For 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, emotion-laden defense of his pet theory that he has done earlier. 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 hypothesis. There are some facts that he has simply not absorbed. In a critical analysis of the guidance-theory model published in 1995, the striking lack of concordance of essential conditions was noted in the following paragraph:
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. Furthermore, less than 10% of maxillary quadrants with absent or pegged reduction of the lateral incisor were found to have a PDC anomaly. 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 Baccetti 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? 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. 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.
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 mid-20th-century ideas. The best current knowledge points 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.”