amount of genetic variance increased, producing ‘new’ types of malocclusions that are modulated by environmental influences in the new, urbanized condition. Thus, anterior open-bite, unilateral poste-rior open-bite, vertical maxillary excess (‘gummy smile’), etc. may be regarded as relatively ‘new’ develop-mental compensations produced by genetic variance and environmental interactions. In addition, however, there is no doubt that there is a certain genetic susceptibility to developing a malocclusion, as genes that encode for skeletal, muscular and dental tissues have been identi-fied and sequenced. The famous Hapsburg’s jaw is one example of this familial tendency for the devel-opment of a malocclusion. Familial hypodontia (oligodontia) is another example. Therefore, bone remodel-ing should be an integral part of treatment planning prior to the deployment of aligners. Generally speaking, a cranio-caudal gradient of development exists in the human embryo i.e. structures in the head region appear first and undergo development prior to those located further distally. Thus, an altered maxilla, due to temporo-spatial patterning and gene-environmental interac-tions, has concomitant effects on the developing mandible; and these effects can sometimes be clearly seen in children who manifest a malocclusion as part of a craniofa-cial syndrome. In order to explain these associated phenomena the Spatial Matrix Hypothesis 15 was developed using the Functional Matrix hypothesis as a starting point, which according to Moss 19 was first formulated by van der Klaauw. 20 As noted above, the crowns of teeth are unique in the human body because once fully developed there is no innate devel-opmental mechanism by which they can change their size or shape unless subjected to interproximal reduction or slenderizing. They can, however, change their spatial posi-tion/orientation secondary to other tissues that are capable of: remodel-ing, such as bone; hypertrophy/atrophy, such as 20 November/December 2010 JAOS muscle; or regeneration, such as epithelia and the periodontium. Using this concept as a premise, it is likely that an underdeveloped midface presenting with palatal insufficiency (due to gene-environ-mental interactions) could be asso-ciated with malocclusions, and may simultaneously predispose to temporo-mandibular joint dysfunc-tion (TMD) and upper airway compromise, such as obstructive sleep apnea (OSA). Indeed, prelimi-nary findings 21 suggest that a rela-tionship may exist between TMD and upper airway morphology, as well as OSA and (nocturnal) brux-ism. These findings interface well with the Spatial Matrix Hypothesis; a lack of functional space (to breathe at night) might set off an orthodontic treatment or inappro-priate ‘prophylactic’ occlusal equili-bration protocols may exacerbate a precarious state of developmental stability 23 . Thus, in order to re-establish or enhance craniofacial homeostasis, special attention must be given to non-mandibular constraints in patients who present with a retrusive mandible, OSA or TMD. In other words, the cran-iomaxillary structures might need to be more thoroughly assessed before planning the final positions of the crowns of teeth. Form and Function The concept that ‘Form follows Function’ is replete in the medical and dental literature. If that premise is true then, conversely, the notion that ‘Deformity follows Dysfunc-tion’ is also true. It has been suggested that functional appliances somehow alter function, yet there is a dearth of evidence to support this notion. Nevertheless, it is likely that functional alterations occur secon-darily to the implementation of functional appliances, and the primary mode of correction may reside elsewhere in the craniofacial system. For example, when a func-tional appliance is used to re-posi-tion a retrusive mandible, there is a functional change in the upper airway. This mandibular advance-ment usually changes/improves the caliber of the upper airway and thereby improves airway function, according to Poiseuille’s equation -but the mechanism of correction of the malocclusion is not dependent upon the change in airway function. It was thought that by changing the position of the mandible, muscles or soft tissues were stretched, and that this stretch produces forces that somehow correct the malocclusion. This is but partly true 7 . Recent evidence 24 suggests that by changing the spatial relations of the mandible, a change in the pattern of gene expression is induced. This finding provides scientific evidence for the pertinence of the Spatial Matrix Hypothesis. Put simply, a change in jaw relations provides the impetus for a skeletal (foundational) correction, which is one component “Recent evidence suggests that by changing the spatial relations of the mandible, a change in the pattern of gene expression is induced.” anxiety response that manifests with a patient grinding the teeth in an ineffectual, subconscious attempt to alleviate the airway. Indeed, it can be surmised that the existence of wear facets on perma-nent or deciduous teeth is indica-tive of latent airway issues. Although currently there is a dearth of evidence for this notion, prelimi-nary findings support the above contention that midfacial develop-ment is associated with airway improvements in adults 22 . However, according to the Spatial Matrix Hypothesis, in the presence of developmental compensation, retraction/extraction and IPR/slen-derizing procedures during
Journal of the American Orthodontic Society November-December 2010: Page 20
