We 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 this tooth develops late (as is usual with the peg lateral) or is congenitally absent, there is little or no guidance, and the chances of canine eruption disturbance are thus increased compared with the normal situation. Perhaps this depends on how much root has developed and how much downward movement of the canine has occurred. The canine could go in several directions—palatally, facially, horizontally, or mesially—into the lateral incisor location.
As we pointed out in our article with appropriate references, environmental changes produced by extracting deciduous teeth, distalizing molars, and expanding arches will encourage improvement in the eruption path of a good proportion of palatally displaced canines.
Dr Peck quoted from our article in which we studied the prevalence of anomalous and missing lateral incisors in a random population of schoolchildren and found that 7.1% were affected. He then compared this to one of our earlier articles in which we found 47.3% of anomalous and missing lateral incisors in a sample of children suffering from a displaced canine in the same geographic area. For a mechanical system, 47.3% represents a significant influence, compared with 7.1% in the random population. However, the 100% concordance in this situation which he demanded as proof of this line of argument is a blatantly illogical and spurious requirement.
Dr Peck claims total genetic control, yet he failed to ask himself how an overriding majority of impacted canine cases occur unilaterally, since the right and left sides of every person are genetically identical. Genetics doesn’t play games. If genetics is the whole answer, impacted canine cases would all be bilateral: that is where one must look for 100% concordance!
There can be no argument that genetics is the sole determinant that dictates late development and final root length of the lateral incisor root. To our knowledge, the more advanced development and eruptive progress of the canine in relation to those of the incisor have never been investigated. Specific genes have been identified for missing and anomalous teeth, but none has been isolated for impacted canines. The authors quoted by Dr Peck have each assumed that the long list of clearly genetic factors that are associated with an aberrant canine (missing, small, and peg-shaped lateral incisors, missing and small other teeth, distally tipped mandibular second premolars, infraoccluded deciduous molars, and other items outside the maxillary canine’s local surroundings) includes the canine itself as a genetically determined factor.
The genetic and guidance theories differ on only 1 critical question: Is the canine itself just 1 more genetic link in a totally genetic scenario, or is it a normal tooth whose eruptive behavior is influenced by the genetically altered environment (anomalous incisors) in which it finds itself?
We have sought to study the canine as a separate entity, apart from this scenario, and have tried to avoid ascribing to it exceptional properties and behavioral tendencies that are not characteristics of other teeth. It has been our view that the canine is like any other tooth and is the victim of circumstances that may divert its eruptive path. None of this contradicts the findings of the investigations referred to in Dr Peck’s letter. The “solid investigations” that Dr Peck quoted in relation to genetics are not at odds with our 1981 proposal of a causal relationship between lateral incisor anomaly and canine eruption disturbance. The findings are there for all to see, but their interpretation has been biased by the unproven or mistaken assumption that the missing or anomalous lateral incisor/ectopic canine scenario evolves from a single genetic unit. The guidance theory offers the reader an alternative way to interpret these same findings, which an experienced orthodontist will recognize from seeing these patients in his or her daily practice.
At the end of his letter, Dr Peck contradicted himself and finally admitted that “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.”
But, isn’t that precisely the message that our article conveyed?
We confess to having been deeply shocked by the tone and language that Dr Peck used in his letter decrying the publication of our article. In response, we can only apologize for having had the chutzpah to offer a reasoned alternative hypothesis, which seems to have rattled his belief system!