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Misleading article on palatally displaced canines
READERS' FORUM
Letters to the editor* Misleading article on palatally displaced canines
F
or a while, I was reluctant to submit a letter challenging another of Dr Adrian Becker's attempts to restore some dignity to the embattled “guidance theory,” his personal view on how maxillary canines become displaced in the palate (Becker A., Chaushu S. Etiology of maxillary canine impaction: a review. Am J Orthod Dentofacial Orthop 2015;148:557-67). I reasoned that there have been so many solid investigations with results that counter Becker's 1981 proposal of a causal relationship between maxillary lateral incisor root structure and subsequent palatal displacement of the adjacent canine that surely few readers would take him seriously on this in 2015. But in the guise of an impartial “review,” Dr Becker presented much the same confusing, emotionladen defense of his pet theory that he has done earlier.1-3 We clinicians and readers deserve better. As is often the case in ungrounded theorizing, the article's construction tends to be somewhat incomprehensible logically or confounding, to say the least. By the third sentence of the Abstract, the authors rhapsodized anthropomorphically about “the abnormal milieu in which the canine is reared,” as if the tooth were in an orphanage. Nomenclature is surprisingly abused in this article. By using the broad mechanical term “impaction” in their title and text, Becker and Chaushu carelessly conflate all maxillary canine malpositions, including labial and palatal displacements. They know better, since they have separated these 2 distinct phenotypes in previous articles. Furthermore, why would the authors use the blanket term “impaction” when the guidance theory they are focused on concerns only canines that are displaced palatally? In their so-called review, they showed examples of several dental rarities (odontoma, enlarged follicle, and infected deciduous canine) that frankly do not belong in a specific discussion of the palatally displaced canine (PDC), an anomaly that orthodontists experience regularly in practice. They seemingly use these odd and rare cases to bait the clinician into believing that a PDC is usually caused by local conditions, thus keeping their guidance theory alive. Dr Becker still needs to come to grips with the hard evidence against his shaky mechanical guidance * The viewpoints expressed are solely those of the author(s) and do not reflect those of the editor(s), publisher(s), or Association.
hypothesis. There are some facts that he has simply not absorbed. In a critical analysis of the guidancetheory model published in 1995, the striking lack of concordance of essential conditions was noted in the following paragraph:4 Frequency of trait expression is a parameter that Becker and his group studying PDC have failed to reconcile. They found anomalous maxillary lateral incisors in less than half of the individuals with the PDC anomaly.5 Furthermore, less than 10% of maxillary quadrants with absent or pegged reduction of the lateral incisor were found to have a PDC anomaly.5 Were these anomalies interrelated mechanically in a cause-and-effect manner—such as control of the expression of the PDC trait through canine misguidance from an anomalous lateral incisor—close to 100% concordance in both directions would be expected. In other words, within the “guidance” model of causality nearly all individuals with PDC would be expected to have a missing or severely reduced adjacent lateral incisor and vice versa.
Sacerdoti and Baccetti6 found similarly dismal concordances. How can Becker reconcile his theory built on mechanical reactions between 2 contiguous teeth, if in most cases there is no quadrant concordance in the presence or absence of anomalous lateral incisor and anomalous canine? Moreover, how can Dr Becker continue to ignore the plethora of recent reports—most of which are not cited in his review—of significant associations of PDC and concomitant dental anomalies outside the maxillary canine's local surroundings?6-13 Simultaneous occurrences of molar and premolar agenesis, deciduous molar infraocclusion, distally displaced mandibular second premolars, delay in dental eruption, and generalized tooth-size reductions are hardly explainable by a lateral incisor-canine guidance theory. Family studies in the Czech Republic, Finland, and Malta have shown unquestionable evidence of classical genetic transmission of the PDC anomaly.13-15 A family study in Israel, which Dr Becker coauthored, also demonstrated that the PDC trait was clearly heritable, but for some reason it stopped short of acknowledging genetic mechanisms.16 It's time to move on. PDC and associated patterns of dental abnormalities should continue to be studied vigorously. However, we should not be narrowly and rigidly limited by a quaint mechanical “theory” based on mid20th-century ideas. The best current knowledge points 149
150
Readers' forum
to a biologic, familial predilection of some people for PDC originating from a likely combination of genetic, epigenetic, and environmental influences. Although conjecture about lateral-incisor control of canine position is now properly fading, the concept has served as a valuable stepping-stone on the pathway to better understanding of biologic relationships among dental anomalies. As Claude Bernard, the 19th-century founder of experimental medicine, once wrote, “Even mistaken hypotheses and theories are of use in leading to discoveries.” Sheldon Peck Boston, Mass Am J Orthod Dentofacial Orthop 2016;149:149-150 0889-5406/$36.00 Copyright Ó 2016 by the American Association of Orthodontists.
http://dx.doi.org/10.1016/j.ajodo.2015.11.016 REFERENCES 1. Becker A. Etiology of maxillary canine impactions. Am J Orthod 1984;86:437–8. 2. Becker A. In defense of the guidance theory of palatal canine displacement. Angle Orthod 1995;65:95–8. 3. Becker A, Gillis I, Shpack N. The etiology of palatal displacement of maxillary canines. Clin Orthod Res 1999;2:62–6. 4. Peck S, Peck L, Kataja M. Sense and nonsense regarding palatal canines. Angle Orthod 1995;65:99–102. 5. 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;8:12–6. 6. Sacerdoti R, Baccetti T. Dentoskeletal features associated with unilateral or bilateral palatal displacement of maxillary canines. Angle Orthod 2004;74:725–32. 7. Langberg BJ, Peck S. Tooth-size reduction associated with occurrence of palatal displacement of canines. Angle Orthod 2000;70: 126–8. 8. Peck S, Peck L, Kataja M. Concomitant occurrence of canine malposition and tooth agenesis: evidence of orofacial genetic fields. Am J Orthod Dentofacial Orthop 2002;122:657–60. 9. Shalish M, Chaushu S, Wasserstein A. Malposition of unerupted mandibular second premolar in children with palatally displaced canines. Angle Orthod 2009;79:796–9. 10. Shalish M, Peck S, Wasserstein A, Peck L. Increased occurrence of dental anomalies associated with infraocclusion of deciduous molars. Angle Orthod 2010;80:440–5. 11. Garib DG, Peck S, Gomes SC. Increased occurrence of dental anomalies associated with second-premolar agenesis. Angle Orthod 2009;79:436–41. 12. Baccetti T, Leonardi M, Giuntini V. Distally displaced premolars: a dental anomaly associated with palatally displaced canines. Am J Orthod Dentofacial Orthop 2010;138:318–22. 13. Bartolo A, Calleja N, McDonald F, Camilleri S. Dental anomalies in first-degree relatives of transposed canine probands. Int J Oral Sci 2015;7:169–73. 14. Racek J, Sottner L. Our views on the heredity of retention of canines. Sborn Lek 1984;86:355–60. 15. Pirinen S, Arte S, Apajalahti S. Palatal displacement of canine is genetic and related to congenital absence of teeth. J Dent Res 1996; 75:1346–52.
February 2016 Vol 149 Issue 2
16. Zilberman Y, Cohen B, Becker A. Familial trends in palatal canines, anomalous lateral incisors, and related phenomena. Eur J Orthod 1990;12:135–9.
Authors' response
W
e believe that it possible to argue a case objectively, without the need to descend to disparaging, gratuitous, and ad hominem remarks regarding different views held by another person. We further believe that this may be achieved in a professional manner that is appropriate to a journal of the repute accorded to the AJO-DO. With the notable exception of your esteemed correspondent, few will argue that there is no single, exclusive, across-the-board, all-encompassing, infallible cause for eruption disturbance of the maxillary permanent canine. There is no question that genetics plays a part in the etiology of this phenomenon in most patients, and nowhere in our article do we say otherwise. On the contrary, a careful reading of our text will show how we stated categorically that, in many instances, genetics is almost certainly the direct cause. We can only assume that your respected correspondent, in his obvious hurry to write the letter (at the time of writing, we have not received the October issue of the Journal), has not read the article attentively. The aim of our article was to classify the known etiologic factors concerned with canine displacement into 4 groups, which include local hard tissue impediments (supernumerary teeth, odontomes), soft tissue pathologic lesions (granulomas associated with carious deciduous canines, enlarged dental follicles/dentigerous cysts, and so on), absence of guidance (late-developing anomalous lateral incisors), and genetic factors (primary displacement of the tooth bud, abnormal long-axis orientation). In some cases, the etiology can belong to more than one of these groups; in others, the etiology may remain obscure. Despite his claims to the contrary, we doubt whether Dr Peck would deny that a suitably located supernumerary tooth or odontome, however rare, will cause canine impaction, and similarly, that a relatively common granuloma at the apex of a nonvital deciduous tooth or an enlarged dental follicle of the canine could do the same. These have nothing to do with genetics or the guidance theory; yet they are etiologic factors and are therefore included in our review. Guidance for the developing canine derived from the distal aspect of the root of the lateral incisor is indeed a mechanical factor, which in our view depends on timely and normal growth of the root of the lateral incisor. If
American Journal of Orthodontics and Dentofacial Orthopedics
Letters to the editor* Misleading article on palatally displaced canines
F
or a while, I was reluctant to submit a letter challenging another of Dr Adrian Becker's attempts to restore some dignity to the embattled “guidance theory,” his personal view on how maxillary canines become displaced in the palate (Becker A., Chaushu S. Etiology of maxillary canine impaction: a review. Am J Orthod Dentofacial Orthop 2015;148:557-67). I reasoned that there have been so many solid investigations with results that counter Becker's 1981 proposal of a causal relationship between maxillary lateral incisor root structure and subsequent palatal displacement of the adjacent canine that surely few readers would take him seriously on this in 2015. But in the guise of an impartial “review,” Dr Becker presented much the same confusing, emotionladen defense of his pet theory that he has done earlier.1-3 We clinicians and readers deserve better. As is often the case in ungrounded theorizing, the article's construction tends to be somewhat incomprehensible logically or confounding, to say the least. By the third sentence of the Abstract, the authors rhapsodized anthropomorphically about “the abnormal milieu in which the canine is reared,” as if the tooth were in an orphanage. Nomenclature is surprisingly abused in this article. By using the broad mechanical term “impaction” in their title and text, Becker and Chaushu carelessly conflate all maxillary canine malpositions, including labial and palatal displacements. They know better, since they have separated these 2 distinct phenotypes in previous articles. Furthermore, why would the authors use the blanket term “impaction” when the guidance theory they are focused on concerns only canines that are displaced palatally? In their so-called review, they showed examples of several dental rarities (odontoma, enlarged follicle, and infected deciduous canine) that frankly do not belong in a specific discussion of the palatally displaced canine (PDC), an anomaly that orthodontists experience regularly in practice. They seemingly use these odd and rare cases to bait the clinician into believing that a PDC is usually caused by local conditions, thus keeping their guidance theory alive. Dr Becker still needs to come to grips with the hard evidence against his shaky mechanical guidance * The viewpoints expressed are solely those of the author(s) and do not reflect those of the editor(s), publisher(s), or Association.
hypothesis. There are some facts that he has simply not absorbed. In a critical analysis of the guidancetheory model published in 1995, the striking lack of concordance of essential conditions was noted in the following paragraph:4 Frequency of trait expression is a parameter that Becker and his group studying PDC have failed to reconcile. They found anomalous maxillary lateral incisors in less than half of the individuals with the PDC anomaly.5 Furthermore, less than 10% of maxillary quadrants with absent or pegged reduction of the lateral incisor were found to have a PDC anomaly.5 Were these anomalies interrelated mechanically in a cause-and-effect manner—such as control of the expression of the PDC trait through canine misguidance from an anomalous lateral incisor—close to 100% concordance in both directions would be expected. In other words, within the “guidance” model of causality nearly all individuals with PDC would be expected to have a missing or severely reduced adjacent lateral incisor and vice versa.
Sacerdoti and Baccetti6 found similarly dismal concordances. How can Becker reconcile his theory built on mechanical reactions between 2 contiguous teeth, if in most cases there is no quadrant concordance in the presence or absence of anomalous lateral incisor and anomalous canine? Moreover, how can Dr Becker continue to ignore the plethora of recent reports—most of which are not cited in his review—of significant associations of PDC and concomitant dental anomalies outside the maxillary canine's local surroundings?6-13 Simultaneous occurrences of molar and premolar agenesis, deciduous molar infraocclusion, distally displaced mandibular second premolars, delay in dental eruption, and generalized tooth-size reductions are hardly explainable by a lateral incisor-canine guidance theory. Family studies in the Czech Republic, Finland, and Malta have shown unquestionable evidence of classical genetic transmission of the PDC anomaly.13-15 A family study in Israel, which Dr Becker coauthored, also demonstrated that the PDC trait was clearly heritable, but for some reason it stopped short of acknowledging genetic mechanisms.16 It's time to move on. PDC and associated patterns of dental abnormalities should continue to be studied vigorously. However, we should not be narrowly and rigidly limited by a quaint mechanical “theory” based on mid20th-century ideas. The best current knowledge points 149
150
Readers' forum
to a biologic, familial predilection of some people for PDC originating from a likely combination of genetic, epigenetic, and environmental influences. Although conjecture about lateral-incisor control of canine position is now properly fading, the concept has served as a valuable stepping-stone on the pathway to better understanding of biologic relationships among dental anomalies. As Claude Bernard, the 19th-century founder of experimental medicine, once wrote, “Even mistaken hypotheses and theories are of use in leading to discoveries.” Sheldon Peck Boston, Mass Am J Orthod Dentofacial Orthop 2016;149:149-150 0889-5406/$36.00 Copyright Ó 2016 by the American Association of Orthodontists.
http://dx.doi.org/10.1016/j.ajodo.2015.11.016 REFERENCES 1. Becker A. Etiology of maxillary canine impactions. Am J Orthod 1984;86:437–8. 2. Becker A. In defense of the guidance theory of palatal canine displacement. Angle Orthod 1995;65:95–8. 3. Becker A, Gillis I, Shpack N. The etiology of palatal displacement of maxillary canines. Clin Orthod Res 1999;2:62–6. 4. Peck S, Peck L, Kataja M. Sense and nonsense regarding palatal canines. Angle Orthod 1995;65:99–102. 5. 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;8:12–6. 6. Sacerdoti R, Baccetti T. Dentoskeletal features associated with unilateral or bilateral palatal displacement of maxillary canines. Angle Orthod 2004;74:725–32. 7. Langberg BJ, Peck S. Tooth-size reduction associated with occurrence of palatal displacement of canines. Angle Orthod 2000;70: 126–8. 8. Peck S, Peck L, Kataja M. Concomitant occurrence of canine malposition and tooth agenesis: evidence of orofacial genetic fields. Am J Orthod Dentofacial Orthop 2002;122:657–60. 9. Shalish M, Chaushu S, Wasserstein A. Malposition of unerupted mandibular second premolar in children with palatally displaced canines. Angle Orthod 2009;79:796–9. 10. Shalish M, Peck S, Wasserstein A, Peck L. Increased occurrence of dental anomalies associated with infraocclusion of deciduous molars. Angle Orthod 2010;80:440–5. 11. Garib DG, Peck S, Gomes SC. Increased occurrence of dental anomalies associated with second-premolar agenesis. Angle Orthod 2009;79:436–41. 12. Baccetti T, Leonardi M, Giuntini V. Distally displaced premolars: a dental anomaly associated with palatally displaced canines. Am J Orthod Dentofacial Orthop 2010;138:318–22. 13. Bartolo A, Calleja N, McDonald F, Camilleri S. Dental anomalies in first-degree relatives of transposed canine probands. Int J Oral Sci 2015;7:169–73. 14. Racek J, Sottner L. Our views on the heredity of retention of canines. Sborn Lek 1984;86:355–60. 15. Pirinen S, Arte S, Apajalahti S. Palatal displacement of canine is genetic and related to congenital absence of teeth. J Dent Res 1996; 75:1346–52.
February 2016 Vol 149 Issue 2
16. Zilberman Y, Cohen B, Becker A. Familial trends in palatal canines, anomalous lateral incisors, and related phenomena. Eur J Orthod 1990;12:135–9.
Authors' response
W
e believe that it possible to argue a case objectively, without the need to descend to disparaging, gratuitous, and ad hominem remarks regarding different views held by another person. We further believe that this may be achieved in a professional manner that is appropriate to a journal of the repute accorded to the AJO-DO. With the notable exception of your esteemed correspondent, few will argue that there is no single, exclusive, across-the-board, all-encompassing, infallible cause for eruption disturbance of the maxillary permanent canine. There is no question that genetics plays a part in the etiology of this phenomenon in most patients, and nowhere in our article do we say otherwise. On the contrary, a careful reading of our text will show how we stated categorically that, in many instances, genetics is almost certainly the direct cause. We can only assume that your respected correspondent, in his obvious hurry to write the letter (at the time of writing, we have not received the October issue of the Journal), has not read the article attentively. The aim of our article was to classify the known etiologic factors concerned with canine displacement into 4 groups, which include local hard tissue impediments (supernumerary teeth, odontomes), soft tissue pathologic lesions (granulomas associated with carious deciduous canines, enlarged dental follicles/dentigerous cysts, and so on), absence of guidance (late-developing anomalous lateral incisors), and genetic factors (primary displacement of the tooth bud, abnormal long-axis orientation). In some cases, the etiology can belong to more than one of these groups; in others, the etiology may remain obscure. Despite his claims to the contrary, we doubt whether Dr Peck would deny that a suitably located supernumerary tooth or odontome, however rare, will cause canine impaction, and similarly, that a relatively common granuloma at the apex of a nonvital deciduous tooth or an enlarged dental follicle of the canine could do the same. These have nothing to do with genetics or the guidance theory; yet they are etiologic factors and are therefore included in our review. Guidance for the developing canine derived from the distal aspect of the root of the lateral incisor is indeed a mechanical factor, which in our view depends on timely and normal growth of the root of the lateral incisor. If
American Journal of Orthodontics and Dentofacial Orthopedics