5: Eruption and Shedding of Teeth

Eruption and Shedding of Teeth

Göran Koch, Sven Kreiborg, and Jens O. Andreasen

Chronology of normal tooth eruption

Primary dentition

The chronology of eruption of primary teeth for Swedish children is given in Box 5.1. The sequence of eruption and the timing of eruption for each tooth are similar for both sexes. The variability in the age of the children at emergence of the individual teeth is relatively small, with standard deviations of 2–3 months. On average, the eruption of primary teeth begins at about the age of 8 months with the mandibular central incisors, and ends at the age of about 30 months with the maxillary second molars. Thus, in most children the total period of eruption of primary teeth spans about 2 years.

Permanent dentition

The chronology of eruption of permanent teeth (except for the third molars) for Danish children is given in Box 5.2. The sequence of tooth eruption is almost identical for both sexes. However, all teeth erupt significantly earlier in girls than in boys. The sex difference in eruption times averages approximately 6 months. There is, however, no appreciable difference in the variability of the eruption times between the sexes. In general, the variability in eruption times for the permanent dentition is much larger than the variability observed in the primary dentition, with standard deviations of 8–18 months (about five times greater than in the primary dentition). The smallest variability in time of emergence is observed for the first molars and incisors, whereas the largest variabilities are found for the canines and premolars in each jaw. The eruption of the permanent dentition begins with eruption of the mandibular central incisors at 6 years of age and ends with the eruption of the maxillary second molars at 12 years. Thus, in most children, the total period of eruption of permanent teeth (except for the third molars) spans about 6 years. In both sexes, a tendency for grouped emergence is noted, the teeth within a group showing similar mean times of emergence. The following groups are distinguishable:

  • first molars in each jaw and the mandibular central incisors
  • maxillary central and mandibular lateral incisors
  • mandibular canines and the first premolars in both jaws
  • maxillary canines and the second premolars in both jaws
  • second molars in both jaws.

Mechanism and theories of tooth eruption

Tooth eruption is defined as the movement of a tooth, primarily in the axial direction, from its site of development in the jaw bone to its functional position in the oral cavity. This process continues, in principle, until the tooth meets the teeth in the opposing jaw. However, with the subsequent growth of the jaws and alveolar processes the teeth will exhibit continued vertical, mesial, and transverse drift until adult age. In addition, even through the second to fifth decade of life very slow but continuous eruption and alveolar growth have been documented.

The eruption phase has been divided into the following stages: pre‐eruptive; intraosseous; mucosal penetration; preocclusal; and postocclusal.

In the pre‐eruptive stage, the tooth crown is formed and the position of the tooth in the jaw bone is relatively stable. When the root begins to form, the tooth starts moving inside the jaw bone towards the oral cavity (the intraosseous stage). The eruption path is, for most teeth, not only through the bone, but also through the roots of the primary teeth. The mucosal penetration stage occurs, in general, when half to three‐fourths of the root of the erupting tooth is formed. The preocclusal stage is relatively short (a few months), whereas the postocclusal stage is much longer (several years) and is characterized by much slower tooth movement. Although the movement of teeth during eruption primarily occurs in the axial direction, the teeth actually move in all three planes of space. Apart from the rather precise eruption pattern of various tooth types there appears to be an individual very precise eruption time for homologous teeth, i.e., that left–right‐side eruption should not deviate by more than 2–4 months. If that is not the case then an eruption obstacle may be present [1].

Until recently, clinical studies of tooth eruption have been based on two‐dimensional X‐rays. However, with newer medical imaging techniques, such as computed tomography and magnetic resonance scanning, three‐dimensional analysis of tooth eruption has become possible (Figure 5.1a,b). With these technologies more accurate determination of the eruption path of individual teeth is now possible.

Frontal (a) and lateral views (b) of the transparent mandible, displaying symphysis menti, mental foramen, mandibular canals, and teeth in discrete colors, with lines indicating the eruption paths.

Figure 5.1 Transparent mandible at age 10 years. (a) Frontal view. Mental foramina, and segmented teeth (posterior to the incisors) from four different ages (0, 1, 7, and 10 years) are aligned automatically on the symphysis menti and the mandibular canals. Only the teeth and the mental foramen on the right side are illustrated. Lines indicate the eruption paths of the individual teeth. Tooth color code: purple = permanent third molar, blue = permanent second molar, red = permanent first molar, green = permanent premolars and the permanent canine. The mental foramen = blue. The symphysis menti = yellow. The mandibular canals = pink. (b) Lateral view. Lines indicate the eruption paths of the individual teeth. Color coding is the same as in part (a).

The eruption path is determined by genetic and local environmental factors. One of the most important local environmental factors is crowding among the developing and erupting teeth [2].

Tooth eruption is a biological process which is still not fully understood. The process is accompanied by multiple tissue changes, such as resorption and apposition of the alveolar bone, and development of the root and periodontium.

The eruption mechanism has for a long time been under investigation and several theories have been proposed, including eight different explanations of how eruption takes place [2,3]. At present, the “polarized follicle theory” is possibly the one which can best explain the initial stages of tooth eruption in humans (Figure 5.2). According to this theory, the coronal part of the follicle will start its resorbing activity when root formation starts. This process is coordinated by selective bone growth in the apical part of the follicle. Due to this coordinated osteoclast/osteoblast activity an eruptive movement of the tooth will take place. The direction of this movement is apparently directed by an eruption canal, a canal in the bone filled with an odontogenic mesenchymal tissue with odontogenic epithelial islands. This will expand during eruption, and thereby guide the tooth into its right position in the jaw. When the erupting permanent tooth has resorbed the overlying primary tooth and/or bone, the next step is to penetrate the oral mucosa (usually when half to three‐fourths of the root is formed). The coronal part of the follicle with the reduced enamel epithelium has been shown to possess the necessary collagenase activity to allow the permanent tooth germ to penetrate the mucosa (however, large amounts of fibrous tissue may present an obstacle to eruption; see later). After mucosal penetration, a fast extraalveolar eruption takes place, possibly related to periodontal ligament (PDL) traction and/or apical alveolar bone formation. Finally, when occlusion has been reached, vertical and horizontal changes can occur and the mechanisms for these events are largely unknown.

Micrograph displaying histologic section of a human second premolar in initial stage of eruption, with arrows denoting mechanisms in eruption pointing to numbers.

Figure 5.2 Histologic section of a human second premolar in its initial stage of eruption. In the figure various theories behind eruption are presented. Experimental studies have shown that the following mechanisms might only play a minor role in eruption, namely: PDL and pulp tissue pressure (6 and 7), coiled vessels creating a slight tissue pressure (8 and 6), pulpal growth (4) and root elongation (3). The most important mechanisms appear to be tissue changes induced by the follicle, namely, induced coronal resorption and apical bone apposition (1 and 5). PDL traction (2) may play a role after penetration of the oral mucosa.

Source: Marks et al. 1997 [3]. Reproduced with permission of Munksgaard.

Longitudinal studies of aplasia sites with persistent primary teeth have shown that over a 10‐year period, approximately 10% of the teeth showed very little resorption whereas the remaining teeth showed an average loss of approximately 5% root length each year [4].

Mechanism of shedding of primary teeth

Prior to shedding of primary incisors, canines and molars, the roots of the primary teeth are resorbed and their crowns shed. Dentinoclasts appear on the apical surface of the roots of the primary teeth, possibly initiated by the pressure created by the dental sac of the erupting permanent teeth. However, even if a permanent tooth is missing, the primary predecessor usually undergoes root resorption, although commonly at a much slower pace. The role of pulpal dentinoclasts in this process is still being investigated.

Figure 5.2 illustrates the histologic picture during resorption of the roots of a primary mandibular second molar in connection with eruption of the second premolar. Figure 5.3 shows the histologic picture of the resorption of the palatal part of the root in a primary maxillary central incisor during eruption of the permanent maxillary central incisor.

Micrograph displaying histology of palatal resorption of primary maxillary central incisor during eruption of permanent incisor, with arrow pointing to the presence of eruption canal.

Figure 5.3 Histologic findings associated with the palatal resorption of a primary maxillary central incisor during eruption of the permanent incisor. Note also the presence of the eruption canal (arrow).

Systemic disturbances affecting tooth eruption and shedding

A number of systemic diseases and syndromes affect tooth eruption and shedding of primary teeth. Premature tooth eruption and shedding of primary teeth are far more common than delayed eruption and shedding. In general, delay in eruption in the primary dentition is associated with delay in the permanent dentition, and the delay in the permanent dentition is mostly more pronounced than in the primary dentition.

Premature tooth eruption

Natal or neonatal teeth have been shown to occur in about 50 different syndromes. Of these, about 10 syndromes are associated with chromosomal aberrations, e.g., trisomy 13. Among other syndromes are Hallermann–Streiff syndrome and Ellis–van Creveld syndrome.

Delayed tooth eruption

In general, children with chronic diseases show delay in both physical and dental development, and will, consequently, show delayed tooth eruption. Several general diseases, including more than 150 different syndromes, have been shown to exhibit delayed tooth eruption [5].

Endocrinopathies and chromosomal aberrations

Endrocrinopathies, such as hypopituitarism, hypothyroidism, and hypoparathyroidism, often result in retardation of dental emergence in both the primary and the permanent dentition. Many chromosomal aberrations, including trisomy 21 (Down syndrome), are associated with delayed tooth eruption.

Syndromes

Many syndromes, and especially those involving skeletal dysplasias with disturbed bone metabolism, show severely retarded or arrested tooth eruption.

In the following, a few relevant examples will be given.

Subjects with cleidocranial dysplasia (CCD) are characterized by short stature, aplasia or hypoplasia of the clavicles, and severe disturbances in cranial ossification. These patients often develop numerous supernumerary permanent teeth occlusal to the normal permanent teeth. Tooth eruption is delayed in both the primary and permanent dentitions, but the delay is most severe in the permanent dentition, often with arrest of eruption and multiple retentions of both normal and supernumerary teeth. The disturbances in tooth eruption are related both to the skeletal pathology with retardation of osteoblast, osteoclast, and odontoclast differentiation, and to the presence of supernumerary teeth. Thus, even in regions without supernumerary teeth, shedding of primary teeth and eruption of permanent teeth can be extremely delayed or arrested (Figure 5.4). Therefore, children with CCD should be monitored for disturbances in tooth eruption (and other dental abnormalities) from early childhood, and treatment should be instituted as early as possible [6–9].

Orthopantomogram displaying supernumerary permanent teeth and arrested eruption of many of the normal permanent teeth of a boy with cleidocranial dysplasia.

Figure 5.4 Orthopantomogram of a 16‐year‐old boy with cleidocranial dysplasia. Note the numerous supernumerary permanent teeth and the arrested eruption of many of the normal permanent teeth.

Subjects with tricho‐dento‐osseous syndrome (TDO) are characterized by disturbances in the development of hair, teeth, and bones. The patients are of normal height, but the skeleton, including the craniofacial skeleton, is dense and reveals disturbed bone remodeling with reduced osteoclastic activity. Tooth eruption is delayed in both dentitions, but most severely so in the permanent dentition, which may also show arrested eruption leading to retention of several permanent teeth (Figure 5.5). The cause of the eruption problems is related to the reduced osteoclastic activity. Therefore, children with TDO should be monitored for disturbances in tooth eruption (and other dental abnormalities) from early childhood, and treatment should be carried out as early as possible [9].

Orthopantomogram displaying severely delayed eruption of several permanent teeth and dense jaw bones of a girl with tricho‐dento‐osseous syndrome.

Figure 5.5 Orthopantomogram of a 13‐year‐old girl with tricho‐dento‐osseous syndrome. Note the severely delayed eruption of several permanent teeth and the dense jaw bones.

Subjects with pycnodysostosis are characterized by short stature, caused by shortening of the extremities. The skeleton, including the craniofacial skeleton, is characterized by osteopetrosis with increased bone fragility. The increased bone density of the jaws, combined with pronounced crowding, leads to delayed eruption in both dentitions, but is most pronounced in the permanent dentition. Thus, the permanent dentition may even show arrested tooth eruption and several other dental abnormalities (Figure 5.6). These children should be monitored for disturbances in tooth eruption from early childhood, and treatment should take place as early as possible [10].

Orthopantomogram displaying delayed eruption of several permanent teeth and osteopetrotic bones of a boy with pycnodysostosis.

Figure 5.6 Orthopantomogram of a 10‐year‐old boy with pycnodysostosis. Note the delayed eruption of several permanent teeth and the osteopetrotic bones.

Premature shedding of primary teeth

Systemic diseases that are associated with premature shedding of primary teeth include histiocytosis, hypophosphatasia, and neutropenia.

Histiocytosis is a symptom complex, which includes multiple eosinophilic granulomas, Hand–Schüller–Christian disease, and Letterer–Siwe disease. Early loss of posterior primary teeth is frequently observed, whereas the anterior teeth are less commonly involved.

Hypophosphatasia is a metabolic disease with impaired bone mineralization. The activity of alkaline phosphatase in plasma and tissues is reduced. Premature loosening and shedding of primary teeth are often seen. The anterior teeth are most frequently affected, whereas the primary molars are rarely involved. The teeth have a defect in cementum. There is often severe loss of alveolar bone with no or little gingival inflammation. The teeth are often shed without any signs of root resorption.

In neutropenia, the decrease in circulating neutrophils leads to lack of resistance to infection, which may predispose the children to gingivitis and periodontitis.

Premature shedding of primary teeth can occur in other diseases where the periodontium undergoes pathologic breakdown as seen in Papillon–Lefèvre syndrome (hyperkeratosis palmoplantaris with periodontoclasia), Down syndrome, and Ehlers–Danlos syndrome.

Other causes of premature shedding of primary teeth can be cystic lesions of the jaws, as seen in cherubism (Figure 5.7).

Orthopantomogram displaying large cystic lesions in the maxilla and mandible of a boy with cherubism.

Figure 5.7 Orthopantomogram of 10‐year‐old boy with cherubism. The large cystic lesions in the maxilla and mandible have caused premature loss of primary teeth.

Local disturbances affecting tooth eruption and shedding

It is essential to diagnose where the obstacle for the eruption process is located. The overwhelming cause is crowding, which may lead to impaction, and if this is the case, dental arch expansion or extraction is indicated. Crowding often leads to follicle collisions where one follicle is placed on top of the other thereby leaving both teeth unerupted. Another frequent cause is an ectopic eruption path, and in these cases extraction of primary predecessors and/or surgical creation of a new eruption path are the treatments of choice. Sometimes orthodontic traction must be used. In the case of follicle and PDL pathology, arrest of eruption may occur; this condition is termed retention. Retention has further been divided into primary retention and secondary retention. Primary retention means that the eruption is arrested in the intraosseous stage due to pathology of the follicle and sometimes an ankylosis affecting either the crown or the root. Secondary retention means that an already erupted tooth due to ankylosis of the root is prevented from further eruption and thereby gradually comes more and more into infraocclusion. In the case of primary retention, the treatment of choice will normally be denudation of the tooth. In the case of secondary retention, the tooth is ankylosed, and should be surgically removed. Finally, an eruption disturbance can be diagnosed to be a delayed eruption. In asymmetric cases where expected eruption time on one side is exceeded by more than 4 months, surgical exposure is indicated.

In Table 5.1 various causes for noneruption of permanent teeth are listed according to tooth type.

Table 5.1 Most frequent causes of noneruption for various types of permanent teeth and suggested treatment

Cause Treatment
Maxillary incisors Dilaceration (trauma) Surgical exposure
Supernumerary teeth Surgical removal of supernumerary teeth
Maxillary canines, palatal impaction Unknown Surgical exposure and orthodontic traction
Maxillary canines, labial impaction Crowding Expansion of dental arch or removal
Mandibular canines, ectopic position Unknown Surgical removal or transplantation
Maxillary second premolar Crowding Expansion of dental arch or removal
Mandibular second premolar Unknown According to tilting extraction of primary molar, surgical exposure or transplantation
Maxillary first molar, mesial tilt Unknown None or distalization of first molar
Mandibular first molar, mesial tilt Unknown None or distalization of first molar
Maxillary first molar, infraocclusion Ankylosis Extraction
Mandibular first molar, infraocclusion Ankylosis Extraction
Second maxillary molar Follicle collision with third molar Remove third or second molar (usually third molar)
Second mandibular molar Follicle collision with third molar Remove third or second molar (usually third molar)

Local aberrations in primary dentition

Natal and neonatal tooth eruption

The frequency of natal or neonatal teeth is estimated at one case per 2000–3000 births and is equally common in boys and girls. Most of these premature erupting teeth are mandibular central incisors belonging to the normal dentition and they have a normal shape. The root has not yet developed and the tooth is loosely attached to the gingiva (Figure 5.8). The symptoms related to natal/neonatal teeth include gingivitis, extreme mobility, self‐mutilation of the tongue, and trauma to the mother’s breasts. Natal and neonatal teeth should be extracted only if they are loose enough to involve risk of aspiration or if feeding is severely disturbed.

Photo displaying natal teeth in a 2-day-old girl.

Figure 5.8 Natal teeth in a 2‐day‐old girl.

Symptoms associated with “teething”

Often, the primary teeth pierce the gums without causing any symptoms. However, in some children local symptoms such as redness and swelling in the oral mucosa overlying the erupting tooth is found. These symptoms appear a few days before clinical eruption. The child may also show signs of local irritation, drooling, and sometimes slight fever. Treatment for teething troubles was formerly directed at both local and supposed general symptoms. Since local massage of the gum pads obviously relieves the discomfort, various remedies with which the gums can be rubbed have been proposed. A bite‐ring of rubber may be recommended because it is easy to clean, cannot be swallowed, and does not injure the gums.

Fibrotic mucosa and eruption cysts

Changes in the oral mucosa overlying the erupting tooth may cause eruption disturbances. If the child is chewing intensively on hard objects, the alveolar mucosa may turn more fibrotic and cause delayed eruption (Figure 5.9). In some cases surgical removal of the changed tissues might be necessary due to pain at chewing. A common finding in small children is eruption cysts. They are often swellings overlying an erupting tooth and may vary in size. They contain tissue fluid and sometimes some blood (eruption hematoma) accumulated superficially to the reduced enamel epithelium. In most cases no treatment is indicated since the changed mucosa will delay the eruption by only a few weeks. However, if the cyst is causing discomfort or the alveolar mucosa is pathologically thickened, surgical exposure of the tooth may be necessary. Similar changes are also found in the permanent dentition (Figure 5.10a,b).

Photo displaying fibrous gingival tissue delaying eruption of primary molars.

Figure 5.9 Fibrous gingival tissue delaying eruption of primary molars.

Photos of eruption cyst (a), and gingival overgrowth caused by phenytoin medication influencing tooth eruption (b).

Figure 5.10 (a) Eruption cyst. (b) Gingival overgrowth caused by phenytoin medication influencing tooth eruption.

Infraocclusion of primary molars

The definition of infraocclusion is that a tooth is positioned 1 mm or more below the normal occlusion plane/level. Infraoccluded primary molars mostly reach occlusal contact before they develop ankylosis. Following vertical growth of the surrounding alveolar bone, the ankylosed tooth seems to gradually be submerged into an infraoccluded position. The diagnosis of ankylosis is difficult to verify by radiography but easy to establish by percussion test and the clinical picture. Infraocclusion of primary molars can be found as early as 3–4 years of age but is more predominant at 10 years of age; the aberration is then found in about 10% of the children. Infraocclusion has been found to be genetically influenced. The treatment depends on the presence of permanent successors to the infraoccluded tooth. If there is a permanent successor, normal exfoliation can be expected with a delay of 6–12 months (Figure 5.11) without removal of the ankylosed tooth. If the neighboring permanent tooth is severely tilting over the ankylosed tooth, early orthodontic correction may be indicated. In cases with no successor, the therapy planning must be based on the conclusion that normal exfoliation cannot be expected.

Radiographs of infraoclusion of primary molars of a boy from 11 years 7 months to 14 years 2 months of age displaying nonextraction (left) and extraction sides (right).

Figure 5.11 Infraocclusion of primary molars. Periapical radiographs of a boy followed from 11 years 7 months to 14 years 2 months of age. Left side, extraction side. Extraction resulted in the eruption 1 year earlier of the successor compared to the nonextraction side. Normal marginal alveolar bone height at end of observational period.

Source: J. Kurol, 1984. Reproduced with permission of Swedish Dental Association.

Retention of primary teeth

The primary tooth that is most commonly involved is the maxillary second molar. The tooth anlage is malpositioned and often the roots bend and follow the wall of the sinus during development (Figure 5.12). This means that spontaneous eruption cannot be expected. The impacted tooth can cause tilting of the permanent molar and disturbance in eruption of the permanent premolars. The impacted primary tooth has to be surgically removed. Also the primary second molar in the mandible may become retained and thereby lead to severe eruption problems for the permanent successor.

Radiograph of impacted primary maxillary second molar causing eruption disturbances for permanent premolars indicated by arrow.

Figure 5.12 Impacted primary maxillary second molar (arrow) causing eruption disturbances for the permanent premolars.

Local aberrations in permanent dentition

Disturbances in eruption are common in the permanent dentition. Besides the normal variation in eruption time a number of genetic disorders, diseases, and syndromes can affect tooth eruption as has been described earlier in this chapter. However, the most frequent disturbances in tooth eruption in the permanent dentition are local in origin (Box 5.3).

Apr 26, 2017 | Posted by in General Dentistry | Comments Off on 5: Eruption and Shedding of Teeth
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