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The European Journal of Orthodontics Advance Access originally published online on August 10, 2005
The European Journal of Orthodontics 2005 27(5):450-456; doi:10.1093/ejo/cji040
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© The Author 2005. Published by Oxford University Press on behalf of the European Orthodontics Society. All rights reserved. For permissions, please email: journals.permissions@oxfordjournals.org.

Maxillary canine anomalies and tooth agenesis

Simon Camilleri

Faculty of Dental Surgery, University of Malta Medical and Dental School, Guardamangia, Malta

Address for correspondence Simon Camilleri, Faculty of Dental Surgery, University of Malta Medical and Dental School, Guardamangia, Malta. E-mail: simon.camilleri{at}um.edu.mt


   Summary
Top
 Summary
Introduction
 Subjects and method
 Results
 Discussion
 Conclusion
 References
 
The aims of the study were to analyse the records of 26 subjects (18 females, eight males) with maxillary canine–first premolar transposition (Mx.C.P1) together with 160 subjects with a palatally displaced canine (PDC) to determine the pattern of tooth agenesis in these cases and to compare them with similar samples reported in the literature.

A strong association between Mx.C.P1, lateral incisor and lower second premolar agenesis was found, with a 20 per cent prevalence of lateral incisor agenesis and a 24 per cent prevalence of lower second premolar agenesis. There was a lesser association with third molar (M.3) agenesis, with a prevalence of 52.2 per cent. Weaker associations were found for a PDC, with a prevalence of 5 per cent for lateral incisor agenesis. The prevalence of lower second premolar (5 per cent) and M.3 (27.5 per cent) agenesis approached reference values. Evidence for the implication of the MSX1 or PAX9 genes in the aetiology of PDC was weak.


   Introduction
Top
 Summary
 Introduction
Subjects and method
 Results
 Discussion
 Conclusion
 References
 
Tooth transposition is defined as a form of ectopic eruption where a permanent tooth develops and erupts in the position normally occupied by another permanent tooth (Shapira et al., 1989Go). The commonest form of transposition is between the maxillary canine–first premolar (Mx.C.P1). Tooth transpositions are rare. The prevalence of this particular anomaly is between 0.135 and 0.51 per cent and varies according to the race and region studied (Ruprecht et al., 1984Go; Chattopadhyay and Srinivas, 1996Go; Burnett, 1999Go).

Several authors (Joshi and Bhatt, 1971Go; Peck et al., 1993Go; Chattopadhyay and Srinivas, 1996Go; Plunkett et al., 1998Go; Shapira et al., 2000Go; Shapira and Kuftinec, 2001Go) have studied transposed teeth in an attempt to shed light on the aetiology of the condition. The weight of evidence is that canine transposition is a disturbance of eruption under a measure of genetic control (Feichtinger et al., 1977Go; Peck et al., 1993Go, 1997Go, 2002Go; Shapira et al., 2000Go). Other theories proposed are an interchange in the position at the anlage stage of the involved teeth during odontogenesis (Joshi and Bhatt, 1971Go; Mader and Konzelman, 1979Go; Laptook and Silling, 1983Go) and trauma (Dayal et al., 1983Go; Shah, 1994Go).

A palatally displaced canine (PDC) is a more common developmental disorder with a prevalence of 0.8–2.8 per cent (Shah et al., 1978Go; Grover and Lorton, 1985Go). This, too, may have a genetic aetiology (Zilberman et al., 1990Go; Peck et al., 1994Go). Inheritance on an autosomal dominant basis has been proposed (Pirinen et al., 1996Go).

Both Mx.C.P1 and PDC are associated with hypodontia (Svinhufvud et al., 1988Go; Peck et al., 1993Go), another autosomal dominant condition. Hypodontia may be caused by one major gene mutation, but is very often heterogenic (Arte, 2001Go).

Peck et al. (1994)Go pointed out similarities between PDC and Mx.C.P1 and argued that both conditions are genetic in origin and frequently occur in association with other, genetically interrelated, dental anomalies.

Peck et al. (2002)Go analysed the pattern of hypodontia associated with PDC, Mx.C.P1 and other variations of canine transposition. Third molar (M.3) agenesis was found to be strongly associated with mandibular incisor–canine transposition (Mn.I2.C) and PDC. Mx.C.P1 was associated with lateral incisor agenesis, but not with M.3 agenesis. In view of this, the homeobox genes MSX1 and PAX9, associated with posterior field (molar) hypodontia, have been suggested by Peck et al. (2002)Go as candidate genes for the control of Mn.I2.C and PDC.

The Maltese population has a high prevalence of PDC, over 4 per cent (Camilleri, 1995Go). The most likely genetic explanation for this is the founder effect, the local population having grown rapidly from less than 20 000 to over 350 000 in the past 500 years (Cassar, 2000Go). This high prevalence causes a considerable drain on the resources of the School Dental Service. Seventeen per cent of the consultant caseload involves dealing with ectopic canines. Consequently, the aetiology of PDC is of considerable interest.

The aim of this study was to analyse a large sample of subjects with Mx.C.P1 and PDC and to compare the prevalences and patterns of tooth agenesis in these groups with similar samples reported in the literature.


   Subjects and method
Top
 Summary
 Introduction
 Subjects and method
Results
 Discussion
 Conclusion
 References
 
One hundred and sixty non-syndromic consecutive subjects with PDC were ascertained from the files of the School Dental Clinic, Floriana, and from private practice over the past 3 years. Diagnosis was made by both clinical and radiographic examination and confirmed at the time of surgery, where appropriate. Patients under 13 years of age were eliminated from the M.3 study. All subjects were Caucasian and resident in the Maltese Islands.

Twenty-six non-syndromic subjects with Mx.C.P1 transposition were gathered from private practice over the past 10 years and from the files of the School Dental Clinic over the last 3 years. A general dental practitioner contributed study models of one further case. Transposition was confirmed clinically or by radiographic or photographic evidence for all cases except one, which was documented with study models only and used solely for assessment of lateral incisor agenesis. Two Mx.C.P1 subjects were under 13 years of age and therefore were excluded from the M.3 assessment, as was the study model case.

Fisher's exact test was used to compare the frequencies of agenesis of specific teeth with earlier published population prevalences (Grahnén, 1956Go; Bot and Salmon, 1977Go; Bredy et al., 1991Go). The significance level was set at P < 0.05.

Data were also obtained from previously published articles on PDC and Mx.C.P1 transposition. The ratios of tooth agenesis were compared with each other and with the present sample, using chi-squared tests.


   Results
Top
 Summary
 Introduction
 Subjects and method
 Results
Discussion
 Conclusion
 References
 
Table 1 shows the data for the Mx.C.P1 subjects. The sample comprised 18 females and eight males. Various other anomalies were observed to occur in these subjects, apart from the transposed canines and hypodontia. Six patients presented with ectopic contralateral canines. Of these, five were palatally displaced (Figure 1) and one was buccally impacted. In one subject, the transposed canine had erupted palatally (Figure 2). Other anomalies were submerged primary teeth, ectopically erupting premolars and supernumerary teeth (Table 1). In one patient, a dental panoramic tomogram (DPT) had been taken at 10 years of age, prior to the diagnosis of the transposition. The second DPT was taken at 15 years of age (Figure 3). In another case, the transposition was found to have corrected spontaneously after extraction of the adjacent submerged primary teeth. Following this, the contralateral canine erupted palatally (Figure 4).


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  		Table 1 The subject data, recording the position and number of transposed teeth together with associated dental anomalies. Subjects under 13 years of age at the time of the study are listed as ‘<13 years’.

 


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  		Figure 1  Case 12: transposed right maxillary canine with palatally displaced left maxillary canine.

 


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  		Figure 2  Case 13: transposed maxillary canine erupted palatally. The bracket was bonded post-eruption in an attempt to bring it into the arch.

 


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  		Figure 3  Case 8: (a) dental panoramic tomogram (DPT) taken at 10 years of age. The apex of the upper right canine is much further distal than normal, over the bud of the developing second premolar. Both first premolars are markedly distally inclined. (b) DPT taken at 15 years of age. The upper right canine has erupted into a transposed position, buccal to the first and second premolars. The upper left canine is impacted high and buccal to the arch.

 


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  		Figure 4  Case 11: (a) the apex of the upper left canine seems to be in the correct position, over the root of the first primary molar. The first and second premolars seem to be ectopic, being mesial to their normal positions. (b) Following extraction of the submerging primary molars, the teeth erupted in the correct sequence, with the upper left canine buccal to the retained primary canine crown, and the second premolar palatal to the line of the arch. Had the primary molars not been extracted, transposition would probably have occurred, due to ectopic eruption of the premolar. The upper right canine had spontaneously erupted palatally.

 
Table 2 shows the tooth agenesis frequencies for the PDC and Mx.C.P1 samples for the three studied tooth types, M.3, mandibular second premolar (Mn.P.2), maxillary lateral incisor (Mx.I.2). The number of affected subjects in each category is reported along with the computed relative frequency of agenesis.


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  		Table 2 Agenesis according to tooth type in maxillary canine–first premolar (Mx.C.P1) transposition and palatally displaced canine (PDC) cases. The data are compared with reference values.

 

   Discussion
Top
 Summary
 Introduction
 Subjects and method
 Results
 Discussion
Conclusion
 References
 
Mx.C.P1 transposition seems to be strongly associated with incisor agenesis but less so with premolar and M.3 agenesis.

Comparison of the data reported previously on Mx.C.P1 (Table 3) with the present sample showed remarkable similarity. There was no significant difference between the figures for lateral incisor, premolar and M.3 agenesis (P = 0.1114, P = 0.1977, P = 0.0953, respectively). The prevalence ratios quoted were quite similar in most cases.


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  		Table 3 Comparison of data for tooth agenesis and ectopic maxillary canines in different published samples of maxillary canine–first premolar transposition.

 
The ratios for incisor and premolar agenesis were remarkably consistent for all Mx.C.P1 transposition samples throughout the world.

There was no significant difference between the studies of Plunkett et al. (1998)Go and Shapira and Kuftinec. (2001)Go for maxillary canine impaction (P = 0.0636). The prevalences of canine impaction reported in those studies (1.9 and 2.7 per cent) were well within the quoted range. However, in the present study, the prevalence was markedly higher at 20.8 per cent (P = 0.0041). This is an unusual finding, as PDC has not been reported as being associated with Mx.C.P1. Plunkett et al. (1998)Go and Shapira and Kuftinec (2001)Go documented one case each, while Peck et al. (2002)Go reported no such case in their sample or in a search of the literature.

There were highly significant differences between all samples and the reference values for Mx.I.2 agenesis (Table 4). The same applied for Mn.P.2 agenesis, apart from the findings of Shapira and Kuftinec (2001)Go, where there was no significant difference from the reference value.


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  		Table 4 Proportion of congenitally missing teeth in different published samples of maxillary canine–first premolar transposition as compared with reference data.

 
The figures for the Maltese Mx.C.P1 group were elevated when compared with the published prevalences for lateral incisor, premolar and M.3 hypodontia (P = 0.0006, P = 0.0002, P = 0.0234, respectively).

The PDC samples (Table 5) also showed no significant differences between each other, although the level of agreement was low for both Mx.I.2 and Mn.P.2 agenesis. The ratios for Mx.I.2 agenesis were also consistent, except for the figure given by Mossey et al. (1994)Go. This may be due to ethnic or sampling differences.


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  		Table 5 Comparison of data for congenitally missing teeth in palatally displaced canine cases.

 
There was no significant difference in M.3 agenesis between the Maltese PDC sample and the published population prevalences (Table 6). The figure for lateral incisor agenesis for the control sample was significantly different from the PDC sample (P = 0.0324), but not for premolar hypodontia (P = 0.1246). A comparison of previous PDC data with the reference values showed that PDC in this sample was also associated with incisor agenesis, while the association with premolar agenesis was variable.


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  		Table 6 Proportion of congenitally missing teeth in different published samples of palatally displaced canines as compared with reference data.

 
Separation of the Maltese PDC sample into unilateral and bilateral subsamples and comparison of these samples gave interesting results (Table 7). The ratio of tooth agenesis in the bilateral sample was much higher than in the unilateral sample. This is not surprising, as one would expect the bilateral PDC subjects to have more complex problems. However, the ratios of Mn.P.2 and M.3 agenesis in the unilateral sample approached the reference values.


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  		Table 7 Comparison of congenitally missing teeth in unilateral and bilateral palatally displaced canine cases in the present study with reference values.

 
The data do not support the theory that PDC is specifically associated with M.3 agenesis. Rather, it points to an incisor/premolar/M.3 agenesis gradient, more pronounced in bilateral than in unilateral PDC cases, and even stronger in Mx.C.P1 cases. This supports previous work (Bjerklin et al., 1992Go; Pirinen et al., 1996Go; Baccetti, 1998Go; Arte et al., 2001Go) where a relationship was found between incisor/premolar hypodontia and PDC.

MSX1 mutations have been associated with facial clefting (Lidral et al., 1998Go; van den Boogaard et al., 2000Go) and also premolar/M.3 agenesis (Vastardis et al., 1996Go). However, no association has been shown with MSX1 mutations and incisor/premolar hypodontia (Lidral and Reising, 2002Go). Lidral and Reising (2002)Go and Arte et al. (2001)Go are of the opinion that, as one of the features of MSX1 hypodontia is multiple missing teeth, MSX1 and PAX9 mutations are unlikely to be the cause of incisor/premolar hypodontia, where one or two teeth are usually missing.

The evidence for an association of PDC with posterior orofacial genetic fields, as proposed by Peck et al. (2002)Go, seems weak. It seems unlikely that MSX1 or PAX9 would be candidate genes in the aetiology of PDC.

In all Mx.C.P1 studies where gender was reported (Shapira, 1980Go; Peck et al., 1993Go; Plunkett et al., 1998Go) a gender bias was evident, with the proportion of girls ranging from 60 to 80 per cent. The present sample showed a similarly high proportion of females (69 per cent). This finding cannot simply be explained by the increased ratio of females over males seeking orthodontic treatment and supports the view of Peck et al. (1993)Go that a degree of gender linkage seems to be present.

It is controversial whether the anlages develop in the transposed position or whether the tooth buds develop correctly and subsequently migrate to ectopic positions. The maxillary permanent canine starts to calcify at 1.5 years of age, between the roots of the first primary molar. As the jaws grow, the canine moves apically, away from the first primary molar. The first premolar then develops in the same site as the canine (Broadbent, 1941Go). As the jaws grow rapidly in depth and width, the teeth move to maintain their correct relationship to each other. As the maxilla grows, the first premolar moves distally relative to the canine, providing space for the canine to erupt. This involves precise co-ordination of the movement of the tooth germs in the growing maxilla. This movement is probably effected by osteoblast–osteoclast interaction, controlled by the dental follicle, as part of the eruption process. A deficiency in the cell signalling process of one tooth or more adjacent teeth, at an early stage, could well cause the tooth buds to move in the wrong direction (or fail to move), leading to transposition of the tooth germ.

The genes identified with the failure of eruption in experimental animals and humans are those associated with osteoclast/osteoblast function, such as cleidocranial dysostosis and osteopetrosis (Walker, 1975Go; Cooper et al., 2001Go), although tooth agenesis is not usually a feature.

It is possible that the gene or genes responsible for both PDC and Mx.C.P1 are those involved with the control of tooth eruption. These in turn seem to be linked with the gene or genes causing incisor/premolar hypodontia. The heterogenic nature of tooth agenesis has made it difficult to identify the culpable genes (Arte, 2001Go).


   Conclusion
Top
 Summary
 Introduction
 Subjects and method
 Results
 Discussion
 Conclusion
References
 
The weight of available evidence points to a genetic association between PDC and hypodontia. This association is even more marked in the case of Mx.C.P1. Family studies to establish the mode of heredity and the prevalence of other anomalies are indicated for the latter group. The difference in prevalence of hypodontia in cases of unilateral and bilateral PDC warrants further research.


   Acknowledgement
 
I would like to thank Professor A. Buhagiar, Department of Mathematics, University of Malta, for his help and advice with the statistics, Mr K. Mulligan, School Dental Clinic, Floriana, for contributing several Mx.C.P1 cases, and the general dental practitioners who referred Mx.C.P1 cases and co-operated enthusiastically in the compilation of the data.


   References
Top
 Summary
 Introduction
 Subjects and method
 Results
 Discussion
 Conclusion
 References
 

    Arte S 2001 Phenotypic and genotypic features of familial hypodontia. Thesis, University of Helsinki (http://www.ethesis.helsinki.fi)

    Arte S, Nieminen P, Apajalahti S, Haavikko K, Thesleff I, Pirinen S 2001 Characteristics of incisor–premolar hypodontia in families. Journal of Dental Research 80: 1445–1450[Abstract/Free Full Text]

    Baccetti T 1998 A controlled study of associated dental anomalies. Journal of Dental Research 68: 267–274

    Bjerklin K, Kurol J, Valentin J 1992 Ectopic eruption of maxillary first permanent molars and association with other tooth and developmental disturbances. European Journal of Orthodontics 14: 369–375[Abstract/Free Full Text]

    Bot P L, Salmon D 1977 Congenital defects of the upper lateral incisors (ULI): condition and measurements of the other teeth, measurements of the superior arch, head and face. American Journal of Physical Anthropology 46: 231–243[CrossRef][ISI][Medline]

    Bredy E, Erbring C, Hubenthal B 1991 The incidence of hypodontia with the presence and absence of wisdom teeth. Deutsche Zahn Mund Kieferheilkunde Mit Zentralblatt 79: 357–363 (in German)

    Broadbent B H 1941 Ontogenic development of occlusion. Angle Orthodontist 11: 223–241

    Burnett S E 1999 Prevalence of maxillary canine–first premolar transposition in a composite African sample. Angle Orthodontist 69: 187–189[ISI][Medline]

    Camilleri S 1995 The prevalence of impacted permanent canines in Maltese schoolchildren – a pilot study. Maltese Medical Journal 7: 42–45

    Cassar C 2000 A concise history of Malta. Mireva Publications, Msida

    Chattopadhyay A, Srinivas K 1996 Transposition of teeth and genetic etiology. Angle Orthodontist 66: 147–152[ISI][Medline]

    Chaushu S, Sharabi S, Becker A 2002 Dental morphologic characteristics of normal versus delayed developing dentitions with palatally displaced canines. American Journal of Orthodontics and Dentofacial Orthopedics 121: 339–346[CrossRef][ISI][Medline]

    Cooper S C, Flaitz C M, Johnston D A, Lee B, Hecht J T 2001 A natural history of cleidocranial dysplasia. American Journal of Medical Genetics 104: 1–6[CrossRef][ISI][Medline]

    Dayal P K, Shodhan K H, Dave C J 1983 Transposition of canine with traumatic etiology. Journal of the Indiana Dental Association 55: 283–285

    Feichtinger C, Rossiwall B, Wunderer H 1977 Canine transposition as autosomal recessive trait in an inbred kindred. Journal of Dental Research 56: 1449–1452[Abstract/Free Full Text]

    Grahnén H 1956 Hypodontia in the permanent dentition. Odontologisk Revy 7: 1–100

    Grover P S, Lorton L 1985 The incidence of unerupted permanent teeth and related clinical cases. Oral Surgery, Oral Medicine, Oral Pathology 59: 420–425[CrossRef][ISI][Medline]

    Joshi M R, Bhatt N A 1971 Canine transposition. Oral Surgery, Oral Medicine, Oral Pathology 31: 49–54[CrossRef][ISI][Medline]

    Laptook T, Silling G 1983 Canine transposition – approaches to treatment. Journal of the American Dental Association 107: 746–748[Abstract]

    Lidral A C, Reising B C 2002 The role of MSX1 in human tooth agenesis. Journal of Dental Research 81: 274–278[Abstract/Free Full Text]

    Lidral A C et al. 1998 Association of MSX1 and TGFB3 with nonsyndromic clefting in humans. American Journal of Human Genetics 63: 557–568[CrossRef][ISI][Medline]

    Mader C, Konzelman J L 1979 Transposition of teeth. Journal of the American Dental Association 98: 412–413[Abstract]

    Mossey P A, Campbell H M, Luffingham J K 1994 The palatal canine and the adjacent lateral incisor: a study of a west of Scotland population. British Journal of Orthodontics 21: 169–174[Abstract]

    Oliver R G, Mannion J E, Robinson J M 1989 Morphology of the maxillary lateral incisor in cases of unilateral impaction of the maxillary canine. British Journal of Orthodontics 16: 9–16[Abstract]

    Peck L, Peck S, Attia Y 1993 Maxillary canine–first premolar transposition, associated dental anomalies and genetic basis. Angle Orthodontist 63: 99–109[ISI][Medline]

    Peck S, Peck L, Kataja M 1994 The palatally displaced canine as a dental anomaly of genetic origin. Journal of Dental Research 64: 249–256

    Peck S, Peck L, Hirsh G 1997 Mandibular lateral incisor–canine transposition in monozygotic twins. ASDC Journal of Dentistry for Children 64: 409–413[Medline]

    Peck S, Peck L, Kataja M 2002 Concomitant occurrence of canine malposition and tooth agenesis: evidence of orofacial genetic fields. American Journal of Orthodontics and Dentofacial Orthopedics 122: 657–660[CrossRef][ISI][Medline]

    Pirinen S, Arte S, Apajalahti S 1996 Palatal displacement of canine is genetic and related to congenital absence of teeth. Journal of Dental Research 75: 1742–1746[Abstract/Free Full Text]

    Plunkett D J, Dysart P S, Kardos T B, Herbison G P 1998 A study of transposed canines in a sample of orthodontic patients. British Journal of Orthodontics 25: 203–208[Abstract]

    Ruprecht A, Sastry K A, Batniji S 1984 Transposition of teeth. Journal of the Canadian Dental Association 50: 308–309[Medline]

    Shah N 1994 Extraoral tooth eruption and transposition of teeth following trauma. Endodontics and Dentofacial Traumatology 10: 195–197

    Shah R M, Boyd M A, Vakil T F 1978 Studies of permanent tooth anomalies in 7,886 Canadian individuals. I: Impacted teeth. Journal of the Canadian Dental Association 44: 262–264[Medline]

    Shapira J, Chaushu S, Becker A 2000 Prevalence of tooth transposition, third molar agenesis, and maxillary canine impaction in individuals with Down syndrome. Angle Orthodontist 70: 290–296[ISI][Medline]

    Shapira Y 1980 Transposition of canines. Journal of the American Dental Association 100: 710–712[Abstract]

    Shapira Y, Kuftinec M M 2001 Maxillary tooth transpositions: characteristic features and accompanying dental anomalies. American Journal of Orthodontics and Dentofacial Orthopedics 119: 127–134[CrossRef][ISI][Medline]

    Shapira Y, Kuftinec M M, Stom D 1989 Maxillary canine–lateral incisor transposition – orthodontic management. American Journal of Orthodontics and Dentofacial Orthopedics 95: 439–444[CrossRef][ISI][Medline]

    Svinhufvud E, Myllarniemi S, Norio R 1988 Dominant inheritance of tooth malpositions and their association to hypodontia. Clinical Genetics 34: 373–381[ISI][Medline]

    van den Boogaard M J, Dorland M, Beemer F A, van Amstel H K 2000 MSX1 mutation is associated with orofacial clefting and tooth agenesis in humans. Nature Genetics 24: 342–343[CrossRef][ISI][Medline]

    Vastardis H, Karimbux N, Guthua S W, Seidman J G, Seidman C E 1996 A human MSX1 homeodomain missense mutation causes selective tooth agenesis. Nature Genetics 13: 417–421[CrossRef][ISI][Medline]

    Walker D G 1975 Bone resorption restored in osteopetrotic mice by transplants of normal bone marrow and spleen cells. Science 190: 784–785[Abstract/Free Full Text]

    Zilberman Y, Cohen B, Becker A 1990 Familial trends in palatal canines, anomalous lateral incisors, and related phenomena. European Journal of Orthodontics 12: 135–139[Abstract/Free Full Text]


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