Biological Foundations of Orthodontics and Dentofacial Orthopaedics

Lecture 1: Molecular genetics of craniofacial development

Over the past twenty years craniofacial biology has been revolutionized by major developments in our understanding of the cellular, molecular and genetic mechanisms underlying embryonic development. Many of these advances have been based on animal models, most notably the fruitfly Drosophila, the chick and the mouse. Since these developmental processes have been highly conserved during evolution, this information is relevant not only to understanding normal human development, but also to understanding how genetic mutations produce particular malformations or inherited diseases. This lecture highlights some of these developments regarding the more common craniofacial deformities, and in a form accessible to clinicians with an interest in the head and neck.

Lecture 2: Remodelling the dentofacial skeleton

Orthodontic tooth movement is dependent upon the remodelling (deposition and resorption) of the periodontal ligament (PDL) and alveolar bone by mechanical means. Facial sutures are also fibrous articulations and by remodelling these joints, one can alter the positional relationships of the dentomaxillary complex. As might be expected from the structure and function of the temporomandibular joints these articulations are more resistant to remodelling activity and whether functional mandibular displacement can alter the growth of the condyle remains controversial. Clinical investigations of the effects of the Andresen activator and its variants on dentofacial growth suggest the changes are essentially dentoalveolar. However, with the popularity of active functional appliances such as the Herbst and twin-block based on ‘jumping the bite’, attention has focused on how they might achieve dentofacial change. Animal experimentation enables informed decisions to be made regarding the effects of treatment on the dentofacial skeleton at the tissue, cellular and molecular levels. This lecture discusses the evidence from rat and monkey experimental models and the conclusions that can be drawn from such experimentation to understand what can be achieved clinically.

Lecture 3: Evolving concepts of orthodontic tooth movement

After 100 years of experimentation we have a reasonably good understanding of the sequence of events involved in remodelling the PDL during orthodontic tooth movement at the tissue, cellular and molecular levels; in this lecture a new experimental model for applying compressive mechanical strain to human PDL cells in vitro will be presented. The mechanobiology of the supporting alveolar bone, however, remains poorly understood. It has been an article of faith based on Wolff’s law dating back to Edward Angle, that orthodontic appliances have a positive effect on bone mass. New evidence from an in vivo rat model suggests the contrary and that an orthodontic appliance produces stress-shielding of the inter-radicular bone, leading to osteopenia similar to that associated with prolonged bed rest and spaceflight, or the implantation of any rigid metallic device into bone. These observations are also consistent with the findings of experimental masticatory hypofunction in rats, showing that reduced occlusal loading leads to a reduction in alveolar bone mass and bone mineral density

Lecture 4: Orthodontic randomized clinical trials: the complex issues involved in evaluating treatment outcome

The prospective randomized clinical trial (RCT) is seen by many to be the ‘gold standard’ for analyzing treatment outcome and the only valid source of clinical data. In orthodontics, most RCTs have been designed to resolve the controversy surrounding the ability of functional appliances to significantly modify dentofacial growth. However, the issues involved in analyzing treatment outcome are complex and include: variability in the timing, magnitude and duration of pubertal dentofacial growth, differing levels of motivation and patient compliance, the inherent inaccuracy of cephalometry and the questionable validity of the measurements themselves used to quantitate change. It is therefore not surprising that the conclusions have not been as clear-cut as anticipated. Unlike a laboratory experiment in which it is possible to limit the differences between experimental and control groups to the single factor being investigated, in a clinical trial an orthodontic appliance is just one of several variables affecting the outcome. The aim of this lecture is to highlight these elephant traps awaiting the unwary clinical investigator, and to emphasize that Homo sapiens is characterized by endless morphological variation. As orthodontists we treat individuals, not averages.