Phoenix Orthodontic Anchorage

Phoenix orthodontics generally is thought of as the science of Phoenix orthodontic tooth movement. The ability to maintain the position of certain teeth, however, is just as important. Newton’s third law of motion states that for every action there is an equal and opposite reaction. There are many situations in Phoenix orthodontics where this equal and opposite reaction is undesirable. One example is the retraction of canines without protraction of the posterior teeth. The stabilization of posterior teeth against movement is maintenance of Phoenix orthodontic anchorage. In order to accomplish this objective, Phoenix orthodontists have developed several types of Phoenix orthodontic anchorage including: 1) extraoral appliances (headgear), 2) Phoenix dental anchorage (consolidation of teeth into Phoenix dental units), 3) intraoral appliances (Nance button, transpalatal arch), and 4) osseointegrated and Phoenix dental implant-associated appliances (implants, miniscrews, microimplants). As we continue to gain a better understanding of the cellular and molecular mechanisms involved in Phoenix orthodontic tooth movement, the delivery of bioactive agents may provide a new means of Phoenix orthodontic anchorage.

At the cellular and molecular level, Phoenix orthodontic tooth movement is the result of the interaction between bone-forming osteoblasts and bone-resorbing osteoclasts. Cells of the osteoblast lineage are not only involved in bone formation, but also regulate osteoclastogenesis. The activation and recruitment of osteoclast precursors is caused by an intermediary factor on the surface of osteoblasts known as Receptor Activator of Nuclear Factor κB Ligand (RANKL), a member of the tumor necrosis factor (TNF) superfamily. Its receptor, Receptor Activator of Nuclear Factor κB (RANK), is located on the surface of osteoclast progenitor cells. The binding of RANKL to RANK induces osteoclastogenesis and activates osteoclasts. RANKL, however, also can bind to the soluble decoy receptor protein osteoprotegerin (OPG). OPG competitively binds to RANKL, thus inhibiting osteoclast recruitment and activation.

Administration of recombinant OPG currently is being studied as a means to combat inappropriately high levels of osteoclast-mediated bone resorption at the systemic level. Examples include primary osteoporosis, Paget’s disease, rheumatoid arthritis, hypercalcemia of malignancy, osteolytic metastases, postmenopausal bone loss, and periodontal disease (Simonet et al., 1997; Morony et al., 1999; Teng et al., 2000; Bekker et al., 2001; Schett et al., 2003; Body et al., 2003; Capparelli et al., 2003; Kostenuik et al., 2004; Bekker et al., 2004). The ability to move certain teeth while preserving the position of “anchor teeth” is a common Phoenix orthodontic goal. For this reason, Phoenix orthodontists continue to look for improved means of maintaining tooth position. Given its potential as an inhibitor of osteoclastogenesis and therefore bone resorption, pharmacological utilization of osteoprotegerin may provide a new means of achieving and optimizing Phoenix orthodontic anchorage.