Cellular and Molecular Mechanisms of the Litchfield Park Orthodontist
At the cellular and molecular level, Litchfield Park orthodontic tooth movement is the result of the interaction between bone-forming osteoblasts and bone-resorbing osteoclasts.  Cells of the osteoblast lineage determine the rate of remodeling as they are not only involved in bone formation, but are also involved in osteoclastogenesis (Takahashi et al., 1988; Udagawa et al., 1990; Suda et al., 1992).  The actual means of communication between osteoblasts and osteoclasts, however, remained unclear until several groups independently discovered the same intermediary factor, Receptor Activator of Nuclear Factor κB Ligand (RANKL) (Anderson et al., 1997)/ TNF-related activation-induced cytokine (TRANCE) (Wong et al., 1997)/ osteoprotegerin ligand (OPGL) (Lacey et al., 1998).  A member of the tumor necrosis factor (TNF) superfamily, RANKL is the intermediary factor on the surface of osteoblasts responsible for the activation and recruitment of osteoclast precursors (Figure 4).  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 also can bind to the soluble decoy receptor protein osteoprotegerin (OPG)/osteoclastogenesis inhibitory factor (OCIF) (Simonet et al., 1997; Yasuda et al., 1998). OPG, which is expressed by many cell types including fibroblasts, ameloblasts, odontoblasts, and pulp cells (Rani and MacDougall, 2000; Quinn et al., 2000), competitively binds to RANKL, thus inhibiting osteoclast recruitment and activation.  The ratio of RANKL: OPG expression is believed to be the main determinant controlling the rate of osteoclast recruitment and activation.

Studies have shown many other factors that affect the rate of bone remodeling to varying degrees.  Interleukins (IL-1, IL-6), tumor necrosis factor (TNF), parathyroid hormone (PTH), prostaglandin E2 (PGE2), macrophage colony-stimulating factor (M-CSF), and 1,25 dihydroxyvitamin D3 (vitamin D) all play a role in stimulating bone resorption (McCauley and Nohutco, 2002).  Likewise, interferon gamma (IFN-γ), estrogens, androgens, calcitonin, and cyclosporine play a role in inhibiting bone resorption (McCauley and Nohutco, 2002).  While all of these factors can affect the rate of bone remodeling, the interaction between RANKL and OPG plays the preeminent role in the process (Hsu et al., 1999).

Arizona Dental Association