Postretention relapse of mandibular anterior crowding

Or is it a combination of all the above?

The literature is filled with quality research studies attempting to discover answers to why relapse occurs, and despite decades of research, lower anterior crowding is still unpredictable (Freitas, K., Freitas, M., Henriques, J., Pinzan, A., & Janson, G., 2004). “The degree of post-retention anterior crowding is both unpredictable and variable and no pre-treatment variables either from clinical findings, casts, or cephalometric radiographs before or after treatment seem to be useful predictors” (Little, 1999, p.191).

For many years, the implication has been that nonextraction orthodontic cases might result in a higher percentage of postretention lower anterior crowding compared to extraction cases, but do they? Review of the literature regarding the effects that third molars have on lower anterior crowding presents both agreement and opposition for both sides of the problem, but the bulk of the evidence seems to indicate that third molars play an insignificant role in lower anterior crowding.

Parallel studies often show dissimilar deductions, and, more than likely, the problem is multifactorial. Bramante (1990) noted that in the 1930s Dr. Charles Tweed redirected orthodontic treatment procedures to extraction therapy with the removal of four first premolars as a more disciplined approach to effective orthodontic treatment. He added: “Fifty years later, we have found that extraction treatment and uprighting lower incisors does not prevent long-term post-retention crowding and that flattened profiles are not always esthetically desirable” (p. 91).

Form and function certainly underlie growth and development in the craniofacial skeleton and the role that the biological environment plays. According to Carlson (1999), the “form-function” principle of craniofacial biology in general was attractive but primarily to account for the factors that may have influenced broad morphological variation and change associated with the evolution of the whole complex. Carlson added that the form-function principal is much less effective in explaining variations of craniofacial form, growth and treatment outcomes associated with causes of skeletal discrepancies and malocclusion.

So where does the discussion of lower incisor crowding end? Is the problem multifactorial, a product of improper orthodontic treatment modalities (or techniques), form vs. function, or does genetics play a large part in creating or solving the problem?

We can go on and on discussing virtues of the many possibilities and causative factors involved with post-retention relapse of lower incisor crowding, but here we are in the 21st century and cannot provide an absolute answer to the riddle of postreatment stability. It is still an important objective but also still a scar of orthodontics.

Answers may never be absolutely identified, which, of course, begs consideration for some form of indefinite retention in almost all cases. However, we shouldn’t feel totally alone with regard to our knowledge (or lack of knowledge) for an absolute answer to why relapse of postretention tooth movement occurs because, according to our medical colleagues at the Mayo Clinic (n.d.), even after years of research, physicians still have no cure for the common cold either.

Note: This article was published in Ortho Tribune U.S. Edition, Vol. 8 Nos. 3/4, AAO Review 2013. A complete list of references is available from the publisher.