Spatial matrix hypothesis

Sir, I read with some interest the recent articles on the aetiology and management of TMD (BDJ 2007; 202: E2 and E3). As mentioned previously,¹ I understand that malocclusions and TMD are most commonly encountered in modern societies, most likely in association with changes in environmental conditions, such as feeding behaviour inter alia. The foundations for malocclusions and TMD might begin at birth, as modern mothers are less likely to breastfeed a child. Similarly, other environmental/behavioural changes, such as pacifier-use or bottle-feeding during infancy, might predispose to, or be associated with, malocclusions and TMD in later life.

In terms of cause and effect, there is little doubt that genetic susceptibility is involved in a child's development of a malocclusion and perhaps TMD. Moreover, a cranio-caudal gradient of ontogeny means that an altered maxilla will have concomitant effects on the developing mandible, and these midfacial disparities may have primacy over dento-occlusal parameters that dental professionals tend to focus on. In order to explain these associated phenomena I developed the spatial matrix hypothesis.² The crowns of teeth are unique in the human body because once fully developed there is no innate developmental mechanism by which they can change their size or shape. They can, however, change their spatial position/orientation secondary to other tissues that are capable of: remodelling, such as bone; hypertrophy/atrophy, such as muscle; or regeneration, such as epithelia. Using this idea as a premise, it is likely that an underdeveloped midface presenting with palatal insufficiency (due to gene-environmental interactions) could be associated with malocclusions, TMD and may simultaneously predispose to upper airway obstruction. I am currently investigating 3D airway changes to establish this association, and the preliminary findings suggest that a relationship may exist between TMD and upper airway morphology.³ Dr Luther's contentions on sleep (nocturnal) bruxism interface with my own hypothesis at this juncture; a lack of functional space (to breathe at night) might set off a chronic anxiety response that manifests with the TMD-patient grinding the teeth in an ineffectual, subconscious attempt to alleviate the airway. Indeed, I surmise that the existence of wear facets on deciduous or permanent teeth is indicative of latent airway issues, although currently there is a dearth of evidence for this notion. However, according to the spatial matrix hypothesis, in the presence of developmental compensation, retraction/extraction procedures during orthodontic treatment or inappropriate 'prophylactic' occlusal equilibration protocols may exacerbate a precarious state of developmental stability.⁴ Perversely, in order to re-establish or attain craniofacial homeostasis, special attention must first be given to non-mandibular constraints prior to addressing the signs and symptoms of TMD.