**2.1. Pharmacological methods**

Orthodontic forces cause a fluid movement in the periodontal ligament space and distortion of the matrix and cells. There is release of molecules which initiate bone remodelling for tooth movement [1]. There are a number of researches on pharmacological agents that act as biomodulators for increased orthodontic tooth movement. These are examples of such biomodulators:

> Calcitriol or 1,25-dihydroxycholecalciferol which is the most active metabolite of vitamin D acts in a similar fashion to PTH by facilitating osteoblastic proliferation and function [12]. Calcitriol facilitates alveolar bone remodelling which leads to increase in tooth movement

> Recently intravenous immunoglobulin (IVIg) preparations which are used in immunodeficient patients as replacement therapy. These preparations have been shown to induce COX-2

> Bichmalyr in 1931, put forward a surgical technique with orthodontic appliances for rapid correction of severe maxillary protrusion. First, wedges of bone were removed to reduce the volume for which the roots of the maxillary anterior teeth would require for retraction. Kӧle further looked into this technique in 1959 by including special movements like crossbite correction and space closure. He believed that he was able to move bony blocks using the crowns of teeth as handles as the blocks were connected by only less-dense medullary bone [16].

> In 2001, Wilcko et al. had introduced a method which combines corticotomy surgery and alveolar bone grafting which is referred to as accelerated osteogenic orthodontics or recently

and cytokine production [14, 15]. Future potential of these preparations could

synthesis.

Accelerated Orthodontics

25

http://dx.doi.org/10.5772/intechopen.80915

while force application [6, 13].

be used to modulate orthodontic movement via PGE2

**Figure 1.** Injection of a biomodulator in the periodontium.

• Periodontally accelerated osteogenic orthodontics

Currently there are few surgical methods being practiced, they are:

mediated PGE2

• Piezocision

• Micro-osteoperforations

**2.2. Surgical methods**


Prostaglandin E2 (PGE2 ) is an arachidonic acid metabolite is an often-tested substance to increase orthodontic tooth movement [2]. Animal studies have shown PGE2 to increase tooth movement and facilitate bone resorption [3–6]. Camacho and Velásquez Cujar conducted a study that showed that it required repeated injections due to its short half-life [7]. Particular synthases that are required for the synthesis of PGE2 could be targeted to control the production of the prostaglandins [8].

Another prostaglandin that has been reported to speed up orthodontic tooth movement is Prostaglandin E1 (PGE1 ). Prostaglandin E1 (PGE1 ) has also been seen to be induced by mechanical stress and cause bone remodelling, Patil and his co-workers had shown that even minimal amounts of PGE1 injection had significant increase in tooth movement [9]. Due to the hyperalgesia that accompanies with the local injection of PGE1, an analogue of it which is misoprostol was tried out. It was seen that it was effective in increasing orthodontic tooth movement (**Figure 1**) [10].

The parathyroid hormone (PTH) acts directly on osteoblasts and on osteoclasts indirectly by binding to the PTH type 1 receptor on osteoblasts. This causes the expression of insulin like growth factor 1. There is promotion of osteoblast survival, osteoblastogenesis and receptor activator for nuclear factor κ B ligand (RANKL) which induces osteoclast activation [2]. PTH facilitates bone remodelling in intermittent treatment by enhancing activities of osteoblasts and osteoclasts [11].

**Figure 1.** Injection of a biomodulator in the periodontium.

Calcitriol or 1,25-dihydroxycholecalciferol which is the most active metabolite of vitamin D acts in a similar fashion to PTH by facilitating osteoblastic proliferation and function [12]. Calcitriol facilitates alveolar bone remodelling which leads to increase in tooth movement while force application [6, 13].

Recently intravenous immunoglobulin (IVIg) preparations which are used in immunodeficient patients as replacement therapy. These preparations have been shown to induce COX-2 mediated PGE2 and cytokine production [14, 15]. Future potential of these preparations could be used to modulate orthodontic movement via PGE2 synthesis.
