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The etiology of maxillary canine impaction: Part 2

Published: May 2013

Bulletin #22 May 2013

The etiology of maxillary canine impaction: Part 2

In part 1 of this article, published in the April 2013 Bulletin #21 in this series, local causes of maxillary canine impaction were described. These included local anatomical obstructions and hard and soft tissue pathological entities that cause a deflection in the normal eruption path of the canine. It was also pointed out that, when these etiological factors are eliminated, there is a fair degree of autonomous correction in the eruption path, which may often lead to spontaneous eruption of the canine.

Ipso facto, the unerupted maxillary permanent canine is subject to the influence of environmental factors.

On the other hand, impaction of the maxillary canine sometimes runs in families and, in these cases, it is seen in association with other features of the dentition that are clearly hereditary1. So, it is perhaps reasonable to assume that canine impaction is also hereditary. Let’s present the evidence for and against and try to understand the biological mechanisms by which the tooth fails to erupt normally.

As a starting point to understanding abnormal development that creates canine ectopy, it is important to first understand how normal development occurs and how the canine manoeuvers its way in relation to the roots of the adjacent teeth. As it does so, it influences the alignment of the adjacent teeth while, at the same time, its own eruption and alignment are influenced by them, until it erupts into the mouth and into its final position.

The normal eruption mechanism

The mechanism of normal eruption and normal alignment of the maxillary anterior teeth was first described by Broadbent, over 70 years ago.2 He outlined how the eruption of the two central incisors produces an initial temporary arrangement, which is quite different from the final alignment seen just 4 or 5 years later. He called this temporary arrangement the Ugly Duckling stage. He described the orientation of the two newly-erupted maxillary central incisors and the initial wide space between them - the midline diastema - and how this closes up quite naturally, in the fullness of time, with the eruption of the canine teeth. At the outset, he considered that the diastema was caused by the early developmental location of the unerupted lateral incisors, high up on the distal side of the roots of the central incisors. With one lateral incisor on each side in the narrow apical area, the roots of the central incisors are pushed together, to cause a distal flaring of their crowns, with their crown-to-root long axes converging somewhere above their developing apices.

In the ensuing months of normal development, the lateral incisors migrate downwards on the distal side of the central incisors, surrendering their constricting effect on the apices of the central incisors. As they move down past the CEJ, they eventually erupt, distally flared, into interproximal contact with the crowns of the central incisors. The outcome of this is that their relationship to the incisors becomes reversed. The central incisor crowns are influenced to tip mesially, reducing the wide diastema and partially uprighting the long axes of these teeth.

ww._Fig.1

Fig. 1a Diagrammatic representation of the relationship between the maxillary incisors and between them and the unerupted canines in normal development in a 9-10 year old individual. The canines restrict the roots into a narrowed apical area, causing lateral flaring of the incisor crowns. Courtesy of Informa Healthcare Publishers, Abingdon.

Fig. 1b. Diagrammatic representation of the final alignment and long axis re-orientation following eruption of the canines.

At the age of 8 years, normally developing unerupted canines may be seen on a periapical radiograph to be mesially angulated, high on the distal side of the apical third of the roots of the lateral incisors, in much the same relationship that existed between the lateral and central incisors, a year or so earlier. The canines constrict the four developing incisor apices into a small space and their crown-to-root long axes converge to a virtual point high above their apices (Fig. 1a).

During the ensuing 2 or 3 years, the downward eruptive movements of the canines are guided along the distal aspect of the roots of the lateral incisors and, as they move down, they release their “stranglehold” on the incisor apices and generate a progressive mesial uprighting of all four incisor crowns as they go. This results in an integral chain of interproximal contacts between the crowns of the anterior 6 teeth, which also finally closes off what remains of the midline diastema (Fig. 1b).

This account of the natural dynamics of eruption and alignment of the maxillary anterior teeth, described by Broadbent so long ago2, has become a well-recognized and established cornerstone of our orthodontic literature and has withstood the test of time. It is widely quoted in the literature and is accepted as axiomatic to the narrative of normal growth and development. This is the Guidance Theory of Eruption of the maxillary anterior teeth.

From this description it is clear that there is much that can go wrong in this scheme of events that may have an effect on the eruption path of the canine. Indeed, Broadbent speculated that because of the long path of eruption taken by the maxillary canine, from close to the floor of the orbit to its final destination – a distance of 22mms - it had a greater chance of going off-course. It clearly requires a relatively small discrepancy in direction or degree of influence of one of the factors involved to “throw a spanner in the works” and undermine this fragile scheme. It was his view that this was the reason that the canine occasionally became palatally displaced.

About 50 years ago, Miller3 and Bass4 observed that the prevalence of palatal displacement was higher when lateral incisors were congenitally missing. They concluded that the absence of the lateral incisor denied the canine of its guidance, which then allowed it to migrate palatally. It is important to understand that these conclusions were based on clinical impressions from viewing a number of cases in the clinic and not from any disciplined study of a large sample of affected cases versus an appropriate random control group, such as epidemiologic population figures.

In a study by our group in Jerusalem5, we noted that in a large sample of palatal canine cases, only half the patients had normal lateral incisors – the other half had missing, peg-shaped or small lateral incisors. By comparison in random studies in the same geographic area, normal lateral incisors were present in 93% of the general population sample6. We subsequently initiated a study of the families of our palatal canine patients and found an exceptionally high incidence of hereditary lateral incisor anomaly. We also found a high incidence of palatal canine displacement among the siblings and parents of our affected patients.1 These results have been confirmed in many subsequent studies in other countries 7-12.

Armed with this convincing information, the obvious, facile and simplistic conclusion is to deduce that palatally impacted canines and anomlous or missing lateral incisors are each genetically determined and mutually linked - a view that was held by the authors of most of these studies.

The Guidance Theory of Canine Impaction

ww._Fig._2

Fig. 2. Anterior section of a panoramic view of a 10 year old boy with delayed dental development conforming to age 8 overall. The crown of the unerupted lateral incisor is reduced in size and mildly peg-shaped, while its developing root is of a length normally seen at age 4-5 years.

But let’s look at this from a different perspective. Maxillary lateral incisors normally erupt at age 8 years, when their root development is between a half and three-quarters complete. However, these teeth are notoriously variable in their development and they are among the most frequent to be congenitally missing from the dentition. Confirmed as a microform or lesser degree of severity of agenesis,.these teeth are also among the most frequently seen to have deficient form, with small and peg-shaped crowns13-17 and, in these circumstances their development can be as much as 3 or 4 years later than a normal lateral incisor. Thus a 10 year old child may be seen with an unerupted lateral incisor and, from the radiograph, it will be determined that the crown is peg-shaped and, typically, there is only 1/3 of the expected root development (Fig. 2). These features are well recognized as genetically-determined traits.

ww._Fig._3

Fig. 3a-d. A series of periapical radiographs of an untreated girl, taken between age 8 and age 15. The lateral incisor (#12) is peg-shaped and extremely late-developing. It provides no guidance for the canine (#13), which may be seen to progressively move to the mesial, passing by the lateral incisor, to finally erupt palatally and mesial to it.

If we now refer back to the above description of the normal development of the anterior teeth, we are reminded that at the age of 10 years, the unerupted canine is normally to be found at the distal aspect of the root of the lateral incisor. Maxillary canines are ontogenically stable teeth, in terms of shape, size and developmental timing, but lateral incisors are not. If a late-developing peg-shaped or small lateral incisor is present, with only the very earliest degree of root development, it will be clear that the canine will not find the guidance that would enable it to descend along its normal eruption path (Fig. 3). Thus, the tooth frequently moves down in a more palatal path into the downward converging, V-shaped, alveolar ridge until it comes into close proximity of the periosteum of the medial aspect of the alveolar process. This process acts as a secondary guide, encouraging the canine to descend further until it arrives, a year or two later, on the lingual side of the now-erupted anomalous lateral incisor. The incisor then takes on the role of an obstruction which impacts the canine on its palatal side.

ww._Fig._4

Fig. 4. This is the full panoramic view of Fig. 2 and shows congenital absence of the lateral incisor. The left canine appears to be migrating mesially into a position where it may be expected to cause the resorption of the root of the deciduous lateral incisor and, probably, the canine.

It follows, too, that guidance of the canine is also lacking when there is congenital absence of the lateral incisor. The difference, however, occurs in later vertical development, at around the normal eruption time. At that time, the canine is not secondarily obstructed and often may erupt in mid-ridge and in the lateral incisor location. This is quite common. It may even serve as the stimulus for the normal shedding of a retained deciduous lateral incisor, on its way (Fig. 4)! This may account for a greater frequency of canine impaction in the presence of anomalous lateral incisors, compared to their congenital absence.

This description is the essence of what has been termed the Guidance Theory of Canine Impaction and a fuller description of it may be found elsewhere.18 Its salient keys are that:-

1. the immediate environment surrounding the unerupted canine is governed by genetically-controlled factors (late development of small lateral and peg-shaped incisors or by congenitally absent incisors).19

2. the direction and progress of canine eruption is strongly influenced by environmental factors. This is particularly relevant when there is a lack of chronologic coordination between normal canine eruption, on the one hand, and growth of a developed and guiding incisor root of adequate length, on the other.

Problems with the Genetic Theory of Canine Impaction

The right side of any patient is genetically identical with the left side and, as such, any genetic condition of one side will also affect the other. One cannot find a sufferer of Huntington’s disease or Cystic fibrosis or Marfan’s syndrome or Cleidocranial dysplasia affected on just one side of his body. Notwithstanding, in several hereditary conditions the degree of penetrance may affect one side more, resulting in varying degrees expressions of the characteristics of that condition. Cleidocranial dysplasia (CCD) is an autosomal dominant inherited disease, for which the RUNX2 gene is specifically responsible. An affected patient may show variation in gene expression and have more supernumerary teeth on one side than the other, but left and right sides are undoubtedly affected. As we have noted above, missing, small and peg-shaped lateral incisors are 3 varieties of expression of a single genetic factor and, so, we frequently see a peg-shaped or small lateral incisor on one side of the mouth and a missing antimere. In genetics, bilateralism is the rule rather than the exception.

Therefore, if canine impaction were under hereditary control, we would expect to see bilateral canine impaction in the overriding majority of the cases, with a small percentage of cases showing lesser degrees of impaction on one side than on the other. From the epidemiological information gleaned from the many studies reported in the orthodontic literature, findings indicate a 60-75% preponderance of unilateral canine impaction.

In monozygous versus dizygous twins and on the assumption that canine impaction is genetic, one would expect to find monozygous (identical) twins to show a higher degree ofconcordance for impacted canines than dizygous (fraternal) twins. The outcome of such a study found similar degree of concordance for ectopic canines in both groups, suggesting a non-genetic etiology. 20

It was from our earlier studies that we had found that the small and peg-shaped incisors appeared to be more frequently seen in association with the displaced canine than congenital absence5,6

In order to confirm this, we undertook a study21 of a highly selected group of patients each of whom exhibited all of the following characteristics:- 

1. Unspecified unilateral maxillary canine impaction

2. Unspecified unilateral congenitally absence of the maxillary lateral incisor

3. Anomalous lateral incisor (small or peg-shaped) on the other side.

The aim was to see which side showed a greater association with the impacted canine: the side with congenital absence of the incisor or the side with the anomalous lateral incisor. The findings of the study were that the overwhelming majority of canine impactions were associated with the peg-shaped lateral incisor – 7 times more than on the side of congenital absence.21

There is a contradiction here with which the proponents of the Genetic theory have difficulty. We have just pointed out that anomalous lateral incisors represent a microform (a.k.a. lesser degree of severity or weak/partial expression or incomplete penetrance) of total absence. 13-15

If the behavior of the canines is truly governed by genetics, one would expect that the stronger genetic trait (congenital absence) would be associated with a greater frequency of canine impaction. It is surely paradoxical that canine impaction is more frequent with the weaker genetic pattern (anomalous incisors)!

Canine eruptive behavior changes with proactive environmental alteration

ww. Fig.5a_1ww._Fig.5b

Fig. 5a. A panoramic view of the dentition of a boy aged 11 years, showing unerupted maxillary canines with enlarge follicles and mesially angulated. They both a mildly palatally displaced (confirmed with supplementary views). N.B. over-retained and long-rooted deciduous canines, congenital absence of mandibular right second molar and late developing left second mandibular molar

Fig. 5b. A panoramic view taken 1 year after extraction of the deciduous canines shows a favorable alteration in the orientation of the canines, whose normal eruption appears imminent.

It has been our contention, over the years, that genetically-determined lateral incisor anomaly creates an alteration in the local environmental which encourages an abnormal, palatally-deflected, path of eruption of the canine. There is ample evidence to show that spontaneous changes of eruption path of the canine occurs due to alteration of environmental conditions. These conditions include:-

1. extraction of the deciduous canines (Fig. 5)

2. increasing space in the arch in the immediate area with routine orthodontic treatment 22 extraction of deciduous canines with or without the use of cervical headgear.23, 24

3. rapid maxillary expansion.25

4. extraction of first premolars in a serial extraction procedure.18 The entire justification for this is to alleviate anterior crowding by encouraging the canine to adopt a more distal eruption path

5. extraction of a peg-shaped lateral incisor.18 This will also increase the chances of spontaneous eruption of an adjacent impacted canine.

The Guidance theory and the Genetic theory for the causation of palatal displacement of the maxillary canine share the belief that certain genetic characters occur in association with this phenomenon. These include small, peg-shaped and missing lateral incisors, spaced dentitions and late-developing dentitions. According to the Genetic theory, the palatal displacement of the canine is just another associated genetic character. According to the Guidance Theory of Canine Impaction, these factors create a genetically-determined environment in which the developing canine is deprived of its guidance, thus influencing it to adopt an abnormal eruption path.

There is room to doubt that the eruption path of the palatal canine is itself under genetic control26, 27. The cogent alternative explanation promoted here is that a genetically-induced, abnormal environment is highly influential in determining the outcome.

Canine impaction which is exclusively genetic in origin

Are there other forms of canine tooth impaction that are exclusively hereditary? Absolutely!

In normal dentofacial development, the teeth are arranged in a mesio-distal line along the dental arch – incisors, canines, premolars and molars – each in its place, because each has originated from a specific point in the embryonic dental lamina.

For the vast majority of impacted maxillary canines, the root is long, its apex is correctly located in the line of the dental arch and in its appropriate mesiodistal location, high above the apices of the roots of the adjacent teeth. Orientation of the long axis of these canines will have, by and large, caused there to be an abnormal inclination of its long axis which, together with other strictly local environmental factors, brings the crown to an abnormal location. But it is the root apex of the canine which is indicative of the original location of the tooth germ and, as with other teeth, mislocation is rare. Such mislocation, when it occurs, is dictated by genetic factors and is largely to be seen bilaterally – because the left side of the individual is genetically identical to the right. There is undoubtedly room for variation of expression, but this will usually take the form of right-left differences in the orientation of the long axis of the teeth, due to local factors. Apex location is most likely to be similar on each side, although gene penetrance may account for a non-compliant minority.

ww._Fig.6aww. Fig.6b_1

Fig. 6a. The panoramic view taken after space was created in the arch for the bilaterally impacted maxillary canines. Note the ectopic location of the apices of these teeth in the first/second molar region. There is an obvious abnormal orientation of the long axes of these teeth.

Fig 6b. The axial (horizontal) cut from the CBCT shows the apices of the canines to be both posteriorly and medially displaced from their normal location and the tooth to be orientated horizontally with buccally directed long axes.


ww. Fig.6c_1

Fig. 6c. 3-D reconstruction images viewed from the anterior, right, left and from above confirm the location of the root apex and the orientation of the tooth in space.

Thus, one may see a relatively high degree of bilateral occurrence of canines whose root apices are displaced distal to the premolar teeth or medially (towards the midline raphe) in the palate (Fig. 6a-c). Similarly, transposition of the canine with the premolar is also due to apex displacement.

These situations have nothing to do with guidance and cannot be satisfactorily treated by extraction of deciduous canines or other interceptive modalities. These cases exhibit what has been termed “primary displacement of the tooth bud”18. The etiology of these teeth with mislocated root apices is exclusively heredity. The location of the apex is the diagnostic key to distinguishing it and requires sophisticated imaging, best provided by cone beam computerized tomography (CBCT).

Twenty years ago, Kokich and Mathews declared that the etiology of impacted maxillary canines is unknown! Insofar as we can say that there is no single and exclusive cause, they are correct28. But that does not mean that we know nothing about agents that are etiologically associated with its occurrence. On the contrary, we are manifestly confused by the wealth of existing information that relates to the etiology of impacted canines. Our only problem is interpreting its meaning.

References:                  

1.     Zilberman Y, Cohen B, Becker A. Familial trends in palatal canines, anomalous lateral incisors and related phenomena. Eur J Orthod 1990; 12: 135–139

2.     Broadbent BH. Ontogenic development of occlusion. Angle Orthod 1941; 1: 45.

3.     Miller BH. The influence of congenitally missing teeth on the eruption of the upper canine. Dent Pract Dent Rec 1963; 13: 497–504

4.     Bass TB. Observations on the misplaced upper canine tooth. Dent Pract Dent Rec 1967; 18: 25–33

5.     Becker A, Smith P, Behar R. The incidence of anomalous lateral incisors in relation to palatally-displaced cuspids. Angle Orthod 1981;51: 24–29.

6.     Brin I, Becker A, Shalhav M. Position of the maxillary permanent canine in relation to anomalous or missing lateral incisors: a population study. Eur J Orthod 1986; 8: 12–16

7.     Oliver RG, Mannion JE, Robinson JM. Morphology of the maxillary lateral incisor in cases of unilateral impaction of the maxillary canine. Br J Orthod 1989;16:9-16:

8.     Mossey PA, Campbell HM, Luffingham JK. The palatal canine and the adjacent lateral incisor: a study of a West of Scotland population. Br J Orthod 1994; 21: 169–174).

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13.   Grahnen H. Hypodontia in the permanent dentition. A clinical and genetic investigation. Odontol Revy 1956; 79 (Suppl 3): 1–100.

14.   Alvesalo L, Portin P. The inheritance pattern of missing, peg-shaped and strongly mesio-distally reduced upper lateral incisors. Acta Odontol Scand 1969; 27: 563–575.

15.   Garn SM, Lewis AB. The gradient and the pattern of crown-size reduction in simple hypodontia. Angle Orthod 1970; 40: 51–58.

16.   Brook AH. A unifying aetiological explanation for anomalies of human tooth number and size. Arch Oral Biol 1984; 29:373–378.

17.   Pinho T, Tavares P, Maciel P, Pollmann C. Developmental absence of maxillary lateral incisors in the Portuguese population. Eur J Orthod 2005; 27: 443–449.

18.   Becker A. The orthodontic treatment of impacted teeth. 3rd edition. Oxford: Wiley Blackwell Publishers, 2012.

19.   Chosack A, Eidelman E, Cohen T. Hypodontia: a polygenic trait – a family study among Israeli Jews. J Dent Res 1975; 54: 16–19.

20.   Camilleri S, Lewis CM, McDonald F. Ectopic maxillary canines: segregation analysis and a twin study. J Dent Res. 2008;87:580-3.

21.   Becker A, Gillis I, Shpack N. The etiology of palatal displacement of maxillary canines. Clin Orthod Res. 1999;2:62-6.

22.   Olive RJ. Orthodontic treatment of palatally impacted maxillary canines. Aust Orthod J 2002; 18: 64–70.

23.   Leonardi M, Armi P, Franchi L, Baccetti T. Two interceptive approaches to palatally displaced canines: a prospective longitudinal study. AO 2004; 74: 581–586.

24.   Baccetti T, Leonardi M, Armi P. A randomized clinical study of two interceptive approaches to palatally displaced canines. Eur J Orthod 2008; 30: 381–385.

25.   Baccetti T, Mucedero M, Leonardi M, Cozza P. Interceptive treatment of palatal impaction of maxillary canines with rapid maxillary expansion: a randomized clinical trial. Am J Orthod Dentofac Orthop 2009; 136: 657–66

26.   Baccetti T. Risk indicators and interceptive treatment alternatives for palatally displaced canines. Semin Orthod 2010; 16: 182–192

27.   Rutledge MS, Hartsfield, JK Jr. Genetic Factors in the etiology of palatally displaced canines, Semin Orthod 2010; 16: 165–171

28.   Kokich VG, Mathews DP. Surgical and orthodontic management of impacted teeth. Dental Clinics of North America, 1993 37:181-204