascular mucosa.

The normal sequence of tooth formation is outlined in eTable 376.1. The earliest sign of tooth formation is seen at about the sixth week of embryonic life. The tooth buds of the primary teeth develop at 10 specific sites in the developing maxilla and mandible. The 20 succedaneous permanent teeth develop beneath the primary teeth while the permanent molars develop distally in sequential order. Calcification of the primary teeth begins at about 4 months in utero, and the enamel of all crowns is completed by 10 months after birth. The permanent teeth begin to calcify with the first molar around the time of birth, and the process is complete for all the teeth, with the exception of the third molars, by the seventh to eighth year of life.

In both the primary and permanent dentitions, the process of tooth eruption correlates with root development. When the crown emerges through the gingiva, the root usually comprises one half to two thirds of its final length. Eruption continues until the antagonist in the opposing jaw is contacted in occlusion. As tooth wear occurs throughout life, eruption continues but at a much reduced rate, keeping the teeth in occlusion. The primary cause of tooth eruption has not been definitively identified.

Exfoliation of the primary teeth is a normal physiological process that takes place as root development occurs in the permanent successors beneath them. The eruptive process stimulates the formation of osteoclasts, which results in the resorption of the roots of the primary teeth and their subsequent loss. Girls generally precede boys in the eruption of their permanent teeth.

The Primary Dentition

The primary (deciduous) dentition is comprised of 20 teeth, which begin to erupt at approximately 6 months of age and usually complete their eruption before the age of 3 years1 (Fig. 376-1A). In each quadrant, from anterior to posterior, there is a central incisor, a lateral incisor, a canine, and first and second molars. The timing of eruption varies considerably from child to child, but the sequence of eruption is usually as follows: central incisor, lateral incisor, first molar, canine, and second molar with the mandibular teeth erupting somewhat earlier than the maxillary teeth and bilateral symmetry usually the case. Ideally there should be spacing present between all of the teeth, although any space present between the posterior teeth usually closes prior to the eruption of the first permanent molar. Absence of spacing in the primary dentition suggests a greater than 50% probability of crowding in later stages of the dentition.2

Normal occlusion is characterized by maxillary and mandibular teeth that are related properly to each other in the sagittal, transverse, and vertical dimensions. The maxillary incisors and canines are positioned slightly forward of the mandibular incisors (normal overjet with no anterior crossbite), and the maxillary molars are positioned so that their buccal cusps occlude slightly to the outside of the mandibular molars and their palatal cusps occlude onto the center of the biting surface of the mandibular molars (normal buccal overjet with no posterior crossbite). Furthermore, there should be only a mild to moderate amount of vertical overlap of the maxillary and mandibular incisors (normal overbite). The midlines of the maxillary and mandibular dentitions should be approximately coincident with each other and with the facial midline (as approximated by the center of the philtrum), and there should be no significant shifting of the mandible laterally or anteriorly as the teeth come into contact (Fig. 376-2).

The relative position of the jaws, and therefore the occlusion, is reflected in the profile, which is also affected by the position of the teeth and by the soft tissues themselves. It is normal for the profile to be convex during the primary dentition stage of dental development, with this convexity usually decreasing during the subsequent stages as a result of greater forward growth of the mandible when compared with the maxilla (consistent with the overall cephalocaudal growth gradient).3

The Mixed Dentition

The mixed dentition is characterized by the presence of both primary and secondary teeth (eFig. 376.2), beginning with the eruption of the permanent incisors and molars between 6 and 7 years of age (Fig. 376-1B). The central incisors usually erupt prior to the lateral incisors, with the mandibular teeth erupting before the maxillary teeth. If any tooth has erupted normally and the contralateral tooth is delayed in eruption by greater than 6 months’ time, the patient should be referred for evaluation. Delayed tooth eruption is the most commonly encountered deviation from normal eruption time and may indicate systemic problems such as endocrine disorders or Down syndrome. Most frequently, delayed tooth eruption is the result of local factors such as the presence of a supernumerary tooth or ectopic eruption4 (Table 376-1). Ectopic eruption of the first permanent molar occurs in 2% to 6% of children, more frequently in the maxilla than in the mandible. Its timely diagnosis and treatment is important in preventing space loss and the malocclusion that might result.5

Once the permanent incisors and molars have completely erupted, there is usually a period of 2 to 3 years when no exfoliation of deciduous teeth or eruption of secondary teeth is observed. The transition to the permanent dentition begins between 9 and 11 years of age and continues to approximately age 14. The sequence of eruption is different in the mandible and the maxilla. In the mandible, the pattern is usually canine, first premolar, second premolar (premolars or bicuspids replace the primary molars), and second molar. In the maxilla, the sequence is usually first premolar, canine, second premolar, and second molar. It is during this stage of development that one or both maxillary canine teeth may encounter difficulty in erupting. Ectopic maxillary canines occur in 1% to 3% of the population and can cause the resorption of the roots of the neighboring permanent teeth (usually the lateral incisors), possibly even resulting in the complete loss of a tooth or teeth6 (eFig. 376.3).

The spaces between the anterior teeth that may have been present in the primary dentition are largely consumed when the larger permanent incisors erupt (“incisor liability”). Space may remain between the maxillary central incisors, where a thick labial frenum (Fig. 376-3) can persist and help to prevent its normal closure (83% of the patients with a diastema at 9 years of age do not have one at age 16).7,8 Importantly, the space available to accommodate the teeth from first permanent molar to first permanent molar (arch circumference) increases only marginally in the maxilla and actually decreases in the mandible during the mixed and permanent dentitions. Skeletal growth does not result in more space for the teeth in this region but does help to accommodate teeth posterior to the first permanent molars.9 The permanent canines and premolars are usually slightly smaller in size than the primary teeth that they replace (leeway space). Managing this space in the late mixed dentition may be important in the treatment of crowding and the ability to treat such crowding without extracting permanent teeth.10Normal occlusion in the mixed dentition is similar to that found in the primary dentition; the general relationships between the maxillary and mandibular teeth remain approximately the same but with any crowding present become more evident and the eventual nature of the final occlusion more determined.

Skeletal relationships in the mixed dentition stage are similar to those found in the primary dentition stage. However, it should be noted that the profile might become noticeably straighter as the forward growth of the mandible exceeds that of the maxilla, a process that becomes more evident as the child approaches and enters the pubertal growth spurt that will begin in the late mixed or adolescent dentition.

The Adolescent and Permanent Dentitions

The adolescent or early permanent dentition (eFig. 376.4) begins when the last primary tooth is lost, usually between 10 and 13 years of age. As this happens, the second permanent molars erupt behind the first molars, resulting in subtle changes in the molar occlusion. The occlusion—and the profile—may continue to change as skeletal (particularly mandibular) growth in the vertical and sagittal planes may alter the relationship of the jaws to each other, possibly revealing or exacerbating late-developing problems such as skeletally based class III (underbite) or open-bite malocclusions. This growth can take place even after all other skeletal growth has been completed. The eruption of third molars (wisdom teeth) is expected in the late teenage years but may occur well into the third decade of life. Third molars have often been blamed for the development of late mandibular dental crowding in the late adolescent and permanent dentitions. However, the literature suggests that late mandibular growth is a much more critical variable and that such crowding may develop even in the absence of third molars.11

Facial Analysis

Facial analysis is indispensible in the evaluation of a child’s occlusion. It provides important insight into the relationship between the bones of the facial skeleton and helps to determine the presence and nature of any anteroposterior discrepancies, vertical dysplasias, functional shifts, or craniofacial growth problems. The pediatrician can easily accomplished this during a routine clinical exam by using soft tissue landmarks that estimate the anterior extent of the cranial base, the maxilla, and the mandible. These landmarks are the bridge of the nose, the base of the nose, and the tip of the chin, respectively. Two lines can be mentally constructed between these points to describe the facial profile as convex, straight, or concave (Fig. 376-4). Vertical problems can be assessed using similar landmarks by determining if the portion of the face from the base of the nose to the bottom of the chin (lower face height) is properly related to the total face height (bridge of the nose to the bottom of the chin). Normal lower face height is approximately 55% of the total face height. Facial symmetry is best assessed from the posterosuperior view by determining if the chin point is approximately coincident with the facial midline. Mild asymmetry of the chin or nose (up to several mm) is considered to be within normal limits.12 Both profile and facial symmetry must be assessed when the mandible is in its normal position, not while it is artificially postured, as sometimes happens when children are examined.

The American Association of Orthodontists (AAO) recommends that all children be examined by no later than age 7.13 The rationale for this is that the posterior occlusion is established when the first molar teeth erupt, allowing assessment of the anteroposterior and transverse relationships of the occlusion and identifying the presence of any functional mandibular shift. The incisor teeth have begun to erupt, and problems can be detected such as crowding, anterior crossbites, posterior crossbites, open bites, oral habits, maxillary protrusion, and some facial asymmetries (eTable 376.2). For some, a timely evaluation will lead to significant treatment benefits; for most, the principal immediate benefit is a parent’s peace of mind. The pediatrician who makes timely referrals is rightly regarded as informed, caring, and concerned for the patient’s total well-being. Recognition and basic management of these disorders is summarized briefly in the sections that follow. More detailed guidance is provided on the textbook DVD.

For those patients who have clear indications for early intervention, early treatment presents the opportunity to

• influence jaw growth in a positive manner;
• harmonize widths of the dental arches;
• improve eruption patterns;
• lower risk of trauma to protruded upper incisors;
• correct harmful oral habits;
• improve aesthetics and self-esteem;
• simplify and/or shorten treatment time for later corrective orthodontics;
• reduce the likelihood of impacted permanent teeth;
• improve some speech problems; and
• preserve or gain space for erupting permanent teeth.

Dental Crowding

Crowding is one of the most prevalent components of malocclusion in the mixed, adolescent, and permanent dentitions, affecting as many as 40% of children ages 6 to 11 and 85% of children ages 12 to 17.11 The etiology of crowding is multifactorial and may include tooth-size/jaw-size discrepancies, loss of arch length (due to interproximal caries or the premature loss of primary teeth), ectopic eruption of teeth, or the presence of supernumerary teeth.3,10,11 It is important to emphasize that the premature loss of primary teeth, particularly molars, may require the use of fixed or removable space maintainers to prevent the development of unnecessary crowding or the exacerbation of existing crowding.14 Management of the space within the dental arches is the prime responsibility of the pediatric dentist and orthodontist. Failure to do so may result in the need to extract permanent teeth, difficulty in maintaining adequate oral hygiene, or the need for more complicated and lengthy orthodontic treatment (Fig. 376-5). A healthy and complete primary dentition plays an essential role in maintaining the space needed for the permanent teeth. A patient with prematurely lost, missing, or decayed teeth should be referred to a pediatric dentist or orthodontist for management as soon as the problem is detected. 3

Managing the crowded dentition requires examination and analysis of the space needed to accommodate the teeth, the space available, the occlusion, the profile, the periodontal health, and the oral hygiene status. It must also account for future growth and development of the jaws, the teeth, and the dental arches. Treatment modalities range from space maintenance in the mixed dentition to comprehensive orthodontic treatment involving the extraction of several permanent teeth.15 Pediatricians should encourage their patients with crowded dentitions to be evaluated while in the mixed dentition stage in order to preserve the choice between extraction and nonextraction treatment. Delayed evaluation leads to a need for extraction in the majority of cases.10,14,15

Anterior Crossbite

An anterior crossbite is defined as the lingual position of one or more maxillary anterior teeth in relationship with the corresponding mandibular anterior teeth (Fig. 376-6). The etiology of anterior crossbite malocclusions is summarized in eTable 376.3. Anterior crossbites may be differentiated into dental, functional, and skeletal crossbites, with any combination possible. Correcting anterior crossbites in a timely manner may be important to prevent untoward growth of the skeletal and dentoalveolar components of the craniofacial complex. Treatment may also be helpful in preventing attrition of the incisors and canines, in avoiding periodontal problems around ectopic incisors, in alleviating functional posterior crossbites that can develop from cuspal interferences caused by the anterior crossbite, in preventing habits such as bruxism, and in reestablishing proper muscle balance. Simple recognition of an anterior crossbite by the pediatrician is enough to justify referral to the pediatric dentist or orthodontist. The etiology of anterior crossbite malocclusions is summarized in eTable 376.3.

Diagnosis of a skeletal or functional anterior crossbite may be accomplished by viewing the patient in profile. The child will usually have a concave profile, with the base of the nose deficient in relation to the chin point. It is important for the practitioner to know that the timing of treatment for a skeletal anterior crossbite malocclusion may be critical. Studies have shown the potential for interceptive orthodontic treatment to be effective in correcting this malocclusion in as many as 66% to 75% of the cases if treatment is undertaken before the age of 10.16,17 In the author’s opinion, the pediatrician should question any treatment, or lack thereof, that does not consider this opportunity, because once the child matures, the treatments may become more complicated and less desirable. Similarly, it must be understood that some of these malocclusions cannot be successfully treated without a combined orthodontic and surgical approach and that careful diagnosis and treatment planning is essential in all of these cases.18

Treatment often requires a combined orthodontic and surgical approach.18 The modality of the chosen treatment depends on whether the child is in the primary, mixed, or permanent dentition and if a single tooth or several teeth are involved. A child presenting in the primary dentition (usually age 5 or less) typically has a single incisor tooth in crossbite and may also have an anterior functional shift of the mandible. In the younger child, various treatment options are available, including reassurance and periodic monitoring; occlusal grinding of the tooth responsible for the interference; appropriately timed extraction of the offending tooth if it is close to exfoliation; and use of a removable or a fixed appliance, depending on the child’s level of compliance.

Treatment regimes for the older child presenting in the mixed dentition (usually 6–11 years of age) include removable or fixed appliances and orthopedic devices. Appliance therapy for correcting an anterior crossbite may include expansion of the maxillary arch; this creates room for alignment of a palatally displaced tooth. Proven methods for correcting anterior crossbite malocclusions in young children are using a removable maxillary appliance with auxiliary springs or screws or using a removable mandibular appliance with a labial bow for anterior tooth retraction. Alternatively, in less compliant children, partial fixed appliances (2 molar bands and 4 bonded incisor brackets) may be used to tip the maxillary incisors forward. Orthopedic treatment in the form of extraoral traction can be applied to children with maxillary retrognathia in order to protract the maxillary skeletal and dentoalveolar complex forward.

Posterior Crossbite

A posterior crossbite malocclusion is defined as the abnormal buccolingual relationship between two or more maxillary and mandibular posterior teeth and has a reported prevalence of 7.7% to 17.6% in preadolescent children.19,20 The most common type of posterior crossbite is when the buccal cusps of the maxillary molars occlude palatally to the buccal cusps of the mandibular molars, unilaterally or bilaterally (Fig. 376-7). Much less common is the buccal or “Brodie” crossbite, which is when the palatal cusps of the maxillary molars occlude to the outside of the buccal cusps of the mandibular molars. Posterior crossbites may result from a dental transverse deficiency, the tipping of teeth, a skeletal transverse deficiency, sagittal discrepancies between the jaws, functional shifting of the mandible, or any combination of these factors.

Dentoalveolar crossbites are usually due to insufficient arch length or the prolonged retention of deciduous teeth, both of which can cause ectopic eruption of a tooth or teeth into crossbite. A skeletal crossbite is related to discrepancies between the transverse dimensions of the maxilla and mandible and could be due to a narrow maxilla, a wide mandible, or a combination of both. Since the type of treatment required for correction will depend mainly upon the origin of the problem, determining the dental or skeletal component of posterior crossbite represents the first step in treatment planning.

The pediatrician should be aware of the different types of posterior crossbites previously described and should understand that treatment is available to correct each of these problems. Of particular importance is recognizing that posterior crossbites accompanied by a functional shift of the mandible should be treated as early as possible. These comprise between 67% and 79% of unilateral crossbites found in the growing child, making them the most common type found in this group.20,21 The pediatrician may determine if there is a functional shift of the mandible by assessing the position of the chin from the posterosuperior view when the teeth are in occlusion and when they are not. When this condition is treated at the appropriate time, compensatory growth of the mandible may eliminate any positional and skeletal asymmetries present and may create optimum conditions for normal craniofacial growth and development. If the condition is left untreated, asymmetric growth of the mandible may result in permanent skeletal asymmetry that could have been avoided.22,23

Three points should be considered during the clinical differential diagnosis of dental versus skeletal transverse deficiency:

1. 1. The angulations (buccopalatal) of the posterior teeth. If the posterior teeth are of normal angulations in the presence of a unilateral or bilateral posterior crossbite, then a skeletal discrepancy is present. Consequently, orthopedic correction using a rapid or slow maxillary expander that may be bonded or banded should be considered. However, if the posterior teeth are improperly angulated, the problem is dental in origin and treatment should aim to correct the crossbite by dental uprighting, which will eliminate the crossbite. The exposure and analysis of a frontal (posteroanterior) cephalometric radiograph may be required to determine these angulations and to accurately determine the presence and magnitude of any skeletal discrepancy between the jaws.

   2. The severity of the crossbite. A posterior crossbite that is bilateral, that involves multiple teeth, and that has an increased maxillomandibular arch width discrepancy usually reflects an underlying skeletal problem.

   3. The morphology of the palatal vault. A deep and V-shaped palate is indicative of a skeletal deficiency.

Treatment differs substantially, depending on the underlying cause of the malocclusion. Skeletal crossbites, which usually result from a narrow maxilla but occasionally from an excessively wide mandible, are generally treated by heavy forces to open the midpalatal suture and make the maxilla wider. Dental crossbites are treated by moving the teeth with lighter forces. Although this is a correct concept for adolescents in the late-mixed and early permanent dentition, the lesser interdigitation of the midpalatal suture in the early mixed dentition means that even modest forces will cause both skeletal and dental changes.

Posterior crossbites in children often appear to be unilateral but on close examination are usually found to result from bilateral constriction of the maxillary arch and a shift of the mandible to one side on closure. More severe constriction may result in a bilateral crossbite without a mandibular shift; occasionally, a true unilateral posterior crossbite from an intra-arch or jaw asymmetry will be noted.

Open Bite and Oral Habits

An open-bite malocclusion is defined as the lack of normal vertical overlap (overbite) between the maxillary and mandibular incisors in the case of an anterior open bite (Fig. 376-8) or between the maxillary and mandibular posterior teeth in the case of a posterior or lateral open bite.3,24 Dental open bites are most common and are restricted to malposition of the teeth (proclined maxillary incisors, retroclined mandibular incisors, infraocclusion) and deformation of the surrounding alveolar bone; skeletal open bites are characterized by problems with the underlying growth patterns and the relative positions of the maxilla and the mandible. A patient presenting with a dental open-bite malocclusion will have relatively normal skeletal components, whereas in skeletal open-bite malocclusions, a discrepancy in the cranial base, maxilla, or mandible may be observed. Characteristics observed in skeletal open bites include a distal condylar inclination, short ramus height, antegonial notching, an obtuse gonial angle, excessive maxillary height, a straight mandibular canal, a thin and long symphysis, excessive anterior facial height, short posterior facial height, an anteriorly tipped-up palatal plane, a steep mandibular plane, divergent occlusal planes, a tendency toward a Class II malocclusion, mandibular deficiency, a narrow maxilla, and a posterior crossbite.25,26

Open bites are often found in conjunction with sagittal dysplasias of the jaws (such as overbite and underbite types of malocclusions)27,28 but may also present alone. They are more commonly observed in the younger, mixed dentition age group.29 The literature has reported that African Americans have a greater incidence (6.6%) of open-bite malocclusion than do Caucasians (2.9%) or Hispanics (2.1%).30 The highest reported incidence of anterior open-bite malocclusion is found in mentally retarded and in children with Down syndrome.31

Vertical growth discrepancies have been postulated as causative factors in skeletally based open-bite malocclusions. These involve the direction, pattern, and rotation of mandibular growth, as well as vertical underdevelopment of the middle cranial fossa (producing an elevation of the glenoid fossa) and inadequate alveolar growth in the anterior portion of the maxilla.26,32-35 Transitional dental open-bite malocclusions occur during the mixed dentition stage as the deciduous teeth exfoliate and the permanent teeth erupt, with self-correction reported in over 80% of patients.29 Noninherited factors that result in open bites include trauma to the condyles, muscle dysfunction, pathological disturbances of dental development encompassing the presence of supernumerary teeth, ankylosis, root dilacerations, cysts, and prolonged retention of deciduous teeth.36-38

Chronic oral habits, such as non-nutritive sucking, tongue thrusting, and mouth breathing, are likely to be causative or contributing factors in the majority of open-bite malocclusions the pediatrician will encounter. Prolonged digit and pacifier sucking are the prime offenders in this category, while tongue thrusting is usually an adaptation to the open bite already present. These habits disturb the normal equilibrium of pressures and forces that exist between the orofacial musculature and the dentition, directly resulting in the open bite seen.39

During the primary dentition and early mixed dentition years, many children engage in finger and pacifier sucking. Although it is possible that a prolonged and intense habit may deform the alveolus and dentition during the primary dentition years, much of the effect is on eruption of the permanent anterior teeth. The effect of such a habit on the hard and soft tissues depends on its frequency (hours/day) and duration (months/years). While most children will discontinue sucking habits by the age of 3 or 4 years, some may continue. If the finger sucking habit ceases prior to the eruption of the permanent incisors, any dental changes resulting from the habit may resolve spontaneously. However, persistent sucking habits extending into the mixed and permanent dentition age groups may result in an anterior open-bite malocclusion that requires intervention to resolve.

The etiological relationship of tongue thrusting and open-bite malocclusion is not completely clear. While some of the literature suggests that tongue thrusting may be a direct cause of anterior open bite, most authors believe that it is just an adaptation used to achieve a good oral seal during swallowing, with the open bite actually caused by a sucking habit or the result of skeletal factors. Respiratory patterns and airway obstructions have also been implicated in the etiology of open-bite malocclusions, possibly from a resultant change secondary to abnormal resting head and jaw posture made necessary by the compromised airway. Although experimental studies in primates have demonstrated a relationship between complete nasal obstruction and the development of open bite, other investigations have failed to demonstrate a significant clinical correlation between airway obstruction and the development of open-bite malocclusion.

Open-bite malocclusion therapy in the mixed and early permanent dentition is directed toward addressing obvious etiological factors (eg, removing pathological obstructions of eruption of the anterior teeth and controlling of oral habits). Skeletal discrepancies should be treated through intervention with ongoing growth, focusing on reducing or redirecting the vertical skeletal growth and controlling vertical dentoalveolar development by impeding molar eruption or extruding anterior teeth. Headgear has been traditionally the preferred appliance for treating high-angle open-bite patients, whereas functional appliances such as the Active Vertical Corrector appliance, the Herbst appliance, or the Frankel function regulator (FR-4) may be useful in treating patients presenting with an open bite and concomitant mandibular deficiency. Posterior bite blocks are used to intrude or control eruption of the posterior teeth and to encourage subsequent bite closing through mandibular autorotation.

Some have considered non-nutritive sucking to be a symptom of emotional disturbance. However, the majority of the literature suggests that most oral habits are simply learned behaviors and that treating a habit causing a malocclusion in a child who is mature enough to understand the process will not result in any serious symptom substitution.40 A straightforward discussion with the parent, child, and dentist and counseling the child on the detrimental effects of the habit should be the first attempt at treatment. A reward system that encourages the child to stop the habit may also prove to be effective. Beyond this, physical reminders such as a bandage on the offending finger are the next level of intervention to be considered. These include placing a finger bandage, an elbow splint, a sock, or a glove over the hand. Interceptive therapy using removable or fixed appliances, such as a palatal crib, is the preferred treatment if the malocclusion resulting from the habit warrants the expense and effort required.41 With the use of any appliance, it is imperative that the child be informed that the appliance is meant only as a reminder to assist the child in breaking the habit, not as a punitive measure. A fixed palatal crib (eFig. 376.5) is an effective measure in arresting a persistent digit-sucking habit42 and serves to restrain the tongue, therefore allowing for some degree of self-correction of the open bite to occur. An uncontrolled habit of sufficient frequency, duration, and intensity may maintain or exacerbate the open-bite malocclusion and significantly worsen the prognosis for successful orthodontic treatment.

Maxillary Protrusion

Overjet is the term used to describe the horizontal relationship of the maxillary and mandibular incisor teeth. The incisors are normally in contact, with the maxillary teeth forward of the mandibular teeth by the thickness of their incisal edges (normal overjet is 1–2 mm). Maxillary protrusion is defined as excessive overjet (5 mm or more) and is found in approximately 23% of children, 15% of adolescents, and 13% of adults43 (Fig. 376-9).

Maxillary protrusion may represent a normal developmental period, as seen during the transition from the primary to the mixed dentition or from the mixed to the permanent dentition, but may also be related to an underlying dental or skeletal malocclusion. The key components of this type of malocclusion can include mandibular skeletal retrusion; maxillary dental protrusion; excess vertical skeletal development; and, less frequently, mandibular dental retrusion and maxillary skeletal protrusion.44 The most common causes of increased maxillary incisor protrusion are the presence of oral habits (such as digit sucking or tongue thrusting), dental crowding, ectopic eruption, and discrepancies between the positions of the jaws.

Children with maxillary protrusion are at increased risk for injuries to their maxillary anterior teeth.45 Treatment of excessive overjet should be considered for this reason alone but may also serve to improve the child’s self-image. Studies indicate, however, that children treated in this manner will most often require a second phase of orthodontic treatment and that one-stage treatment at a later time will provide a similar outcome in most cases.46 Overjet is the leading reason why parents seek orthodontic treatment for their children.47 Additionally, addressing an increased overjet can serve to maintain the periodontal health of the anterior gingiva and prevent further development of abnormal soft tissue function and underlying skeletal discrepancies.

The approach to treating maxillary protrusion in children and adolescents is largely determined by the underlying etiology of the malocclusion. If a skeletal discrepancy exists, treatment options include extraoral traction (headgear), the use of a functional appliance, or orthognathic surgery in the case of severe problems. Therapeutic techniques used to address maxillary protrusion of dental etiology include braces, removable appliances, the distalization of the maxillary teeth, or the extraction of teeth.

Acknowledgments

The authors wish to thank Drs. Murray Dock and Robert L. Creedon for their contribution to this chapter. They were the authors of this chapter in the previous edition of this text, and their work is carried over largely intact for sections of this edition.