External Apical Root Resorption in Patients Treated with Passive Self-Ligating System

External apical root resorption (EARR) is an unavoidable pathologic consequence of orthodontic tooth movement. It can be defined as an iatrogenic disorder that unpredictably occurs after orthodontic treatment, whereby the resorbed apical root portion is replaced with normal bone. EARR is a sterile inflammatory process that is extremely complex and involves various disparate components, including mechanical forces, tooth roots, bone, cells, surrounding matrix, and certain known biologic messengers (Krishnan & Davidovitch, 2006; Meikle, 2006). In the relationship between EARR and inflammatory cytokines, Zhang et al. (2003) indicated that interleukin (IL)-1 and tumour necrosis factor (TNF)-alpha are important for the induction and the further processing of mechanically-induced root resorption in the rat. Receptor activator of nuclear factor κB ligand (RANKL) is a cytokine that belongs to the TNF family and is essential for the induction of osteoclastogenesis. Osteoblasts and bone marrow stromal cells produce this cytokine, and its signals are transduced by the specific receptor RANK, which is localized on the cell surface of osteoclast progenitors. The RANKL/RANK system has been suggested to play an integral role in osteoclast activation during orthodontic tooth movement. Shiotani et al. (2001) observed RANKL in osteoblasts, osteocytes, fibroblasts, and osteoclasts during the application of orthodontic forces. The RANKL/RANK system may regulate the natural process of root resorption in deciduous primary teeth (Lossdörfer et al., 2002). Therefore, these inflammatory cytokines contribute to alveolar bone remodeling and to resorption during orthodontic tooth movement and EARR. The wire friction influences the forces acting in a continuous arch system. Damon (2006a) suggested that the nearly friction-free system, using the self-ligation brackets and high-tech wires, may not cause periodontal problems, including alveolar bone loss. Other studies reported that static friction measured in vitro is much less with a passive self-ligating system than with any other type of fixed appliance (Berger, 1990; Sims et al., 1993). The friction force disturb orthodontic tooth movement, thus, it is expected that influence for the periodontal tissue is different from the self-ligating brackets in the conventional appliances. We reported that GCF levels of substance P (SP), one of neuropeptides which cause the local inflammation, SP for the passive self-ligating system sites were significantly lower than for the teeth with conventional brackets at 24 hours (Yamaguchi et al., 2009). Thus, the passive