Prostaglandin E2.pdf orthoodontics op kharbanda

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International Journal of Applied Dental Sciences 2019; 5(3): 176-180
ISSN Print: 2394-7489
ISSN Online: 2394-7497
IJADS 2019; 5(3): 176-180
© 2019 IJADS
www.oraljournal.com
Received: 21-05-2019
Accepted: 23-06-2019
Evelyn Janeth García-Cabral
Universidad Autonoma de
Nuevo Leon, Facultad de
Odontologia, Monterrey, Nuevo
Leon, CP 64460, Mexico
Rosa Isela Sanchez-Najera
Alejandro Mass-Enriquez
Graduate Periodontics Program,
School of Dentistry, Universidad
Autónoma de Nuevo León,
Monterrey, Nuevo León, México
Guadalupe Magdalena Ramirez-
Herrera
Juana Nelly Leal-Camarillo
Maria Concepcion Treviño
Tijerina
Juan Manuel Solis-Soto
Correspondence
Juan Manuel Solis-Soto
Prostaglandin E2, an orthodontic point of view
Evelyn Janeth García-Cabral, Rosa Isela Sanchez-Najera, Alejandro Mass-
Enriquez, Guadalupe Magdalena Ramirez-Herrera, Juana Nelly Leal-
Camarillo, Maria Concepcion Treviño-Tijerina and Juan Manuel Solis-Soto
Abstract
Introduction. Chemical, biological, physical stimulants and surgical procedures are used to accelerate
orthodontic treatment.
Objective. Analyze the literature about Prostaglandin E2 (PGE2) from an orthodontic perspective.
Methods: Review of available literature in scientific articles indexed in PubMed, Cochrane Library and
EBSCO about the effector mechanism of PGE2, its participation during orthodontic movements, as well
as its beneficial and adverse effects.
Results: PGE2 acts in bone resorption through osteoclast activation and acts on osteoblasts to facilitate
osteoclast genesis by increasing the secretion of the RANKL activator. It has been shown that osteoblasts
and gingival fibroblasts respond to mechanical stress with increased production of PGE2, rapid
movement of the teeth is possible without causing root resorption, because they reduce tissue resistance
during orthodontic movement. It has both anti-inflammatory and pro-inflammatory effects, its role is
fundamental in the improvement of immunosuppressive functions, promotes the healing of peptide
ulcers, angiogenesis and re-endothelization as well as the proliferation of stem cells and positive effect on
gene therapies. Its acceleration of the G1-S cycle during mitosis can cause several types of cancer,
including Kaposi's sarcoma.
Conclusion. Promoting therapy to accelerate orthodontic movement with this mediator should be
carefully evaluated, taking into account the risk / benefit that PGE2 can cause.
Keywords: Prostaglandin E2, accelerated orthodontics, RANKL, EP4, dental movement
1. Introduction
In orthodontics, there is no consensus on the most competent manual methods for dental
movements [1]
. Which are complex phenomena that according to the theory of pressure-tension
occurs in three stages: obstruction in blood flow after the application of pressure to the
periodontal ligament, release of chemical messengers, and activation of bone resorption [2]
.
During the last decade, several strategies have been proposed to accelerate orthodontic
treatment, these include chemical agents, physical stimulants and surgical procedures [3]
. They
can help meet the demands of patients. Taking into account the risk factors related to treatment
[4, 5]
. Periodontal ligament fibroblasts perform regulatory functions in the innate immune
response, respond to compressive and tensile forces during orthodontic treatment with the
release of prostaglandins [6]
, which are cytokines involved in inflammation caused by such
movements. Among the subclasses of prostaglandins, PGE2 is strongly related to bone
resorption [7]
, inhibits osteoprotegerin and stimulates the activator of the nuclear factor
receptor kappa-B ligand (RANKL), which regulates the increase in COX- 1 and COX-2 [8]
.
One of the factors that are being investigated for their effects on tooth movement are
prostaglandins (PG), especially E2, which are potent multifunctional regulators of bone
metabolism [9]
. Brudvik was the first author to investigate the effects of PE2 injections [10]
.
Currently animal studies have reported that the rate of orthodontic dental movement, as well as
some growth of the mandibular condyle increases significantly after the administration of
exogenous, intraligamentous and submucosal injections of PGE2 because they substantially
increased the osteoblastic and osteoclastic populations in the alveolar bone, greatly
accelerating orthodontic dental movement [4, 11, 12]
. There is currently a greater desire to
implement less invasive methods to achieve rapid movements during orthodontic treatment.
Therefore, the objective of this study is to review the available literature,

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International Journal of Applied Dental Sciences
about the effector mechanism of prostaglandins specifically
PGE2, their participation during orthodontic movements, the
beneficial effects they cause in humans and their adverse
effects.
2. Materials and methods
Major headings are to be column centered in a bold font
without underline. They need be numbered. "2. Headings and
Footnotes" at the top of this paragraph is a major heading. A
bibliographic search of scientific articles indexed in pages
such as PubMed, Cochrane Library and EBSCO was carried
out, taking into account the most relevant for the realization
of this article. 109 bibliographies were analyzed, of which 50
articles were selected that met the inclusion criteria which
were articles that talked about the effector mechanism of
prostaglandins, their participation during orthodontic
movements, positive or beneficial effects for humans, as well
as adverse effects. Articles that talked about the use of other
cytokines with therapeutic effects were excluded.
3. Results & Discussion
3.1 Role of PGE2
PGs are synthesized in almost all body tissues in response to
physical, chemical, mechanical, immunological or
neurohormonal stimuli [12]
. They are eicosanoids formed from
unsaturated fatty acid of 20 carbons and arachidonic acid,
which is released from membrane phospholipids through
phospholipase A2. Subsequently, specific labile PGH2
isomerases and synthases are converted to active prostanoids,
including prostaglandins [13]
. PGE2 which is one of the most
typical lipid mediators produced from arachidonic acid by
cyclooxygenase (COX) [14]
exerts its biological function
through actions including pyrexia, pain sensation and
inflammation through four subtypes other than receptors (E-
prostanoid (EP) 1-4) [15]
. Of which EP2 and EP4 have been
identified in vivo and in vitro as the receptors responsible for
the mediation of bone formation or prevention of bone loss,
they are expressed in the membrane of human CD34 + cells
[16]
. In addition, EP4 is known for its diverse and sometimes
paradoxical activities in different cells of the immune system
during the different stages of the immune response [17]
as it is
by imposing a general suppressive effect on activation and
production. of T cells, differentially regulates the lineage
specification of CD4 + effector T cells, shifting the type 1
balance towards other forms of immunity, such as Th2, Th17
and Treg [18]
. The concentration of PGE2 increases rapidly in
acute inflammatory processes, promoting local vasodilation,
increasing microvascular permeability and promoting
extravasation of blood granulocytes and mast cell activation
[19]
, plays an important role in the regulation of various cell
lines, works both in physiological and pathological
conditions, such as bone resorption through osteoclast
activation, acts on osteoblasts to facilitate osteoclastogenesis
by increasing the secretion of the RANKL activator in
response to mechanical stress in vitro and in vivo [20]
which is
a key molecule in the differentiation and activation of
osteoclasts. The increase in the level of this molecule is
detected in periodontal disease and orthodontic tooth
movement [21]
. The effector mechanism of PGE2 is a
phenomenon that is related especially during inflammatory
processes, which among its actions within this reaction a very
important one is to promote the activation of several cell
lineages, including osteoblasts and osteoclasts, these cells
having the activity of creating and reabsorbing bone.
3.2 PGE2 during orthodontic movements
Bone tissue is constantly renewed and bone homeostasis is
finely regulated by a balance between bone apposition,
carried out by osteoblasts, and bone resorption, for which
osteoclasts are responsible [22]
. Orthodontic dental movement
is based on the resorption and coordinated formation of tissue
in the surrounding bone and the periodontal ligament.
Compression and tension are associated with particular
signaling factors, which establish local gradients to regulate
bone remodeling and the periodontal ligament for tooth
displacement. Facilitating osteoclastic resorption in the
alveolar bone exposed to continuous compressive force is an
important factor for tooth movement [23]
. Various types of
immune system cells, vascular elements and bone cells
participate in tissue remodeling during orthodontic dental
movement [24]
. Key regulators of inflammation and tissue
turnover include secreted factors such as RANKL and
osteoprotegerin, transcription factors such as RUNX2 and
hypoxia-inducible factor, cytokines such as IL-1α, IL-1β, IL-
6, IL-8, [25]
, prostaglandins, TNF-α and proteases, among
others [26]
. Osteoblasts and gingival fibroblasts have been
shown to respond to mechanical stress with increased PGE2
production [27]
. Experimental studies using prostaglandins,
cytokines, neuropeptides and leukotrienes have shown that
rapid movement of the teeth is possible without causing root
resorption, because they reduce tissue resistance during
orthodontic movement [12]
. It has long been suggested that
nonsteroidal anti-inflammatory drugs (NSAIDs) such as
iburpofen [28]
and Meloxicam [29]
can slow down orthodontic
tooth movement due to inhibition of synthesis of
prostaglandins [30]
. Orthodontic movements cause in the
alveolar bone a place where a pressure and tension occurs that
in turn this mechanical stress will be translated as bone
resorption and apposition, where the synthesis of PGE2 for
the activation of osteoblasts will have an important role.
Osteoclasts, allowing dental movement to the place desired by
the operator, taking into account that there are NSAIDs
commonly prescribed to the patient when he suffers post-
operative pain that causes delayed orthodontic movements.
3.3 Benefit effects of PGE2
PGE2 plays a fundamental role in tissue maintenance and
regeneration; It has been found to induce cell differentiation
of some neuronal cells [31]
, has a substantial influence on
bone, bone remodeling and healing, but its effects are still
controversial and discussed [32]
. However, it has been reported
that it has anti-inflammatory effects because it increases the
synthesis of IL-10 and decreases the production of
proinflammatory cytokines such as TNF-α, IFN-ʏ and IL-12
[33]
. In addition, it inhibits the proliferation of activated T
cells, the cytotoxicity of NK cells and the maturation of
dendritic cells, so their role is essential in improving
immunosuppressive functions [34, 35]
. It also plays an important
role in stem cells. A previous study showed that it promotes
the proliferation of progenitor cells in cell cultures in vitro
and in trials of a spleen transplant [36]
. Through its subtype
EP4, it stimulates anti-inflammation in the lung and provides
a new clinical perspective for chronic inflammatory
conditions of the respiratory tract [37]
. It has also been shown
that PGE2 promotes the proliferation of primary myoblasts by
accelerating the transition of the G1-S phase in the cell cycle
[38]
. It has an intestinal cytoprotective action [39]
, shows a
healing effect on gastric ulcers and lesions of the small
intestine [40]
stimulation of angiogenesis and
reendothelialization through the activation of EP4 receptors

~ 178 ~
[41]
. It has recently been shown to be useful in clinical
applications of gene therapy because the synthesis of PGE2
improves lentiviral transduction and increases the number of
copies of the vector, resulting in increased transgene
expression [42]
. It seems that PGE2 has multiple beneficial
effects for humans that are in a state of immunosuppression,
chronic respiratory disease and intestinal diseases because it
has anti-inflammatory, pro-inflammatory effects, promotes
angiogenesis and repair of the endothelium of blood vessels.
As well as its synthesis promises to be a factor with positive
effect in more innovative therapies with stem cells and gene
therapy.
3.4 Adverse effects of PGE2
In general, it has been shown that prostaglandins interfere
with cytokines and amplify their actions in various types of
inflammatory cells, and drive the pathogenic conversion of
cells by critically regulating their gene expression [43]
. PGE2
is involved in numerous physiological processes, which
include the development of stem cells, inflammation and
cancer [44]
because it promotes the progression of the cell
cycle, by accelerating the transition of the G1-S phase [38]
.
Therefore, its inhibition is considered one of the approaches
to limit the growth and spread of several types of cancers [45]
.
Its subtype EP4 has been shown to be the key receptor in
endometrial cancer [46]
. It has also been reported that PGE2
plays a role in the development of ovarian, breast, colorectal
cancer [47]
and pancreas [48]
. In addition, the secretion of PGE2
and its autocrine and paracrine interactions with EP receptors
(EP1-4) has been involved, signaling of the COX-2 / PGE2 /
EP receptor regulates the pathogenesis and latency of
Kaposi's Sarcoma [49].
Recently, it has been shown that PGE2
can have serious effects on humans, such as the progression
of several types of cancer, including Kaposi's Sarcoma, which
can be detected in the oral cavity, with EP4 being the subclass
most related to tumor development.
4. Conclusions
PGE2 is a lipid mediator that plays an extremely important
role during orthodontic movements, promoting bone
resorption and apposition through the activation of osteoblasts
and osteoclasts. There are certain types of NSAIDs that
inhibit the synthesis of PGE2 caused the delay of dental
movement. In general, its synthesis has multiple beneficial
effects on the body that include an intestinal cytoprotective
action and improvement in patients who are in a state of
immunosuppression and with chronic respiratory disease, is
also a mediator that demonstrates positive effects on gene
therapies and with stem cells. However, it has been observed
that due to its acceleration of the G1-S cycle during mitosis,
several types of cancer can occur in the female reproductive
tract, pancreas and orally Kaposi's Sarcoma. Because of this,
promoting therapy to accelerate orthodontic movement with
this mediator should be thoroughly studied taking into
account the risk / benefit that PGE2 can cause.
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