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Primary failure of eruption: A possible cause of posterior open-bite
William R. Proffit, D.D.S., Ph.D., and Katherine W. L. Vig, B.D.S. Chapel Hill, N. C. Failure of posterior teeth to erupt fully into occlusal contact produces a lateral open-bite. These problems usually are attributed to a mechanical inte$erence with the eruptive process, either ankylosis or some soft-tissue interjerence. In some patients, lateral open-bite is due to a disturbance of the eruption mechanism itself so that nonankylosed teeth cease to erupt. Injluences on the eruption of teeth are reviewed, and possible causes of ’ ‘primary failure of eruption” are discussed. The limitations of treatment for patients with eruption failure are described and illustrated by case reports.
Key words: Eruption failure, posterior open-bite, tooth ankylosis, vertical jaw growth, eruption mechanism
P
artial or complete failure of posterior teeth to erupt produces a lateral (posterior) open-bite. This problem is seen occasionally in all orthodontic practices, although it occurs too infrequently to warrant separate classification in the best United States epidemiologic surveys of malocclusion. l There are two possible causes: (1) mechanical interference with eruption, either before or after the tooth emerges from the alveolar bone, or (2) failure of the eruptive mechanism of the tooth so that the expected amount of eruption does not occur. Mechanical interference with eruption may be caused by ankylosis of the tooth to the alveolar bone, which can occur spontaneously or as a result of trauma, or by obstacles in the path of the erupting tooth. Examples of such obstructions prior to emergence are supernumerary teeth and nonresorbing deciduous tooth roots or alveolar bone (Fig. 1). After the tooth emerges from the bone, pressures from soft tissues interposed between the teeth (cheek, tongue, finger) can be obstacles to eruption. When a tooth erupts into the oral cavity and then ceases eruption before growth is completed, it appears to submerge and may eventually be covered over again by the gingiva. This “submergence” usually denotes ankylosis. The second possible cause of eruption failure, a disturbance of the eruption mechanism itself, often is overlooked. In this article we describe a condition best termed “primary failure of eruption, ” in which nonankylosed teeth fail to erupt fully or partially because of malfunction of the eruption mechanism. These patients have no other recognizable disorder, and no mechanical interferences with eruption seem to exist. The condi-
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Fig. 1. Mechanical obstruction to eruption in a 14-year-old boy with retained deciduous molars.
Fig. 2. Failure of eruption of maxillary and mandibular molars in the absence of ankylosis or other mechanical obstruction in a 20-year-old man, the condition termed “primary failure of eruption.”
tion may be the cause of posterior open-bite which does not respond to orthodontic treatment (Fig. 2). Our goals in this article are to review briefly influences on eruption, describe patients with primary failure of eruption and differentiate them from patients with eruption failure due to other causes, and discuss treatment possibilities and limitations for patients with eruption failure. Influences
on tooth
eruption
In the process of tooth development, the deciduous tooth buds lie in a relatively superticial position and are never completely separated from the oral cavity by bone2 (Fig. 3). The succedaneous tooth buds, however, come to lie in a completely enclosed bony crypt, connected to the oral cavity by the thin gubernacular cord of connective tissue. In order for eruption to occur, the bony covering must be resorbed and the tooth must be
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Fig. 3. Radiograph of mandible at birth (wet specimen). Buds of the first permanent molars, like the deciduous tooth buds, are positioned superficially. (From McCall and Wald: Clinical Dental Roentgenology, Philadelphia, 1957, W. B. Saunders Company, used by permission.)
Fig. 4. Cleidocranial dysplasia and associated delay in eruption of permanent teeth in a lByear-old
girl.
moved to its final position by an active eruption mechanism. Mechanical pressure from the erupting tooth probably plays some role in resorption of the bony covering, perhaps as one initiating factor, but biochemical and cellular changes in the follicular epithelium are necessary to produce bone removal. Tooth eruption will be blocked if bone resorption does not take place or if there are other mechanical obstructions. Resorption can occur in the absence of eruption. Cahill3 prevented the eruption of molars in puppies by ligating the teeth to the lower border of the mandible and found that resorption of overlying bone and deciduous teeth proceeded even when eruption did not. When the ligated teeth subsequently were released, they erupted faster than normal.4 Thus, the rate of bone resorption may be the rate-limiting factor for normal pre-emergence eruption. Once a tooth emerges into the oral cavity, there no longer are restraints to eruption caused by overlying tissues. The tooth then is subject to intermittent forces from function which oppose eruption. Continued eruption of all teeth accompanies growth, of course, and renewed eruption of a tooth is commonly observed late in life if an antagonist tooth is removed, demonstrating that the eruption mechanism remains present and potentially active long after eruption ceases. The origin of the eruption force never has been clearly established. Hydrostatic forces
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expressed in the periodontium but ultimately derived from the vascular system repeatedly have been implicated.“. 6 So have forces derived from active metabolism in the periodontal ligament (PDL).‘. ’ Agents (lathyrogens) which interfere with normal maturation and cross-linking of collagen definitely inhibit eruption,” which indicates that a PDL composed of normal tissue is a prerequisite for normal eruption. Eruption proceeds even after amputation of most of the root,“’ so a totally intact PDL is not required; nor is an actively growing area at the root apex. It has long been recognized that tooth eruption is abnormal in patients with some developmental syndromes. The best known of these is cleidocranial dysplasia (formerly called cleidocranial dysostosis), which is characterized by absence or reduction of the clavicles, alterations in skull proportions, multiple supernumerary teeth. and failure of most permanent teeth to emerge from the alveolar bone (Fig. 4). Cleidocranial dysplasia is inherited as an autosomal dominant trait. ” The underlying biochemical abnormality is unknown. The unerupted teeth in cleidocranial dysplasia are not ankylosed. If they are surgically exposed by removal of overlying tissue, they will respond to orthodontic force and often can be brought into the mouth and into a reasonably normal occlusion. ‘*, I8 Histologic studies have shown that the roots of these unerupted permanent teeth lack the normal layer of secondary (cellular) cementum. i4 The present consensus, however, is that the eruption failure is due to mechanical obstruction from abnormal resorption of overlying bone and not to any root or periodontal abnormality. I’, ifi The absence of cellular cementum is a reflection of eruption failure, not a cause. In addition to nonresorbing bone, a dense layer of fibrotic tissue is present in some cleidocranial dysplasia patients, ii and this also can mechanically impede eruption. Eruption failure not due to some form of mechanical obstruction rarely has been discussed in the literature. In his 1966 Tomes lecture, BallardiR described a “type of failure of vertical adaptation ” which clearly is the same condition that we call “primary failure of eruption. ” Ballard reported having seen nine such cases in 16,000 admissions at the Eastman Dental Hospital and published partial records on one of these patients. Kaban, Needleman, and HertzbergiY discussed molar eruption failure in the oral surgery literature in 1976 and presented five cases, one of which may have represented primary failure of eruption. Three other individual case reports have appeared in the last decade, and we would classify these as examples of primary failure of eruption.20-22 In 1978 Bosker, Ten Kate, and Nijenhuis’” reported “reinclusion of permanent molars” in fiftyfive individuals from nine related families. Radiographs of their index cases show the same characteristics as our “primary failure” patients. In this kindred, there was autosomal dominant transmission with essentially complete penetrance.2” Characteristics
of patients with primary failure of eruption
Primary failure of eruption is rare. Since we first became interested in these patients 10 years ago, we have collected records on eight patients, either from patient flow through moderately busy university clinics or from private practitioners, and have seen approximately eight other such patients. On the basis of this admittedly small number of patients, it appears that these persons share most if not all of the following characteristics: 1. Posterior teeth are involved more than anterior teeth (Fig. 5). First permanent molars seem most likely to be affected, but premolars or canines can be included. Incisors almost never are. Varying degrees of abnormality seem present distal to the first involved
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Fig. 5. Panoramic films of patients with primary failure of eruption. A, Unilateral involvement of maxillary and mandibular molars. B, Bilateral involvement including second deciduous molars.
tooth; that is, if the lirst molar is affected, the second and third molars almost surely are but premolars may be normal. If the canines are affected, premolars and molars almost certainly are affected also. 2. Involved teeth may erupt all the way into occlusion and then cease to erupt, even though they are not ankylosed, or they may fail to erupt, even though the overlying bone has been removed by apparently normal resorption to provide an eruption path. If they erupted initially, affected teeth submerge in the classic fashion of ankylosis. In some instances, a tooth which never erupted at all appears to be at the bottom of a large vertical bony defect because all the bone over it has been resorbed. In other cases, there appears to
be an enlarged follicle around the unerupted crown. From these findings, it seems reasonable to conclude that the problem relates to the eruption mechanism itself and that there are abnormalities of the periodontal ligament structures related to eruption. 3. Deciduous as well as permanent molars are likely to be involved (Fig. 6). Submerged and apparently ankylosed deciduous second molars were noted in most of these patients in the vicinity of a nonerupting permanent molar. Since ankylosis of deciduous molars occurs relatively frequently in normal patients, this in itself does not indicate any particular problem with the eruption mechanism. Darling and Lever? noted that 98 percent of a large sample of submerged deciduous teeth were ankylosed. The other 2 percent may be instances of primary failure of eruption. 4. Involvement may be unilateral or bilateral, but the condition rarely is symmetric and frequently is unilateral. 5. Involved permanent teeth do tend to become ankylosed, but failure of eruption is apparent before definite ankylosis occurs. When an unerupted molar is surgically exposed in a patient with this condition, the surgeon usually observes that the tooth is not ankylosed and can be moved within the crypt. Some involved teeth do erupt slightly during a period of observation, but at rates far below the normal eruption rate. 6. Application of orthodontic force in an attempt to bring involved teeth into the arch leads to ankylosis rather than normal tooth movement. Involved teeth seem never to respond normally to orthodontic forces. At best, they move 1 to 2 mm., but ankylosis invariably results before the tooth can be brought down into occlusion. This can be taken as further evidence of periodontal ligament abnormalities. 7. Our patients seem not to have similarly affected close relatives, and none have any apparent medical problems or syndrome involvement. Ballard *Breported the same finding in his nine cases. There is clear evidence of widespread involvement of persons in the kindred reported by Bosker and colleagues, 2:1but this seems unusual since all other reports concern apparently isolated instances. No cause for the condition can be documented. The age at onset of the condition is not clear, probably because the more teeth are affected, the earlier deviations from normal occlusion will appear. It is clear that some teeth may erupt normally at first and then stop erupting. In at least one patient in our series, a mandibular first molar had erupted far enough into the mouth that an occlusal restoration had been placed at age 7. implying reasonably normal eruption up to that time (see Case 1). This tooth subsequently failed to erupt and was completely covered over by soft tissue as alveolar development continued, although it was not ankylosed. Since both upper and lower molars were involved bilaterally in this patient, it seems unlikely that the simple restoration in itself caused the eruption failure. If only second molars are involved, there will be no apparent abnormality until the patient is 14 years of age or older. It is conceivable that some patients who have delayed eruption of second molars only do fall into the category of a mild eruption failure syndrome. Similarly, some unerupted third molars may be due to failure of the eruption mechanism rather than mechanical interference from lack of space. A gradient of eruption may exist distally along the dental lamina. If so, this could explain why eruption problems not related to mechanical restriction become more frequent with the posterior teeth. Developmentally, the permanent molars are really a distal extension of the deciduous dentition and can be considered deciduous teeth which do not develop permanent succes-
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Fig. 6. Bilateral posterior open-biie due to primary failure in a boy. A, Lateral cephalometric fill n at age 8. 8, F)anoramic film at age 8. C, Study casts at age 10.
sors. This may help to explain the frequent involvement of deciduous second molars along with permanent first molars. Treatment of patients with failure of eruption Patients with eruption failure can be placed into two groups: (1) those whose teeth have not emerged from the alveolar bone and (2) those whose teeth show alveolar emergence but have not come into occlusion. For the first group, it becomes important to evaluate whether the cause of eruption failure is (1) some sort of mechanical obstruction as, for example, a retained deciduous tooth or a supernumerary tooth in the area; (2) failure of normal resorption of overlying bone, as in cleidocranial dysplasia and related syndromes and in some instances of early loss of deciduous teeth; or (3) failure of the eruption mechanism, probably related to a periodontal ligament defect, for which the best evidence is failure of the tooth to erupt despite the absence of any apparent obstruction. Treatment in each of these three circumstances should be different. When eruption failure is due to an ankylosed deciduous molar, a supernumerary tooth, or other mechanical obstruction, the question is whether the tooth beneath the obstruction can be brought into the arch. In this circumstance, it probably is best to remove the mechanical obstruction and observe the unerupted tooth over the next few months (Fig. 7). If it begins to erupt, even though it might not reach the normal location on its own, the periodontal ligament and eruption mechanism are normal. The tooth should respond to orthodontic force, allowing it to be brought into the arch. A tooth whose eruption has been delayed by mechanical interference usually can be brought to its normal position by orthodontic treatment, even if it must be moved over a considerable distance. If the tooth shows no spontaneous eruption on its own, however, there is an increased probability that if it is exposed and orthodontic force is applied, it will ankylose as soon as orthodontic traction is begun. Failure of overlying bone to resorb properly requires surgical exposure of the teeth followed by orthodontic treatment to move the involved teeth into position. This is true whether the problem is cleidocranial dysplasia, other related syndromes,‘“, ” or no apparent developmental anomaly. Since most or all of the patient’s teeth are likely to be involved, treatment can be difficult, but good results are possible with careful coordination of surgery and orthodontics.r2, l3 Patients with primary failure of eruption may or may not have teeth which have emerged from the alveolar bone. Frequently some involved teeth are covered only by soft tissue, while others in the same patient have a layer of overlying bone. If bone resorption is occurring but tooth movement is not, the natural result is an enlarged bony crypt over the crown of the tooth. In patients with primary failure of eruption, therefore, the presence of enlarged crypts around some of the posterior teeth is one indicator of the true nature of the problem. If alveolar emergence of some posterior teeth has occurred but those teeth have not come into occlusion, the differential diagnosis is between primary failure of eruption and mechanical obstruction from interposed soft tissue. Lip or tongue interference produces a lateral open-bite with adjacent teeth at nearly the same vertical level. Each tooth erupts up to the point at which the interference overcomes further eruption; then it stops. In contrast, primary failure of eruption usually results in teeth being at different vertical levels. Failure
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Fig, 7. Failure of eruption of maxillary second premolar because of mechanical obstructia In. A, Par roramic film at age 13. Left maxillary deciduous molar is ankylosed and “submerging” with ob struction and displacement of the permanent successor. B, Following extraction of the ankylosed deck hlous mol ar and second molar, spontaneous eruption of the premolar toward space produced by distal mot rement of the first molar. C, Final position of the second premolar in functioning occlusion , after con rpletion of orthodontic treatment.
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Fig. 8. Case 1. Facial photographs of patient at age 13.
of teeth to resume eruption when the putative interference is removed, as by placement of a lip or tongue shield off an arch wire, indicates a problem with the eruption mechanism. Failure to respond to direct orthodontic force, as from vertical elastics, is an even stronger indicator. Treatment of patients with primary failure of eruption is extremely difficult and frustrating. If the patient truly has primary failure of eruption, orthodontic force will be ineffective. The involved teeth tend to ankylose when orthodontic force is applied. Since an ankylosed tooth is perfect orthodontic anchorage, an effort to pull down a tooth which ankyloses soon after force is applied often results in intrusion of the normal teeth. This converts an isolated posterior open-bite into a more general lateral open-bite (see Case 2). In the absence of a normal response to orthodontic force, the only way to move unerupted teeth into occlusion is to reposition them surgically without disturbing the periodontal ligament. A small-segment alveolar osteotomy (or an osteotomy involving a larger segment, depending on how many teeth are involved) can accomplish this in some instances if the teeth are in an accessible location. When an osteotomy is used to reposition an alveolar segment containing unerupted teeth, a bone graft should be interposed beneath it. Stable results are possible, and for selected patients, this surgical approach can allow treatment of problems which otherwise are almost unmanageable. Such a smallsegment osteotomy may result in a tooth which is 1 to 2 mm. out of occlusion because of some retraction of the segment during healing. Even if the repositioned tooth cannot be held tightly in occlusion, usually it is possible to get it close enough surgically that a restoration can bring it the rest of the way into functional occlusion without too much increase in crown-root ratio. Unfortunately, at times the position of the nonerupting teeth precludes surgery to bring the teeth into occlusion. Then prosthetic replacement becomes the only possible treatment. Treatment difficulties and possibilities are illustrated in the case reports that follow.
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films. A, Prior to treatment. 6, Following surgical repositioning of maxill; w mandibular first molars and maxillary right canine and premolars. C, After 16 lths of orthodontic treatment, prior to extraction of upper left first molar and construction of on lay parti al dentures.
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Fig. 10. Case 1. Vertical elastics from lower arch wire to upper molars in an attempt to bring posterior teeth into occlusion.
Case 1 (Figs. 8 to 10) A 13-year-old girl was referred because of multiple unerupted posterior teeth. Her medical history was unremarkable, consisting only of the usual childhood illnesses. Them were no apparent physical abnormalities except for impaction, ankylosis, and/or eruption failure of various teeth in all four quadrants. It was decided initially that the most severely involved teeth should be exposed surgically and manipulated gently to free them from the presumed ankylosis if possible. On exploration of the maxillary left quadrant, the first and second molars and second premolar could be displaced by pressure and definitely were not ankylosed. At this time, the maxillary left canine was elevated into position after extraction of the deciduous canine; subsequently, endodontic treatment was carried out. One week later, the maxillary right quadrant was explored, and the canine and both premolars were surgically repositioned. The clinical impression was that the canine was lightly ankylosed, but the premolars were not. One month later, the deeply embedded mandibular right first molar was extracted without difficulty. It was not ankylosed. Since the unerupted teeth were not ankylosed, it was decided that orthodontic treatment should be attempted, uprighting the lower molars and using vertical elastics to bring the upper molars into occlusion. After gingival tissue was excised to expose the teeth, a wire loop was placed around the maxillary left first molar. The maxillary right molars and all remaining mandibular teeth were banded. A mandibular 0.016 inch arch wire was placed and vertical elastics were worn between upper and lower molars bilaterally. Six months later there was essentially no progress. All lower teeth except the central incisors now seemed ankylosed, since they showed no mobility at all and had a dull sound on percussion. Bands were placed on the maxillary teeth and A-lastics were applied to close the anterior spaces. After 3 months, the central and lateral incisors were together, but other spaces could not be closed and all maxillary teeth except the incisors appeared ankylosed. Sixteen months after orthodontic treatment began, all appliances were removed. The situation remained essentially what it had been initially except that maxillary anterior diastemas were closed. The upper left first molar was extracted and maxillary and mandibular onlay partial dentures were construe ted.
Case 2 (Figs. 11 to 13) A 13-year-old girl was referred for consultation to plan surgical correction of mandibular prognathism at a later date. When she was seen initially, a full edgewise appliance was in place and she had been under treatment for the previous 12 months. Because of the size of the lower jaw, the initial plan had been mandibular surgery. The orthodontic treatment was aimed at obtaining align-
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Fig. 11. Case 2. A, Lateral cephalometric film after 12 months of orthodontic treatment. Note two levels of maxillary posterior teeth consistent with the right lateral open-bite. B, Panoramic film. Right maxillary premolars and canine are intruded to the level of the ankylosed right first molar. ment of incisors and bringing the maxillary right first molar down into occlusion. After 12 months of treatment, the molar remained some 6 mm. out of occlusion, and a lateral open-bite extended posteriorly on the right side from the lateral incisor. It appeared that, in response to the orthodontic force, the first molar had ankylosed and had provided the anchorage necessary for intrusion of the premolars and canine. At this time, extraction of the maxillary right first molar was advised and was carried out. With a light round arch in place back through the maxillary second premolar, the lateral open-bite improved as the canine and premolar came back down into occlusion. The patient was placed on observation to determine the best time for mandibular surgery. Eighteen months later mandibular growth was almost complete and the patient was seen by an
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Fig. 12. A, Cephalometric film during attempt to bring maxillary right second molar down into occlusion 2 years after extraction of first molar. B, Panoramic film just prior to jaw surgery, after second molar was disconnected and premolars re-erupted.
orthodontist in a city near her home for final orthodontic preparation for the jaw surgery. Since the maxillary right second molar had not erupted, the orthodontist arranged to have this tooth surgically exposed. A band was placed on it and an arch wire was extended posteriorly to include the second molar. Vertical elastics were placed between the upper and lower second molars. When the patient was seen for another surgical consultation, the second molar had not moved appreciably but again the canines and premolars on the maxillary right side were intruding and a lateral open-bite extended posteriorly from the lateral incisor. The othodontist was advised to disconnect the second molar and the open-bite improved forward from the molar. At this stage, the patient was seen for mandibular surgery. A bilateral ramus osteotomy was used to set the mandible back 7 mm., and at the same time an alveolar osteotomy was done to free the bony segment containing the maxillary right second molar. This tooth was surgically moved
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Fig. 13. A, Cephalometric film after mandibular surgery and alveolar osteotomy to position the right second maxillary molar adjacent to the same vertical level as the right premolars. B, Postoperative panoramic film. The upper right molar remained out of occlusion (approximately 2 mm.) but was brought significantly down and forward.
downward and forward to the vertical level of the premolars. A graft of freeze-dried cadaver bone was placed ahove the alveolar segment. Following surgery, light elasticson round arch wires settled the teeth into occlusion. The maxillary right secondmolar remained about 2 mm. out of occlusion, but in a position where a restoration could he used to bring it into function. The right canine and premolars showed no ill effects from inadvertently having been intruded twice during the orthodontic treatment. Discussion Many orthodontists have seemed to take it for granted that open-bite problems are caused by some environmental influence which affects eruption. With the appreciation of skeletal vertical dysplasias in recent years, there has been greater recognition that anterior
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open-bite may be caused by a skeletal growth problem. When this is true, the patient’s tendency to place the tongue in the anterior opening is best regarded as a physiologic adaptation to the presence of the space rather than the tongue being the cause of the opening between the teeth. A similar situation apparently occurs for some patients with posterior or lateral open-bite. The open-bite is due to an abnormality in the eruption mechanism which leads to failure of eruption of the involved teeth and a vertical opening between posterior teeth. Although the tongue fills the vertical space between the teeth, the lateral tongue thrust may be the result, not the cause, of the lateral open-bite. To understand clearly the possible causes of lateral open-bite, it can be helpful to consider the vertical equilibrium of forces on the teeth. After it emerges into the oral cavity, each tooth is subjected to a set of forces which are applied to the occlusal surface and tend to push the tooth back into its socket. Such forces are applied during chewing and during parafunctional activities (clenching of the teeth, bruxism). There also may be vertically directed forces applied by the soft tissues during sleep and at rest as well as during such activities as swallowing. These forces are resisted by the periodontal ligament, alveolar bone, and the dentofacial structures broadly. In normal persons an eruptive force in the opposite direction is generated and tends to move the tooth occlusally along its long axis. In adults there is an equilibrium between the eruptive force and the forces opposing eruption, so that teeth neither erupt nor are intruded although forces in both directions are present. In a child some net eruption accompanies jaw growth, even after a tooth has come into occlusion. This must mean that the forces which oppose eruption do not totally balance out the eruptive force. It is apparent, therefore, that an open-bite between posterior teeth could develop in a growing child either from an increase in the forces applied against the occlusal surface, as from a tongue or cheek interposed between the teeth, or from a decrease in normal eruption in the presence of normal occlusal loadings. It is important for orthodontists to recognize that for some patients the real problem is a failure of the eruption mechanism and not some habit through which the patient is preventing normal eruption. The condition of failure of eruption described in this article seems to be the result of abnormalities in the periodontal ligament. A precise definition of the problem in these patients will have to await elucidation of the eruption mechanisn in normal persons. We can conclude, however, that the problem in primary failure of eruption not only differs from the problem when there is mechanical obstruction to postemergence eruption but also is significantly different from the eruption failure owing to lack of bone resorption which is observed in patients with cleidocranial dysplasia and related syndromes. Distinguishing between lack of eruption due to some external interference with eruption and a primary failure of the eruption mechanism is important clinically because this determines the prognosis for conventional orthodontic treatment. If the eruption mechanism is normal, the response to orthodontic forces also will be normal. This means that even if a tooth whose eruption has been impeded no longer would move on its own to the desired location, it should be possible to move it there by orthodontic treatment. On the other hand, if the periodontal ligament is abnormal and eruption failure has occurred because of this, the problem cannot be treated orthodontically because the periodontal ligament will not respond normally to orthodontic force. Applying orthodontic force to a tooth with eruption failure is likely to lead only to intrusion of other normal teeth within the arch, as the abnormal tooth becomes ankylosed. For some of these patients, the only
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feasible treatment is prosthetic replacement of the abnormal teeth. In other instances, a small-segment osteotomy, with surgical repositioning of the involved tooth and the adjacent bone, leaving the periodontal ligament undisturbed, may provide a successful outcome. Establishment of a realistic prognosis for unerupted teeth based on the probable cause of the problem can prevent disappointment for both patient and clinician. The etiology of primary failure of eruption is entirely unknown. From the two major theories of eruption, it would seem that either metabolism in the periodontal ligament or blood flow to it should be altered in this condition. A systemic problem affecting tissue metabolism in this one area seems improbable. Some metabolic change arising toward the end of the period of dental development could partially explain why posterior teeth are more involved. In several of our patients first molars but not premolars are involved, although the first molars form at an earlier age. In addition, the condition often is asymmetric. It is not clear why a metabolic disturbance would affect only one side. Local alteration in blood flow seems a more likely possibility. In experimental animals, decreasing blood flow in acute experiments immediately affects eruption.5 There are no data for long-term effects. We have observed that a few nonankylosed teeth in orthognathic surgery patients no longer responded normally to orthodontic force. These teeth were always in alveolar segments which had been repositioned surgically, so that blood supply could have been affected. There is no direct evidence for this, however, and no explanation for what might have happened to the vascular system in nonsurgical patients. Whatever the mechanism, it seems likely that primary failure of eruption is related to some sort of genetic disturbance with varying penetrance and expressivity. If this is the case, either the condition shows up only sporadically or a detailed pedigree analysis of the type done by Bosker and associates23would reveal that the condition is much more common than has previously been suspected. Although the autosomal dominant inheritance described by Bosker and co-authors probably is not the usual condition, further investigation of the families of affected persons is indicated. Since hyper- or hypoeruption of teeth in addition to jaw positioning is involved in all types of malocclusion involving the vertical dimension, a more complete understanding of the eruption mechanism and why it sometimes fails should facilitate treatment for many orthodontic patients. Further study of patients with primary failure of eruption offers an interesting opportunity to gain insight into the mechanism and control of eruption. We thank Drs. Herbert Davidson, Michael Simmons, and Richard Peters for sharing records of their patients with us and Drs. James Ackerman and David Bixler for helpful comments. REFERENCES 1. Kelly, J. E., and Harvey, C. R.: An assessmentof the occlusion of the teeth of youths age 12-17 years, Rockville, Md., 1977, National Center for Health Statistics, U. S. Public Health Service. 2. McCall, J. O., and Wald, S. S.: Clinical dental rcentgenology, ed. 4, Philadelphia, 1957, W. B. Saunders Company, p. 154, Fig. 156. 3. Cahill, D. R.: Eruption pathway formation in the presence of experimental tooth impaction in puppies, Anat. Rec. 164: 67-77, 1969. 4. Cahill, D. R.: The histology and rate of tooth eruption with and without temporary impaction in the dog, Anat. Rec. 166: 225-237, 1970. 5. Main, J. H. P., and Adams, D.: Experiments on the rat incisor into the cellular proliferation and blood pressure theories of tooth eruption, Arch. Oral Biol. 11: 163-178, 1966. 6. Moxham, B. J.: The effects of some vaso-active drugs on the eruption of the rabbit mandibular incisor, Arch. Oral Biol. 24: 681-687, 1979.
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7. Melcher, A. H., and Beer&on, W.: The physiology of tooth eruption. In McNamara, J. A. (editor): Biology of occlusal development, Ann Arbor, 1977, University of Michigan Center for Human Growth and Development. 8. Tsuruta, M., Eto, K., and Chiba, M.: Effect of daily or 4-hourly administration of lathyrogens on the eruption rates of impeded and unimpeded mandibular incisors of rats, Arch. Oral Biol. 19: 1221-1226. 1974. 9. Berkovitz, B. K. B., Migdalshia, A., and Solomon, M.: The effect of the lathyritic agent aminoacetonitrile on the unimpeded eruption rate in normal and root-resected rat lower incisors, Arch. Oral Biol. 17: 1755-1763, 1972. 10. Berkovitz, B. K. B., and Thomas, N. R.: Unimpeded eruption in the root-resected lower incisor of the rat with a preliminary note on root transection, Arch. Oral Biol. 14: 771-780, 1969. 11. Gorlin,R.J.,Pindborg,J.J.,andCohen,M.M.:Syndromesoftheheadandneck,ed.2,NewYork, 1976, McGraw-Hill Book Company. 12. Smylski, P. T., Woodside, D. G., and Harnett, B. E.: Surgical and orthodontic treatment of cleidocranial dysostosis, Int. J. Oral Surg. 3: 380-385, 1974. 13. Hall, R. K., and Hyland, A. L.: Combined surgical and orthodontic management of the oral abnormalities in children with cleidocranial dysplasia, Int. J. Oral Surg. 7: 267-273. 1978. 14. Rushton, M. A.: An anomaly of cementum in cleidccranial dysostosis, J. Can. Dent. Assoc. 42: 139-142, 1976. 15. Chapnick, L. A., and Main, J. H. P.: Cementum in cleidocranial dysostosis. J. Can. Dent. Assoc. 42: 139-142, 1976. 16. Fleisher-Peters, A.: Zur Pathohistologie des Alveolar-knochens bei Dysostosis cleidocraniahs, Stoma (Heidelburg) 23: 212-215, 1970. 17. Miller, R., et al.: Cleidocranial dysostosis: A multidisciplinary approach to treatment, J. Am. Dent. Assoc. %: 296-300, 1978. 18. Ballard, C. F.: The adaptive alveolar processes, Ann. R. Coll. Surg. Engl. 39: 299-311, 1966. 19. Kaban, L. B., Needleman, H. L., and Hertzberg, J.: Idiopathic failure of eruption of permanent molar teeth, Oral Surg. 42: 155-163, 1976. 20. Koskinen, K. P., and Rahkamo, A.: A submerged permanent tirst molar, Proc. Finn. Dent. Sot. 71: 191-193, 1975. 21. Brady, F. A., and Blum, M.: An unerupted deciduous mandibular molar, ORAL SURG. 47: 201, 1979. 22. Kapoor, A. K., Srivastava, A. B., and Singh, B. P.: Bilateral posterior open bite: Case report, Oral Surg. 51: 21-22, 1981. 23. Bosker, H., ten Kate, L. P., and Nijenhuis, L. E.: Familial reinclusion of permanent molars, Clin. Gene. 13: 314-320, 1978. 24. Darling, A. J., and Levers, B. G.: Submerged human deciduous molars and ankylosis, Arch Oral Biol. 18: 1021-1040, 1973. 25. Rayne, J.: Gardner’s syndrome, Br. J. Oral Surg. 6: 11-17, 1968. 26. Shokeir, M. H. K.: Complete failure of eruption of all permanent teeth: An autosomal dominant disorder, Clin. Genet. 5: 322-326, 1974.
Key words: Eruption failure, posterior open-bite, tooth ankylosis, vertical jaw growth, eruption mechanism
P
artial or complete failure of posterior teeth to erupt produces a lateral (posterior) open-bite. This problem is seen occasionally in all orthodontic practices, although it occurs too infrequently to warrant separate classification in the best United States epidemiologic surveys of malocclusion. l There are two possible causes: (1) mechanical interference with eruption, either before or after the tooth emerges from the alveolar bone, or (2) failure of the eruptive mechanism of the tooth so that the expected amount of eruption does not occur. Mechanical interference with eruption may be caused by ankylosis of the tooth to the alveolar bone, which can occur spontaneously or as a result of trauma, or by obstacles in the path of the erupting tooth. Examples of such obstructions prior to emergence are supernumerary teeth and nonresorbing deciduous tooth roots or alveolar bone (Fig. 1). After the tooth emerges from the bone, pressures from soft tissues interposed between the teeth (cheek, tongue, finger) can be obstacles to eruption. When a tooth erupts into the oral cavity and then ceases eruption before growth is completed, it appears to submerge and may eventually be covered over again by the gingiva. This “submergence” usually denotes ankylosis. The second possible cause of eruption failure, a disturbance of the eruption mechanism itself, often is overlooked. In this article we describe a condition best termed “primary failure of eruption, ” in which nonankylosed teeth fail to erupt fully or partially because of malfunction of the eruption mechanism. These patients have no other recognizable disorder, and no mechanical interferences with eruption seem to exist. The condi-
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Fig. 1. Mechanical obstruction to eruption in a 14-year-old boy with retained deciduous molars.
Fig. 2. Failure of eruption of maxillary and mandibular molars in the absence of ankylosis or other mechanical obstruction in a 20-year-old man, the condition termed “primary failure of eruption.”
tion may be the cause of posterior open-bite which does not respond to orthodontic treatment (Fig. 2). Our goals in this article are to review briefly influences on eruption, describe patients with primary failure of eruption and differentiate them from patients with eruption failure due to other causes, and discuss treatment possibilities and limitations for patients with eruption failure. Influences
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eruption
In the process of tooth development, the deciduous tooth buds lie in a relatively superticial position and are never completely separated from the oral cavity by bone2 (Fig. 3). The succedaneous tooth buds, however, come to lie in a completely enclosed bony crypt, connected to the oral cavity by the thin gubernacular cord of connective tissue. In order for eruption to occur, the bony covering must be resorbed and the tooth must be
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Fig. 3. Radiograph of mandible at birth (wet specimen). Buds of the first permanent molars, like the deciduous tooth buds, are positioned superficially. (From McCall and Wald: Clinical Dental Roentgenology, Philadelphia, 1957, W. B. Saunders Company, used by permission.)
Fig. 4. Cleidocranial dysplasia and associated delay in eruption of permanent teeth in a lByear-old
girl.
moved to its final position by an active eruption mechanism. Mechanical pressure from the erupting tooth probably plays some role in resorption of the bony covering, perhaps as one initiating factor, but biochemical and cellular changes in the follicular epithelium are necessary to produce bone removal. Tooth eruption will be blocked if bone resorption does not take place or if there are other mechanical obstructions. Resorption can occur in the absence of eruption. Cahill3 prevented the eruption of molars in puppies by ligating the teeth to the lower border of the mandible and found that resorption of overlying bone and deciduous teeth proceeded even when eruption did not. When the ligated teeth subsequently were released, they erupted faster than normal.4 Thus, the rate of bone resorption may be the rate-limiting factor for normal pre-emergence eruption. Once a tooth emerges into the oral cavity, there no longer are restraints to eruption caused by overlying tissues. The tooth then is subject to intermittent forces from function which oppose eruption. Continued eruption of all teeth accompanies growth, of course, and renewed eruption of a tooth is commonly observed late in life if an antagonist tooth is removed, demonstrating that the eruption mechanism remains present and potentially active long after eruption ceases. The origin of the eruption force never has been clearly established. Hydrostatic forces
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expressed in the periodontium but ultimately derived from the vascular system repeatedly have been implicated.“. 6 So have forces derived from active metabolism in the periodontal ligament (PDL).‘. ’ Agents (lathyrogens) which interfere with normal maturation and cross-linking of collagen definitely inhibit eruption,” which indicates that a PDL composed of normal tissue is a prerequisite for normal eruption. Eruption proceeds even after amputation of most of the root,“’ so a totally intact PDL is not required; nor is an actively growing area at the root apex. It has long been recognized that tooth eruption is abnormal in patients with some developmental syndromes. The best known of these is cleidocranial dysplasia (formerly called cleidocranial dysostosis), which is characterized by absence or reduction of the clavicles, alterations in skull proportions, multiple supernumerary teeth. and failure of most permanent teeth to emerge from the alveolar bone (Fig. 4). Cleidocranial dysplasia is inherited as an autosomal dominant trait. ” The underlying biochemical abnormality is unknown. The unerupted teeth in cleidocranial dysplasia are not ankylosed. If they are surgically exposed by removal of overlying tissue, they will respond to orthodontic force and often can be brought into the mouth and into a reasonably normal occlusion. ‘*, I8 Histologic studies have shown that the roots of these unerupted permanent teeth lack the normal layer of secondary (cellular) cementum. i4 The present consensus, however, is that the eruption failure is due to mechanical obstruction from abnormal resorption of overlying bone and not to any root or periodontal abnormality. I’, ifi The absence of cellular cementum is a reflection of eruption failure, not a cause. In addition to nonresorbing bone, a dense layer of fibrotic tissue is present in some cleidocranial dysplasia patients, ii and this also can mechanically impede eruption. Eruption failure not due to some form of mechanical obstruction rarely has been discussed in the literature. In his 1966 Tomes lecture, BallardiR described a “type of failure of vertical adaptation ” which clearly is the same condition that we call “primary failure of eruption. ” Ballard reported having seen nine such cases in 16,000 admissions at the Eastman Dental Hospital and published partial records on one of these patients. Kaban, Needleman, and HertzbergiY discussed molar eruption failure in the oral surgery literature in 1976 and presented five cases, one of which may have represented primary failure of eruption. Three other individual case reports have appeared in the last decade, and we would classify these as examples of primary failure of eruption.20-22 In 1978 Bosker, Ten Kate, and Nijenhuis’” reported “reinclusion of permanent molars” in fiftyfive individuals from nine related families. Radiographs of their index cases show the same characteristics as our “primary failure” patients. In this kindred, there was autosomal dominant transmission with essentially complete penetrance.2” Characteristics
of patients with primary failure of eruption
Primary failure of eruption is rare. Since we first became interested in these patients 10 years ago, we have collected records on eight patients, either from patient flow through moderately busy university clinics or from private practitioners, and have seen approximately eight other such patients. On the basis of this admittedly small number of patients, it appears that these persons share most if not all of the following characteristics: 1. Posterior teeth are involved more than anterior teeth (Fig. 5). First permanent molars seem most likely to be affected, but premolars or canines can be included. Incisors almost never are. Varying degrees of abnormality seem present distal to the first involved
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Fig. 5. Panoramic films of patients with primary failure of eruption. A, Unilateral involvement of maxillary and mandibular molars. B, Bilateral involvement including second deciduous molars.
tooth; that is, if the lirst molar is affected, the second and third molars almost surely are but premolars may be normal. If the canines are affected, premolars and molars almost certainly are affected also. 2. Involved teeth may erupt all the way into occlusion and then cease to erupt, even though they are not ankylosed, or they may fail to erupt, even though the overlying bone has been removed by apparently normal resorption to provide an eruption path. If they erupted initially, affected teeth submerge in the classic fashion of ankylosis. In some instances, a tooth which never erupted at all appears to be at the bottom of a large vertical bony defect because all the bone over it has been resorbed. In other cases, there appears to
be an enlarged follicle around the unerupted crown. From these findings, it seems reasonable to conclude that the problem relates to the eruption mechanism itself and that there are abnormalities of the periodontal ligament structures related to eruption. 3. Deciduous as well as permanent molars are likely to be involved (Fig. 6). Submerged and apparently ankylosed deciduous second molars were noted in most of these patients in the vicinity of a nonerupting permanent molar. Since ankylosis of deciduous molars occurs relatively frequently in normal patients, this in itself does not indicate any particular problem with the eruption mechanism. Darling and Lever? noted that 98 percent of a large sample of submerged deciduous teeth were ankylosed. The other 2 percent may be instances of primary failure of eruption. 4. Involvement may be unilateral or bilateral, but the condition rarely is symmetric and frequently is unilateral. 5. Involved permanent teeth do tend to become ankylosed, but failure of eruption is apparent before definite ankylosis occurs. When an unerupted molar is surgically exposed in a patient with this condition, the surgeon usually observes that the tooth is not ankylosed and can be moved within the crypt. Some involved teeth do erupt slightly during a period of observation, but at rates far below the normal eruption rate. 6. Application of orthodontic force in an attempt to bring involved teeth into the arch leads to ankylosis rather than normal tooth movement. Involved teeth seem never to respond normally to orthodontic forces. At best, they move 1 to 2 mm., but ankylosis invariably results before the tooth can be brought down into occlusion. This can be taken as further evidence of periodontal ligament abnormalities. 7. Our patients seem not to have similarly affected close relatives, and none have any apparent medical problems or syndrome involvement. Ballard *Breported the same finding in his nine cases. There is clear evidence of widespread involvement of persons in the kindred reported by Bosker and colleagues, 2:1but this seems unusual since all other reports concern apparently isolated instances. No cause for the condition can be documented. The age at onset of the condition is not clear, probably because the more teeth are affected, the earlier deviations from normal occlusion will appear. It is clear that some teeth may erupt normally at first and then stop erupting. In at least one patient in our series, a mandibular first molar had erupted far enough into the mouth that an occlusal restoration had been placed at age 7. implying reasonably normal eruption up to that time (see Case 1). This tooth subsequently failed to erupt and was completely covered over by soft tissue as alveolar development continued, although it was not ankylosed. Since both upper and lower molars were involved bilaterally in this patient, it seems unlikely that the simple restoration in itself caused the eruption failure. If only second molars are involved, there will be no apparent abnormality until the patient is 14 years of age or older. It is conceivable that some patients who have delayed eruption of second molars only do fall into the category of a mild eruption failure syndrome. Similarly, some unerupted third molars may be due to failure of the eruption mechanism rather than mechanical interference from lack of space. A gradient of eruption may exist distally along the dental lamina. If so, this could explain why eruption problems not related to mechanical restriction become more frequent with the posterior teeth. Developmentally, the permanent molars are really a distal extension of the deciduous dentition and can be considered deciduous teeth which do not develop permanent succes-
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Fig. 6. Bilateral posterior open-biie due to primary failure in a boy. A, Lateral cephalometric fill n at age 8. 8, F)anoramic film at age 8. C, Study casts at age 10.
sors. This may help to explain the frequent involvement of deciduous second molars along with permanent first molars. Treatment of patients with failure of eruption Patients with eruption failure can be placed into two groups: (1) those whose teeth have not emerged from the alveolar bone and (2) those whose teeth show alveolar emergence but have not come into occlusion. For the first group, it becomes important to evaluate whether the cause of eruption failure is (1) some sort of mechanical obstruction as, for example, a retained deciduous tooth or a supernumerary tooth in the area; (2) failure of normal resorption of overlying bone, as in cleidocranial dysplasia and related syndromes and in some instances of early loss of deciduous teeth; or (3) failure of the eruption mechanism, probably related to a periodontal ligament defect, for which the best evidence is failure of the tooth to erupt despite the absence of any apparent obstruction. Treatment in each of these three circumstances should be different. When eruption failure is due to an ankylosed deciduous molar, a supernumerary tooth, or other mechanical obstruction, the question is whether the tooth beneath the obstruction can be brought into the arch. In this circumstance, it probably is best to remove the mechanical obstruction and observe the unerupted tooth over the next few months (Fig. 7). If it begins to erupt, even though it might not reach the normal location on its own, the periodontal ligament and eruption mechanism are normal. The tooth should respond to orthodontic force, allowing it to be brought into the arch. A tooth whose eruption has been delayed by mechanical interference usually can be brought to its normal position by orthodontic treatment, even if it must be moved over a considerable distance. If the tooth shows no spontaneous eruption on its own, however, there is an increased probability that if it is exposed and orthodontic force is applied, it will ankylose as soon as orthodontic traction is begun. Failure of overlying bone to resorb properly requires surgical exposure of the teeth followed by orthodontic treatment to move the involved teeth into position. This is true whether the problem is cleidocranial dysplasia, other related syndromes,‘“, ” or no apparent developmental anomaly. Since most or all of the patient’s teeth are likely to be involved, treatment can be difficult, but good results are possible with careful coordination of surgery and orthodontics.r2, l3 Patients with primary failure of eruption may or may not have teeth which have emerged from the alveolar bone. Frequently some involved teeth are covered only by soft tissue, while others in the same patient have a layer of overlying bone. If bone resorption is occurring but tooth movement is not, the natural result is an enlarged bony crypt over the crown of the tooth. In patients with primary failure of eruption, therefore, the presence of enlarged crypts around some of the posterior teeth is one indicator of the true nature of the problem. If alveolar emergence of some posterior teeth has occurred but those teeth have not come into occlusion, the differential diagnosis is between primary failure of eruption and mechanical obstruction from interposed soft tissue. Lip or tongue interference produces a lateral open-bite with adjacent teeth at nearly the same vertical level. Each tooth erupts up to the point at which the interference overcomes further eruption; then it stops. In contrast, primary failure of eruption usually results in teeth being at different vertical levels. Failure
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Fig, 7. Failure of eruption of maxillary second premolar because of mechanical obstructia In. A, Par roramic film at age 13. Left maxillary deciduous molar is ankylosed and “submerging” with ob struction and displacement of the permanent successor. B, Following extraction of the ankylosed deck hlous mol ar and second molar, spontaneous eruption of the premolar toward space produced by distal mot rement of the first molar. C, Final position of the second premolar in functioning occlusion , after con rpletion of orthodontic treatment.
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Fig. 8. Case 1. Facial photographs of patient at age 13.
of teeth to resume eruption when the putative interference is removed, as by placement of a lip or tongue shield off an arch wire, indicates a problem with the eruption mechanism. Failure to respond to direct orthodontic force, as from vertical elastics, is an even stronger indicator. Treatment of patients with primary failure of eruption is extremely difficult and frustrating. If the patient truly has primary failure of eruption, orthodontic force will be ineffective. The involved teeth tend to ankylose when orthodontic force is applied. Since an ankylosed tooth is perfect orthodontic anchorage, an effort to pull down a tooth which ankyloses soon after force is applied often results in intrusion of the normal teeth. This converts an isolated posterior open-bite into a more general lateral open-bite (see Case 2). In the absence of a normal response to orthodontic force, the only way to move unerupted teeth into occlusion is to reposition them surgically without disturbing the periodontal ligament. A small-segment alveolar osteotomy (or an osteotomy involving a larger segment, depending on how many teeth are involved) can accomplish this in some instances if the teeth are in an accessible location. When an osteotomy is used to reposition an alveolar segment containing unerupted teeth, a bone graft should be interposed beneath it. Stable results are possible, and for selected patients, this surgical approach can allow treatment of problems which otherwise are almost unmanageable. Such a smallsegment osteotomy may result in a tooth which is 1 to 2 mm. out of occlusion because of some retraction of the segment during healing. Even if the repositioned tooth cannot be held tightly in occlusion, usually it is possible to get it close enough surgically that a restoration can bring it the rest of the way into functional occlusion without too much increase in crown-root ratio. Unfortunately, at times the position of the nonerupting teeth precludes surgery to bring the teeth into occlusion. Then prosthetic replacement becomes the only possible treatment. Treatment difficulties and possibilities are illustrated in the case reports that follow.
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films. A, Prior to treatment. 6, Following surgical repositioning of maxill; w mandibular first molars and maxillary right canine and premolars. C, After 16 lths of orthodontic treatment, prior to extraction of upper left first molar and construction of on lay parti al dentures.
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Fig. 10. Case 1. Vertical elastics from lower arch wire to upper molars in an attempt to bring posterior teeth into occlusion.
Case 1 (Figs. 8 to 10) A 13-year-old girl was referred because of multiple unerupted posterior teeth. Her medical history was unremarkable, consisting only of the usual childhood illnesses. Them were no apparent physical abnormalities except for impaction, ankylosis, and/or eruption failure of various teeth in all four quadrants. It was decided initially that the most severely involved teeth should be exposed surgically and manipulated gently to free them from the presumed ankylosis if possible. On exploration of the maxillary left quadrant, the first and second molars and second premolar could be displaced by pressure and definitely were not ankylosed. At this time, the maxillary left canine was elevated into position after extraction of the deciduous canine; subsequently, endodontic treatment was carried out. One week later, the maxillary right quadrant was explored, and the canine and both premolars were surgically repositioned. The clinical impression was that the canine was lightly ankylosed, but the premolars were not. One month later, the deeply embedded mandibular right first molar was extracted without difficulty. It was not ankylosed. Since the unerupted teeth were not ankylosed, it was decided that orthodontic treatment should be attempted, uprighting the lower molars and using vertical elastics to bring the upper molars into occlusion. After gingival tissue was excised to expose the teeth, a wire loop was placed around the maxillary left first molar. The maxillary right molars and all remaining mandibular teeth were banded. A mandibular 0.016 inch arch wire was placed and vertical elastics were worn between upper and lower molars bilaterally. Six months later there was essentially no progress. All lower teeth except the central incisors now seemed ankylosed, since they showed no mobility at all and had a dull sound on percussion. Bands were placed on the maxillary teeth and A-lastics were applied to close the anterior spaces. After 3 months, the central and lateral incisors were together, but other spaces could not be closed and all maxillary teeth except the incisors appeared ankylosed. Sixteen months after orthodontic treatment began, all appliances were removed. The situation remained essentially what it had been initially except that maxillary anterior diastemas were closed. The upper left first molar was extracted and maxillary and mandibular onlay partial dentures were construe ted.
Case 2 (Figs. 11 to 13) A 13-year-old girl was referred for consultation to plan surgical correction of mandibular prognathism at a later date. When she was seen initially, a full edgewise appliance was in place and she had been under treatment for the previous 12 months. Because of the size of the lower jaw, the initial plan had been mandibular surgery. The orthodontic treatment was aimed at obtaining align-
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Fig. 11. Case 2. A, Lateral cephalometric film after 12 months of orthodontic treatment. Note two levels of maxillary posterior teeth consistent with the right lateral open-bite. B, Panoramic film. Right maxillary premolars and canine are intruded to the level of the ankylosed right first molar. ment of incisors and bringing the maxillary right first molar down into occlusion. After 12 months of treatment, the molar remained some 6 mm. out of occlusion, and a lateral open-bite extended posteriorly on the right side from the lateral incisor. It appeared that, in response to the orthodontic force, the first molar had ankylosed and had provided the anchorage necessary for intrusion of the premolars and canine. At this time, extraction of the maxillary right first molar was advised and was carried out. With a light round arch in place back through the maxillary second premolar, the lateral open-bite improved as the canine and premolar came back down into occlusion. The patient was placed on observation to determine the best time for mandibular surgery. Eighteen months later mandibular growth was almost complete and the patient was seen by an
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Fig. 12. A, Cephalometric film during attempt to bring maxillary right second molar down into occlusion 2 years after extraction of first molar. B, Panoramic film just prior to jaw surgery, after second molar was disconnected and premolars re-erupted.
orthodontist in a city near her home for final orthodontic preparation for the jaw surgery. Since the maxillary right second molar had not erupted, the orthodontist arranged to have this tooth surgically exposed. A band was placed on it and an arch wire was extended posteriorly to include the second molar. Vertical elastics were placed between the upper and lower second molars. When the patient was seen for another surgical consultation, the second molar had not moved appreciably but again the canines and premolars on the maxillary right side were intruding and a lateral open-bite extended posteriorly from the lateral incisor. The othodontist was advised to disconnect the second molar and the open-bite improved forward from the molar. At this stage, the patient was seen for mandibular surgery. A bilateral ramus osteotomy was used to set the mandible back 7 mm., and at the same time an alveolar osteotomy was done to free the bony segment containing the maxillary right second molar. This tooth was surgically moved
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Fig. 13. A, Cephalometric film after mandibular surgery and alveolar osteotomy to position the right second maxillary molar adjacent to the same vertical level as the right premolars. B, Postoperative panoramic film. The upper right molar remained out of occlusion (approximately 2 mm.) but was brought significantly down and forward.
downward and forward to the vertical level of the premolars. A graft of freeze-dried cadaver bone was placed ahove the alveolar segment. Following surgery, light elasticson round arch wires settled the teeth into occlusion. The maxillary right secondmolar remained about 2 mm. out of occlusion, but in a position where a restoration could he used to bring it into function. The right canine and premolars showed no ill effects from inadvertently having been intruded twice during the orthodontic treatment. Discussion Many orthodontists have seemed to take it for granted that open-bite problems are caused by some environmental influence which affects eruption. With the appreciation of skeletal vertical dysplasias in recent years, there has been greater recognition that anterior
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open-bite may be caused by a skeletal growth problem. When this is true, the patient’s tendency to place the tongue in the anterior opening is best regarded as a physiologic adaptation to the presence of the space rather than the tongue being the cause of the opening between the teeth. A similar situation apparently occurs for some patients with posterior or lateral open-bite. The open-bite is due to an abnormality in the eruption mechanism which leads to failure of eruption of the involved teeth and a vertical opening between posterior teeth. Although the tongue fills the vertical space between the teeth, the lateral tongue thrust may be the result, not the cause, of the lateral open-bite. To understand clearly the possible causes of lateral open-bite, it can be helpful to consider the vertical equilibrium of forces on the teeth. After it emerges into the oral cavity, each tooth is subjected to a set of forces which are applied to the occlusal surface and tend to push the tooth back into its socket. Such forces are applied during chewing and during parafunctional activities (clenching of the teeth, bruxism). There also may be vertically directed forces applied by the soft tissues during sleep and at rest as well as during such activities as swallowing. These forces are resisted by the periodontal ligament, alveolar bone, and the dentofacial structures broadly. In normal persons an eruptive force in the opposite direction is generated and tends to move the tooth occlusally along its long axis. In adults there is an equilibrium between the eruptive force and the forces opposing eruption, so that teeth neither erupt nor are intruded although forces in both directions are present. In a child some net eruption accompanies jaw growth, even after a tooth has come into occlusion. This must mean that the forces which oppose eruption do not totally balance out the eruptive force. It is apparent, therefore, that an open-bite between posterior teeth could develop in a growing child either from an increase in the forces applied against the occlusal surface, as from a tongue or cheek interposed between the teeth, or from a decrease in normal eruption in the presence of normal occlusal loadings. It is important for orthodontists to recognize that for some patients the real problem is a failure of the eruption mechanism and not some habit through which the patient is preventing normal eruption. The condition of failure of eruption described in this article seems to be the result of abnormalities in the periodontal ligament. A precise definition of the problem in these patients will have to await elucidation of the eruption mechanisn in normal persons. We can conclude, however, that the problem in primary failure of eruption not only differs from the problem when there is mechanical obstruction to postemergence eruption but also is significantly different from the eruption failure owing to lack of bone resorption which is observed in patients with cleidocranial dysplasia and related syndromes. Distinguishing between lack of eruption due to some external interference with eruption and a primary failure of the eruption mechanism is important clinically because this determines the prognosis for conventional orthodontic treatment. If the eruption mechanism is normal, the response to orthodontic forces also will be normal. This means that even if a tooth whose eruption has been impeded no longer would move on its own to the desired location, it should be possible to move it there by orthodontic treatment. On the other hand, if the periodontal ligament is abnormal and eruption failure has occurred because of this, the problem cannot be treated orthodontically because the periodontal ligament will not respond normally to orthodontic force. Applying orthodontic force to a tooth with eruption failure is likely to lead only to intrusion of other normal teeth within the arch, as the abnormal tooth becomes ankylosed. For some of these patients, the only
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feasible treatment is prosthetic replacement of the abnormal teeth. In other instances, a small-segment osteotomy, with surgical repositioning of the involved tooth and the adjacent bone, leaving the periodontal ligament undisturbed, may provide a successful outcome. Establishment of a realistic prognosis for unerupted teeth based on the probable cause of the problem can prevent disappointment for both patient and clinician. The etiology of primary failure of eruption is entirely unknown. From the two major theories of eruption, it would seem that either metabolism in the periodontal ligament or blood flow to it should be altered in this condition. A systemic problem affecting tissue metabolism in this one area seems improbable. Some metabolic change arising toward the end of the period of dental development could partially explain why posterior teeth are more involved. In several of our patients first molars but not premolars are involved, although the first molars form at an earlier age. In addition, the condition often is asymmetric. It is not clear why a metabolic disturbance would affect only one side. Local alteration in blood flow seems a more likely possibility. In experimental animals, decreasing blood flow in acute experiments immediately affects eruption.5 There are no data for long-term effects. We have observed that a few nonankylosed teeth in orthognathic surgery patients no longer responded normally to orthodontic force. These teeth were always in alveolar segments which had been repositioned surgically, so that blood supply could have been affected. There is no direct evidence for this, however, and no explanation for what might have happened to the vascular system in nonsurgical patients. Whatever the mechanism, it seems likely that primary failure of eruption is related to some sort of genetic disturbance with varying penetrance and expressivity. If this is the case, either the condition shows up only sporadically or a detailed pedigree analysis of the type done by Bosker and associates23would reveal that the condition is much more common than has previously been suspected. Although the autosomal dominant inheritance described by Bosker and co-authors probably is not the usual condition, further investigation of the families of affected persons is indicated. Since hyper- or hypoeruption of teeth in addition to jaw positioning is involved in all types of malocclusion involving the vertical dimension, a more complete understanding of the eruption mechanism and why it sometimes fails should facilitate treatment for many orthodontic patients. Further study of patients with primary failure of eruption offers an interesting opportunity to gain insight into the mechanism and control of eruption. We thank Drs. Herbert Davidson, Michael Simmons, and Richard Peters for sharing records of their patients with us and Drs. James Ackerman and David Bixler for helpful comments. REFERENCES 1. Kelly, J. E., and Harvey, C. R.: An assessmentof the occlusion of the teeth of youths age 12-17 years, Rockville, Md., 1977, National Center for Health Statistics, U. S. Public Health Service. 2. McCall, J. O., and Wald, S. S.: Clinical dental rcentgenology, ed. 4, Philadelphia, 1957, W. B. Saunders Company, p. 154, Fig. 156. 3. Cahill, D. R.: Eruption pathway formation in the presence of experimental tooth impaction in puppies, Anat. Rec. 164: 67-77, 1969. 4. Cahill, D. R.: The histology and rate of tooth eruption with and without temporary impaction in the dog, Anat. Rec. 166: 225-237, 1970. 5. Main, J. H. P., and Adams, D.: Experiments on the rat incisor into the cellular proliferation and blood pressure theories of tooth eruption, Arch. Oral Biol. 11: 163-178, 1966. 6. Moxham, B. J.: The effects of some vaso-active drugs on the eruption of the rabbit mandibular incisor, Arch. Oral Biol. 24: 681-687, 1979.
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7. Melcher, A. H., and Beer&on, W.: The physiology of tooth eruption. In McNamara, J. A. (editor): Biology of occlusal development, Ann Arbor, 1977, University of Michigan Center for Human Growth and Development. 8. Tsuruta, M., Eto, K., and Chiba, M.: Effect of daily or 4-hourly administration of lathyrogens on the eruption rates of impeded and unimpeded mandibular incisors of rats, Arch. Oral Biol. 19: 1221-1226. 1974. 9. Berkovitz, B. K. B., Migdalshia, A., and Solomon, M.: The effect of the lathyritic agent aminoacetonitrile on the unimpeded eruption rate in normal and root-resected rat lower incisors, Arch. Oral Biol. 17: 1755-1763, 1972. 10. Berkovitz, B. K. B., and Thomas, N. R.: Unimpeded eruption in the root-resected lower incisor of the rat with a preliminary note on root transection, Arch. Oral Biol. 14: 771-780, 1969. 11. Gorlin,R.J.,Pindborg,J.J.,andCohen,M.M.:Syndromesoftheheadandneck,ed.2,NewYork, 1976, McGraw-Hill Book Company. 12. Smylski, P. T., Woodside, D. G., and Harnett, B. E.: Surgical and orthodontic treatment of cleidocranial dysostosis, Int. J. Oral Surg. 3: 380-385, 1974. 13. Hall, R. K., and Hyland, A. L.: Combined surgical and orthodontic management of the oral abnormalities in children with cleidocranial dysplasia, Int. J. Oral Surg. 7: 267-273. 1978. 14. Rushton, M. A.: An anomaly of cementum in cleidccranial dysostosis, J. Can. Dent. Assoc. 42: 139-142, 1976. 15. Chapnick, L. A., and Main, J. H. P.: Cementum in cleidocranial dysostosis. J. Can. Dent. Assoc. 42: 139-142, 1976. 16. Fleisher-Peters, A.: Zur Pathohistologie des Alveolar-knochens bei Dysostosis cleidocraniahs, Stoma (Heidelburg) 23: 212-215, 1970. 17. Miller, R., et al.: Cleidocranial dysostosis: A multidisciplinary approach to treatment, J. Am. Dent. Assoc. %: 296-300, 1978. 18. Ballard, C. F.: The adaptive alveolar processes, Ann. R. Coll. Surg. Engl. 39: 299-311, 1966. 19. Kaban, L. B., Needleman, H. L., and Hertzberg, J.: Idiopathic failure of eruption of permanent molar teeth, Oral Surg. 42: 155-163, 1976. 20. Koskinen, K. P., and Rahkamo, A.: A submerged permanent tirst molar, Proc. Finn. Dent. Sot. 71: 191-193, 1975. 21. Brady, F. A., and Blum, M.: An unerupted deciduous mandibular molar, ORAL SURG. 47: 201, 1979. 22. Kapoor, A. K., Srivastava, A. B., and Singh, B. P.: Bilateral posterior open bite: Case report, Oral Surg. 51: 21-22, 1981. 23. Bosker, H., ten Kate, L. P., and Nijenhuis, L. E.: Familial reinclusion of permanent molars, Clin. Gene. 13: 314-320, 1978. 24. Darling, A. J., and Levers, B. G.: Submerged human deciduous molars and ankylosis, Arch Oral Biol. 18: 1021-1040, 1973. 25. Rayne, J.: Gardner’s syndrome, Br. J. Oral Surg. 6: 11-17, 1968. 26. Shokeir, M. H. K.: Complete failure of eruption of all permanent teeth: An autosomal dominant disorder, Clin. Genet. 5: 322-326, 1974.