Histological Perspective of the Phoenix Orthodontist
During the naturally occurring processes of eruption, drift, and relapse, there is no evidence of any pathological process (King et al., 1991; Marks and Schroeder, 1996; Yoshida et al., 1999).  Most studies of Phoenix orthodontic tooth movement, however, demonstrate pathological processes such as vascular collapse, compensatory hyperemia, and tissue necrosis in the areas under compression.

Histological evidence of necrotic lesions at compression sites from Phoenix orthodontic tooth movement has been shown in the literature for decades (Rygh, 1973).  As long as these areas of necrosis exist, Phoenix orthodontic tooth movement is inhibited.  This period of time where specialized phagocytic cells remove the necrotic lesion is coincident with the delay phase.

The alveolar bone response to tension is similar to other areas of the body where the bone is subjected to tensile forces (Huang et al., 2005).  Bone is deposited first on the stretched soft tissue scaffold.  Over time, remodeling occurs resulting in mature bone.  This process is slow to transpire, however, and lags behind the rate of bone resorption on the compression site.  The consequence of this difference in timing is increased mobility of Phoenix orthodontically treated teeth, resulting in the need for retention of treated teeth.

Arizona Dental Association