Читать книгу Biological Mechanisms of Tooth Movement - Группа авторов - Страница 58

Prostaglandins (PGs), products of arachidonic acid metabolism, are local, hormone‐like chemical agents produced by mammalian cells including osteoblasts that are synthesized within seconds following cell injury. One of the derivatives of the arachidonic acid cascade, PGE₂, acts as a vasodilator by causing increases in vascular permeability and chemotactic properties, and also stimulates the formation of osteoclasts and an increase in bone resorption. The cyclooxygenase (COX) family of enzymes consists of two proteins that convert arachidonic acid, a 20‐carbon polyunsaturated fatty acid comprising a portion of the plasma membrane phospholipids of most cells, to PGs. The constitutive isoform (COX‐1) is found in nearly all tissues and is tissue protective. In contrast, COX‐2, the inducible isoform of COX, appears to be limited in basal conditions within most tissues, while de novo synthesis is activated by cytokines, bacterial lipopolysaccharides, or growth factors, to produce PGs in large quantities in inflammatory processes. There are several lines of evidence showing that COX is also closely associated with periodontitis, and that PGs are mediators of gingival inflammation and alveolar bone resorption (Offenbacher et al., 1993).

With the help of in vivo studies, an injection of biochemical agents such as PG has been suggested as one effective method that significantly increases OTM (Yamasaki et al., 1980; Yamasaki, 1983). The mechanism of action of PGE₂ can be explained by the pressure–tension theory of tooth movement, which assumes chemical signals to be cell stimulants that lead to tooth movement (Rygh, 1989). According to this theory, pressure causes changes in the PDL blood circulation and the resultant release of chemical mediators. Inflammatory mediators may act in concert and produce synergistic potentiation of prostanoid formation in cells of the human PDL (Ransjo et al., 1998). There is evidence that PG is released when cells are mechanically deformed (Rodan et al., 1975). Indeed, in vitro studies have shown that the expression and production of PGE₂ is promoted by mechanical stimulation of the PDL (Yamaguchi et al., 1994). COX‐2 is induced in PDL cells by cyclic mechanical stimulation and is responsible for the augmentation of PGE₂ production in vitro (Shimizu et al., 1998). Furthermore, PGE₂ plays an important role as a mediator of bone remodeling under mechanical forces (Yamasaki et al., 1982). Saito et al. (1991) reported that there is a local increase in PGs in the PDL and alveolar bone during orthodontic treatment, while other studies have demonstrated an arrest in tooth movement in experimental animals when nonsteroidal anti‐inflammatory drugs were administered (Chumbley and Tuncay, 1986). Indomethacin, a specific inhibitor of prostaglandin synthesis, reduced the rate of OTM (Yamasaki et al., 1980). Further, when PGE₁ was administered locally or systemically to rats as an adjunct to orthodontic force, accelerated bone resorption and tooth movement were observed (Yamasaki et al., 1984).

Interestingly, HMGB1 can trigger PG synthesis (Leclerc et al., 2013), suggesting that an inducer‐first messenger (PG) cascade can take place in the development of an inflammatory reaction to orthodontic forces. Also, DAMP‐induced PG can modulate cytokines, demonstrating the existence of complex regulatory networks involving different classes of mediators in the response to orthodontic forces (Prockop and Oh, 2012). Therefore, it may be concluded that PGs play an important role in OTM.