Neural factors influence post-natal growth, development, and aging throughout the body. This influence may be mediated through sensory or motor effects interacting with endocrine and immunological factors. Growth effects may be expressed directly by sensory or motor nerves on the tissue or indirectly by motor function. Direct neurotrophic effects have been well-documented in the development of striated muscle, the taste bud, and the amphibian limb. Evidence for a trigeminal neurotrophic effect on tooth development and facial development is lacking. Growth disturbances of the jaws consequent to lesioning of the trigeminal nerve are due most likely to functional disturbances rather than neurotrophism. Examples of function impact on orofacial growth are abundant. Oral and facial target tissues, like those elsewhere in the body, determine the nature of the target tissue innervation and its central organization. Central effects consequent to tooth loss or dental pulp entirpation are well-documented. Inflammation and pain may exert growth effects through release of "wound hormones" or secondarily to somatic and autonomic effects. There is evidence that vasoactive intestinal peptide (VIP) and calcitonin gene-related peptide (CGRP) elaborated from sympathetic and parasympathetic neurons may have a modulatory role in growth.
While the effects of longstanding motor pathologies on skeletal growth are well-known, concomitant sensory deficits and soft tissue disturbances have not been examined. However, the pathological models beg the question of normal regulation. While muscle develops in the absence of innervation, neurotrophic effects are clearly identified. Little is known about the interaction of simple and complex motor behavior on growth.
Regulation of growth is frequently visualized within a form-function paradigm. For example, anterior open bites have been seen as the consequence of tongue thrusting or tongue thrusting as a consequence of open bites. Low tonic forces in posture are thought to be more important in the development of both the face and the dental alveolar complex than the higher intermittent forces in mastication and swallowing. The need for an active (reflex) contribution to growth at the TMJ is in dispute. The specific chemical regulators of bone cartilage and soft tissue growth identified elsewhere in the body probably act in a similar fashion in orofacial development. The lack of chemical regulators common to both lists of growth factors and putative and demonstrated neural transmitters suggests that most post-natal growth regulation is secondary to function.
Short- and long-term strategies are offered to address questions suitable for immediate and future investigation.
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