Sir, I found the editorial in the recent-most issue of the BDJ1 rather intriguing. The notion that an universal theory does not exist to explain orthodontic tooth movement might be somewhat deficient. The pressure-tension theory was promulgated by Oppenhiem2 as first proposed by Sandstedt.3 This unsophisticated notion was substantially challenged by Moss4 (following van der Klaauw5) who described the Functional Matrix Hypothesis.6,7,8,9 More recently, Singh10 described the Spatial Matrix Hypothesis,11 which was presented at the 11th International Facial Orthotropics Symposium in Tokyo, Japan, in November, 2007. If I'm not mistaken, the Spatial Matrix Hypothesis10,11 first proposed that gene-environmental interactions are associated with the formation of malocclusion.12 Thus, growth mechanisms and not growth outcome are inherited. Therefore, the notion that '...the body of the mandible, the length of which is under tight genetic control...' is ostensibly erroneous. For example, many data have shown that adults who wear a mandibular advancement device for the amelioration of obstructive sleep apnoea show a tendency for renewed mandibular growth, sometimes resulting in a Class III malocclusion and skeletal relationship. It is also too simplistic to say that 'families sharing the same diet, environment and genes are likely to be affected in the same way'. For example, in genetically-identical mice, maternal methyl donor supplementation produces offspring with different coat-colour, and different rates of obesity, diabetes and cancer.13 In addition, it is known that human identical twins do not show a 100% correlation in terms of clinical expression of a specific condition.

Nevertheless, the notion that 'Orthotropics believes that teeth have the ability to align themselves if the face grows well' is a welcomed acknowledgement of the well-documented phenomenon of temporo-spatial patterning.14 In terms of challenging 'the orthodontic profession to a debate to test the hypothesis that malocclusion is caused by the environment and modified by the genes', I fear that confrontation might be less productive than collaborative research. First, it might be agreed that the definition of malocclusion is outdated.12 Second, malocclusions, such as anterior open bite, vertical maxillary excess ('gummy smile'), posterior open bite and unilateral posterior open bite etc were not included in Angle's classification. Why not? It is likely that these outcomes were not commonly-observed at the time when Angle's classification was formulated. However, continued genetic variance has increased since then, as the effects of canalisation (buffering) have been modulated. In one study,15 we found that about 25% of children in a specific sub-population had an anterior open bite by the age of five years. To this end, working with an orthodontist, in a new publication entitled Epigenetic orthodontics in adults,16 I looked at both the theory of orthodontic tooth movement and the clinical outcomes in terms of facial, upper arch, lower arch and upper airway changes. Perhaps the most valuable insight is the notion that, despite canalisation, sutural homeostasis is the key to explaining both malocclusion and its clinical correction, with an enhanced level of craniofacial homeostasis.