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On the immutability of location of the developing root apex

Published: December 2013

Bulletin #28 December 2013


On the immutability of location of the developing root apex

Root dilaceration is the outcome of damage to the specialized epithelial layer or layers of dentine-producing cells that are directly concerned with the normal development of the root of a growing tooth bud, due to trauma. Since trauma affects the front of the mouth, rather than other areas, the most common teeth to be adversely affected are the maxillary central incisors. As a general rule, we are not overly concerned with the actual damage that may be inflicted on the deciduous incisors, because they will not figure in the final long term scheme planned for the patient. Certainly, fractured crowns may be repaired. For the more serious cases, the damaged tooth will need to be extracted which, for a young child, rarely demands artificial replacement.

Trauma to the deciduous incisors is more important for the secondary effect that this has in the immediate locale. Should the tooth lose its vitality, there are several possible sequelae. A traumatized non-vital tooth may become discolored. Whether or not there are other untoward symptoms, a non-vital tooth will develop an apical granuloma which is the soft tissue reaction to a necrotic pulpal tissue and, in time, this may become infected to cause pain and swelling. These symptoms are acute and, therefore, serious at the time they occur. Yet, of themselves, they are of little consequence beyond the visit to the dentist that is necessary to treat the child’s major discomfort. However, the physical presence of a granuloma has implications which are sometimes far reaching. A permanent incisor may be stopped in its eruption path by this soft tissue lesion and its further eruption actively prevented until the obstacle is eliminated. It should be remembered that the roots of non-vital deciduous teeth which have been successfully root-treated will resorb normally, often leaving the root filling directly exposed to the surrounding tissues.

In the longer term, an untreated granuloma may occasionally undergo cystic change, which has been assumed to be due to a re-awakening of the dormant epithelial rests of Malassez that are to be found in granulomatous tissue itself. The resulting cyst is termed a radicular cyst and its further enlargement will displace the permanent incisor and, subsequently, other adjacent teeth. On the other hand, the presence of the granuloma, in close relation to the dental follicle of the unerupted central incisor, may stimulate that follicle itself to undergo cystic change and the follicle enlarges to become a dentigerous cyst. This, too, displaces the incisor and, eventually, other adjacent unerupted teeth. Fortunately, the prevalence of cysts from this cause is relatively uncommon.

From the orthodontic point of view, a more significant secondary effect of trauma to the deciduous incisor is potential damage that may be inflicted on the developing permanent incisor. This is caused by the force of the blow being transmitted through the long axis of the deciduous incisor and on through the long axis of the permanent incisor, to the root-forming Hertwig’s root sheath.

The normal mechanism of root formation

During tooth development, after the completion of crown formation, the apical mesenchyme forms the developing periodontium while the inner and outer enamel epithelia fuse below the level of the crown cervical margin to produce a bilayered epithelial sheath termed Hertwig's epithelial root sheath (HERS) which is responsible for root development.1 This very thin circular row of dentinogenic cells encircles the pulp tissue at the extremity of the developed root, creating a hard tissue circular rim. At the same time, the pulp itself fills in the bulk of the root structure through the agency of the odontoblasts, which line the inner aspect of the forming root, causing the pulp chamber to become narrower and narrower until it finally becomes a root canal.

From this description, it becomes clear that the narrowing diameter of the circle of epithelium of Hertwig’s root sheath, being only one cell thick, creates an open and sharp circular rim of dentine – a feature which remains true until the root finally apexifies. Dentinogenesis of the root has the effect of causing a downward migration of the formed part of the tooth, away from the forming part, which is probably the main factor propelling the downward and forward development of the alveolar process. The location of the ring of forming cells itself is probably unchanged over the entire period.

Trauma and its effect on root formation

If trauma is now introduced into this scenario and it is directed in the line of the orientation of the long axis of the tooth, it is easy to understand that there will be a jarring effect at the incomplete root end, in which the sharp and recently calcified hard tissue rim will be pushed upward, to impact against the sensitive epithelial HERS cells. The result would be a disruption of root formation, from which the root sheath may or may not recover. It will not take much much force for this to happen, which is why the traumatic incident itself may not be remembered and why a history of the event may not be elicited. If recovery is good, then the tooth will continue or restart its vertical development, in line with the resumption of dentinogenesis.

Should the damage be so severe as to kill off these cells, then there will be a cessation of root development, although the pulpal tissue is likely to remain vital since the apical area is wide open. In this instance, the odontoblasts would still be contributing to a thickening of the already formed root, but the root will remain stunted. If, on the other hand, there is death of the pulp, then the tooth will not develop further but will become sequestrated and remain in situ.

QQ Fig. 1_1

Fig. 1a panoramic view of a 10 year old child. Trauma at age 4 years caused arrested root development of the four maxillary incisors and failure of the teeth to migrate occlusally. The apices are wide open. Note the dental development of the other permanent teeth corresponds to a dental age of approximately 9 years.

Fig. 1b transaxial cuts taken from the CBCT of the same patient show the rudimentary root development and indicate the proximity of the teeth to the floor of the nose.

The child in Fig. 1 had, according to the history, suffered trauma at age 4 years, when crown formation of the four maxillary incisors was complete and root development was just beginning. The apical areas were wide open but were very high in the basal bone area, close to the floor of the nose. They had ceased to grow and, as a result, had lost their ability for vertical migration. At the age of 10 years (Fig. 1a, b), the roots of the four maxillary incisors showed no further growth. The roots had hardly developed and the apices were wide open. The maxillary canines were also relatively high and late in their root development – they, too, had been affected by the earlier trauma. By contrast, the roots of the erupted first permanent molars and mandibular incisors were completed and the roots of the adjacent unerupted canines and premolars had reached half their expected final length.

QQ_Fig._3

Fig. 2a panoramic view of the same child at age 13 years, following orthodontic treatment which included 10 months of appliance generated eruption of these teeth.

Fig. 2b periapical views of the incisor teeth taken at the same time. Note the impressive increase in length of the roots of the incisors, whose apices are in various stages of closure.

Following orthodontic and surgical treatment to extrude and actively erupt these teeth, a resumption of root development occurred and the teeth finally achieved roots of good length, albeit of abnormal form (Fig. 2a, b). It is reasonable to assume that these roots would not have grown in their previous location. It also seems that using orthodontic extrusive traction, apical areas with the potential for root development will generate long roots, by virtue of the artificially created vertical development of the tooth, while leaving the root-generating apical ring of cells in its former place.

QQ_Fig._2

Fig. 3a panoramic view of a 7 year old girl who suffered a traumatic episode in infancy at a time when the crown of the left permanent central incisor was in the last stages of crown formation. A minimal amount of root formation occurred, resulting in a short and angulated stump, adjacent to the floor of the nose.

Fig. 3b periapical view of the same tooth and taken on the same day, showing the root stump.

In some cases, the traumatic episode results in transitory damage to HERS, which subsequently permits a partial revival of root development. The outcome may be an unerupted tooth, lacking eruptive potential, impacted high in the basal bone, with a much shortened root of abnormal form and with complete closure of the root apex (Fig. 3a, b).

QQ_Fig._4

Fig. 4a panoramic view of the same patient as in Fig. 3 at age 18 years and 4 years post-treatment. There has been no increase in the root length, since the apex had closed before treatment began. However, there is excellent bone height for the implant that will be necessary when this tooth fails.

Fig. 4b periapical view of the same case at age 14 years, at completion of the phase 2 treatment.

Once apexification has occurred, Hertwig’s root sheath disappears and, although the tooth may be mechanically erupted with orthodontic traction, this will not be accompanied by further root development (Fig. 4a, b).

The “classic” dilacerate incisor

QQ_Fig._5aQQ_Fig._5b

Fig. 5a diagrammatic representation of the transmission of trauma via the deciduous tooth and on to the labial aspect of the developing root of the permanent tooth.

Fig. 5b diagrammatic representation of the manner in which the natural vertical development of the tooth is frustrated by a lack of production of dentine at the labial aspect of the tooth, causing a production differential between the labial and palatal aspects. This causes the crown to displace upwards as the roots becomes sickle-shaped in a tight curve. Reproduced from previous edition with the kind permission of Informa Healthcare - Books

The April 2012 bulletin #10 on this website discussed the “classic” dilacerate maxillary incisor and the origin of its unusual shape in relation to a very specifically directed trauma. It was pointed out there that the reason this happens is due to trauma being transmitted from the deciduous incisor to the permanent successor in such a way as to cause damage only to the labial aspect of Hertwig’s sheath. The consequence is that the damaged labial side of the epithelial ring stops producing dentine while the unaffected lingual side continues, causing the root produced to configure into a curved form, with the apical portion continuing on in its former direction (Fig. 5). A video movie is included here (Fig. 6) which vividly illustrates the author’s hypothesis of how the specifically directed trauma alters the growth of a normally developing central incisor. It does so by honing in on the formative cells of HERS on the labial side only, while the remaining cells continue their outpouring of dentine on the lingual side.



Fig. 6 video clip describing the author’s hypothesis of how the “classic” dilacerations occurs. Note the downward and forward direction in which the root carries the formed coronal portion of the tooth initially, causing the initiation of resorption of the root of the deciduous incisor and, at the same time, contributing materially to the growth of the alveolar process. When trauma is directed in the long axis of the deciduous incisor (red arrow), the impact is transmitted upward, to momentarily contact the incisal edge of the permanent successor and then upward till it hits soft tissue, which is Hertwig’s root sheath on the labial side of the newly-formed root end. At that point (red pulsating ball indicator), the sensitive cells are severely damaged and the rate of production of dentine declines or is arrested. On the palatal side of Hertwig’s root sheath, dentine is being churned out unabated, to cause the root to adopt the form of an arc of circle. This curvature is particularly bulbous palatally and frequently causes a markedly palpable bulge in the palatal profile – frequently mistaken for the incisal edge of the crown. Note also that Hertwig’s root sheath does not alter its position or orientation and it acts as a fixed point or base, against which the contortions of the root have no effect. The entire thrust of positional change is borne by the crown and formed portion of the root which displace forward and upward until root formation ceases, which is when the apex closes.


There is a very important observation to be made in this regard. The entire forming tooth is enclosed in alveolar bone, with the crown surrounded by the dental follicle and the root encased in PDL with a root end formed by HERS and the dental papilla. Yet, when trauma strikes, the entire formed part of the tooth is pushed forward and upwards by the lopsided newly forming dentine, to describe the arc of a circle whose centre of rotation is the root end. The location of the root end itself remains unchanged. This represents a misdirected and frustrated eruptive movement, which is nevertheless generated from the same unaltered base line.

The big question that remains unanswered here is: Why does the anomalous development of the root displace the entire body of the crown and root that has already formed rather than the small developing root apex end of the tooth? It is truly remarkable that the apex remains precisely in the expected location of a normal tooth. Surely, one might ask, is it not to be expected that the small apical portion of the root must offer considerably less resistance to change?

The reason that must be deduced from this is that the surviving epithelial tissue will not be affected by environmental influences and its location is immutable. In the normally developing tooth, Hertwig’s root sheath is the base line from which vertical development of the tooth and the alveolar processes occurs in the unaffected individual.

In the case of the dilacerate incisor, it acts as a fixed base, from which changes may only occur in accordance with the relative differential rates of dentine output. It is for this reason that the incisal edge of the crown proceeds in an upward arc of circle until it stops in the root of the nose on the labial side high in the sulcus, only when apexification is complete. It is also the reason why there is often a small but palpable lump on the palatal side, which is due to the excessive curvature that the rate of root development on the lingual side experiences (Fig. 6). This palpable lump is often mistaken for the incisal edge, both by an inexperienced orthodontic and an unsuspecting oral surgeon!2

Notwithstanding these reservations, orthodontic treatment can be offered to a patient for the resolution of the impaction of a dilacerate incisor with the expectation of success in drawing the crown of the tooth down into the dental arch and, performing the much needed labial root torque.3 This movement will bring an open or a closed root apex into close relation to the labial periosteum of the alveolar ridge, often to make it prominent and palpable under the oral mucosa. It is fortunate that the location of an open and developing root apex can be moved by outside (biomechanical) intervention, but it should be understood that the tendency for relapse in this situation may be high. Thus, should treatment be completed before full apexification of the root of the tooth, retention is mandatory. Non-compliance with the retention protocol will result in relapse due to further root development, unless an apicoectomy is performed because of the prominence of the root end in relation to the labial oral mucosa.

References

1. Zeichner-David M, Oishi K, Su Z, Zakartchenko V, Chen LS, Arzate H, Bringas P Jr. Role of Hertwig's epithelial root sheath cells in tooth root development. Developmental Dynamics 2003, 228:651–663

2. Becker A. Orthodontic Treatment of Impacted Teeth. 3rd edition. Oxford: Wiley-Blackwell Publishers. 2012

3. Becker A. Early treatment for impacted maxillary incisors. American Journal of Orthodontics and Dentofacial Orthopedics. 2002;121:586-7