Effect of Low- level laser therapy (LLLT) on Orthodontic Tooth Movement - Cellular Level
Sushma Dhiman* and Saba Khan
Orthodontics and Dentofacial Orthopedics, Aligarh Muslim University, India
Submission: February 04, 2017;Published: February 19, 2018
*Corresponding author: Sushma Dhiman, Orthodontics and Dentofacial Orthopedics, Aligarh Muslim University, India, Tel: 8527214151; Email:email@example.com
How to cite this article: Sudhakara Reddy K, Thokala Dhamodaran, Vaibhav Nagaraj, Swarna Sudeeshna. Basally Osseointegrated Implants as a Viable
Immediate Solution in Cases of Failed Implants in Atrophic Posterior Maxillary Region: A Case Report. Adv Dent & Oral Health. 2018; 7(5): 555722. DOI:10.19080/ADOH.2018.07.555723
Low-level laser therapy has been used to stimulate the orthodontic tooth movements (OTM). Low level laser therapy has biostimulatory effects. In the last decade, researchers have attempted to determine the affect of Low level laser therapy on the pathways and cells directly associated with orthodontic tooth movement. The results of studies on the rate of tooth movement are controversial. While the majority of published research outcomes indicate an increase in the rate of tooth movement after laser therapy compared to controls, but others reported no difference or even indicated the inhibitory effect of laser therapy on the rate of tooth movement. Most of the studies reported the effect of the LLLT on rate of orthodontic tooth movement but only few have dealt with the underlying mechanism of action of low- level laser therapy on cells involved in orthodontic tooth movement. The present paper discusses the effect of low level laser therapy on orthodontic tooth movement at cellular level.
Orthodontic tooth movement occurs in the presence of a mechanical stimuli will cause changes in the microenvironment around the PDL due to alterations of blood flow, leading to the secretion of different inflammatory mediators such as cytokines, growth factors, neurotransmitters, colony-stimulating factors, and arachidonic acid metabolites. As a result of these secretions, remodeling of the bone occurs [1,2]. Bone remodeling involves resorption of bone on the pressure site and bone formation on the tension site . Low level laser therapy has biostimulatory effects . It stimulates the on-going biological process in tissue and has been found to be effective in modulating cell activity and production of endogenous molecules, which are also involved in orthodontic tooth movement [5-7].
In the last decade, researchers have attempted to determine the affect of LLLT on the pathways and cells directly associated with orthodontic tooth movement. The results of studies on the rate of tooth movement are controversial. While the majority of published research outcomes indicate an increase in the rate of tooth movement after laser therapy compared to controls [8-15], but others reported no difference [16-18] or even indicated the inhibitory effect of laser therapy on the rate of tooth movement . Most of the studies reported the effect of the LLLT on rate of orthodontic tooth movement but only few have dealt with the underlying mechanism of action of LLLT on cells involved in orthodontic tooth movement.
Effect of LLLT is photochemical not thermal. Response of a cell to LLLT occurs by absorption of light by photoacceptor molecule also termed as chromophores [20,21]. Cytochrome C oxidase is a key photoacceptor of light in the far-red to near-IR spectral range . Cytochrome C oxidase is an integral membrane protein of mitochondria that contains four redox active metal centers. The Excitation of this molecule with light energy accelerates the rate of electron transfer  and in turn increases the capacity of mitochondria to generate ATP [20,24-26]. Increased ATP results in increased energy available for that cell’s metabolic processes.
In the last few decades, researchers have attempted to determine the affect of LLLT on the biological pathways involved in orthodontic tooth movement. Some authors believe that LLLT induces osteoblasts proliferation (in vivo studies, [27-28] and in vitro studies [29-38]. Which is responsible for the accelerated tooth movement. However, according to other researchers, bone resorption is the rate-limiting step in tooth movement . Therefore, any procedure which has the potential to increase osteoclastic activity may increase the rate of orthodontic tooth movement. Recent studies highlight enhanced osteoclastic activity after low level laser therapy in vivo [39-44] and in vitro .
Low level laser therapy’s effect on osteoclast factors: The
control mechanism of bone turnover is the OPG/RANKL/
RANK system which is also recognized as the final mediator of
osteoclastogenesis [46,47]. Researchers have sought ways to
determine which member(s) of the system is/are affected by LLLT.
LLLT Effects On RANK and RANKL
Activation and maintenance of osteoclastic activity is under
control of binding of RANKL with RANK. When RANKL dock with
RANK, preosteoclasts differentiate and become osteoclasts. Studies
have observed greater number of RANK and RANKL positive cells
in laser treated groups than in both the non-irradiated. [8,40,45]
Osteoprotregrin (OPG) competes with RANK for the binding
of RANKL. OPG decreases the differentiation and activation of
osteoclasts. Fujita et al.  found that the level of OPG expression
between the laser and control group did not vary . Kim’s
group reported a significant increase of the cytokine with
LLLT application. But they also noted that magnitude of OPG
upregulation was not as great as it was for RANK. Because the OPG
to RANK ratio was skewed in favor of RANK, the team observed
a net increase in osteoclastic differentiation and activation .
Dozens of cytokines, hormones, and peptides have been
proven to play a role in bone turnover. A review of the literature
yields a number of reports indicating how some of the factors
involved in osteoclast regulation may be affected by LLLT [45-61].
Transforming Growth Factor Beta 1 (TGF-β1) is integral in
the differentiation and in maintaining the function of osteoclasts
. Research teams have discovered that sufficient expression
of the polypeptide upregulates RANKL levels in the absence of
osteoblasts, while excessive amounts of TGF-β1 in the presence of
osteoblasts decreases RANKL upregulation [66-68]. Two research
teams recently demonstrated increased levels of TGF-β1 after
LLLT in the oral cavity[69,70].
Cyclo-oxygenase is the rate-limiting enzyme in the conversion
of arachidonic acid to prostaglandins, which is an essential
component in osteoclast regulation. Several authors have shown
that both Cox-2 and PGE-2 upregulate RANKL and inhibit OPG
levels [71-73]. Matsumoto and colleagues demonstrated increased
expression of Cox-2 after LLLT during bone repair in rats .
During orthodontic tooth movement the cells and components
of the periodontal membrane matrix surrounding teeth undergo
remodeling as mechanical forces induce biochemical changes
in the microenvironment . Fibronectin and collagen type
1 are important components of PDL organization. Fibronectin
is synthesized in osteoblasts and fibroblasts. Fibroblast plays
an important role in adhesion, growth, cell movement and
differentiation during PDL reorganization . It is particularly
important in wound healing. Collagen type 1 is the main
component in the PDL and is present in the high concentration in
all fibers responsible for maintaining tooth position .
Increased expression of Fibronectin and turnover of collagen
type 1 in LLLT groups compared to controls from day one of the
experiment was found by Kim and his team of researchers. This
may be due to the fact that Fibronectin induce the upregulation
of RANKL which leads to the differentiation of osteoclast [77-78].
Fibronectin could, therefore, serve multiple purposes in PDL and
bone turnover by assisting in phagocytic cells migration as well as
increasing the presence of osteoclast like cells. The increased rate
of collagen type 1 degradation and reorganization may also assist
in minor increases in orthodontic tooth movement.
Vascularization plays a key role in orthodontic tooth
movement. Regardless of the type of bone resorption, whether
frontal or undermining resorption, key cellular constituents arrive
to the sites of bone resorption and deposition through the blood
vessels. Along with nascent osteoclast, other phagocytic cells make
their way through vessels and assist in not only bone but also
tissue remodeling. Histological sections have revealed accelerated
deposition of bony matrix as well as nascent vascularization on
the laser experimental sides after seven days of healing when
compared to controls [79,80]. Other researchers have shown
increased vascularity after laser therapy in non osseous organs
[81-83] as well as an increase in molecular factors related to
vascular proliferation [84,85]. Additionally, some investigators
have also found an upregulation of eNOS gene expression via PI3K
signal pathway allowing for increased angiogenesis, endothelial
migration, and revascularization . The complete biochemical
pathways through which LLLT influences osteoclast activity are
not fully understood. Yet these researchers provide potential
mechanisms whereby LLLT can influence osteoclast regulation
by effecting enzymatic levels of TGF-β1, Cox-2, PGE-2, fibronectin,
collagen turnover, and tissue vascularity preservation. These
enzymes induce the expression or inhibition of members of the
OPG/RANKL/RANK system and subsequently manipulate the
differentiation, maturation, and maintenance of osteoclasts
Orthodontic tooth movement is induced by mechanical stimuli
and facilitated by the remodeling of the periodontal ligament
and alveolar bone. The remodeling activities and the ultimately
tooth displacement are the consequence of an inflammatory
process. Vascular and cellular changes were the first events to be
recognized. It is important for the clinicians to have knowledge
of the effect of low level laser therapy on the cellular elements
involved in orthodontic tooth movement. Orthodontically induced
tooth movement associated with LLLT produced an increase in
the vascularization, controls mechanism of bone turnover by
regulating the OPG/RANKL/RANK system. Low level laser also
regulates Transforming Growth Factor Beta 1, Cyclooxygenase 2
(Cox-2), fibronectin, PDL Collagen Remodeling. Further research
is required to develop more solid scientific bases for the clinical
use of LLLT and to describe the mechanism action of low power
lasers as there are only a few studies in this field and different
methodologies have been employed.
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