Global Journal of Infectious Diseases and Clinical Research

Luciano Silva* Review Article

University of Pernambuco, Brazilian Association of
Odontology, Brazil
Dates: Received: 10 October, 2015; Accepted: 02
A Literature Review of Inflammation
November, 2015; Published: 04 November, 2015

*Corresponding author: Luciano Silva, University

and Its Relationship with the Oral
of Pernambuco, Brazilian Association of Odontology
- ABO – Recife, Tel: 55 81 30316824; E-mail: Cavity
www.peertechz.com
Abstract
ISSN: 2455-5363
Objective: This article presents a literature review which relates the processes, interactions,
Keywords: Inflammation; Cytosine; Leukocytes classification and the vascular and clinical characteristics of inflammation relating it with the oral
cavity and describing the main cell types and chemical mediators used for its establishment.

Materials and Methods: it was used as source of research the following databases: MEDLINE,
LILACS, BBO, Cochrane Library, Scielo, PubMed and the database of CAPES.

Results: much information was obtained concerning the chemical mediators as well as the main
cell types responsible for the establishment of inflammation and its relationships with the oral cavity.

Introduction a cellular component. The vascular component represents changes

in vessel diameter (vasodilation) and consequently increased blood
The earliest known description of inflammation comes from flow (causing redness and heat), and increased vascular permeability
the Edwin Smith Papyrus, one of the Egyptian papyri found in a resulting in loss of plasma into the tissue and formation of fluid
tomb near Thebes. The Papyrus dates from about 1550 B.C., but it is exudate. The exudate contains many valuable proteins such as fibrin
undoubtedly a copy of ancient tests of the archaic period of Egyptian and immunoglobulin but it also gives rise to edema. The swelling
history (3200-2780 B.C.) Documents from Egyptian and other early distends the tissues; it may compress nerve endings and thus cause
civilizations leave no doubt that the features of inflammation were pain.
recognized from very early periods; although the understanding of
the process took a long time to happen. According to its duration, inflammation is described as acute
or chronic. Sometimes the acute process subsides but the stimulus
Inflammation can be considered as the first response of a living persists sufficiently to evoke a subsequent chronic inflammation.
tissue to injury and may be referred to as the innate immunity, and In other cases, with a stimulus that typically induces chronic
may appear due to microbial infections, physical factors (trauma, inflammation, the tissues response may be acute in type for the
radiation, temperature), chemical substances (irritant and corrosive first day or so. Suffice it to say at this stage that the tissue response
chemicals), as well as tissue necrosis and hypersensitivity reactions. differs considerably in acute and chronic. The cellular component
It is didactically characterized by the following quintet: redness involves the movement of white blood cells (leukocytes) from the
(rubor), heat (calor), swelling (tumor), pain (dolor) and dysfunction blood vessels into the inflamed tissue. They extra vasate from the
of the organs involved (functio laesa). The first four characteristics capillaries into tissue, and act as phagocytes, picking up bacteria
were drawn up by Celsus nearly 2000 years ago; function laesa was and cellular debris. They may also aid by walling off an infection
added to the definition of inflammation by Rudolf Virchow in 1858, and preventing its spread. Influx of neutrophils is one of the earliest
considered the predecessor of modern pathology and social medicine. stages of the inflammatory response. These cells mount a rapid, non-
It was the latter who, in the field of inflammation, critically analyzed specific phagocytic response. Later, monocytes/macrophages and
the meaning of the four key symptoms (redness, swelling, heat and cells of other lymphocyte lineages (specific subsets of T cells and B
pain) and postulated that inflammation could not be represented cells) appear at the site of injury; cell types which are associated with
as a single process but rather constituted of various inflammatory antigen-specific and more tightly regulate immune responses and
processes. once activated also produce protective and inflammatory molecules.
Vascular and cellular considerations The lymphocytes are the primary cells of the immunologic
A definition of inflammation is complicated, because the local system, and have developed one of the more sophisticated intelligent
vascular and tissue reactions often are accompanied by systemic effects defense mechanisms in the biological system. The review of ALAM
that include malaise, fever, leukocytosis, metabolic disturbances and and GORSKA [2], enlightens that the T lymphocytes play a major
shock. The process of inflammation can be defined as the succession of role in the organization of the immune response, eliminating
changes which occurs in the living tissue when it is injured, provided intracellular pathogens (virus, and bacteria) through the generation
that the injury is not of such a degree as at once to destroy its structure of cytotoxic T lymphocytes. The B lymphocytes protect the organism
and vitality [1]. The inflammatory response consists of a vascular and against extracellular pathogens by the production of antibodies. The

Citation: Silva L (2016) A Literature Review of Inflammation and Its Relationship with the Oral Cavity. Glob J Infect Dis Clin Res 2(1): 001-007. DOI:
10.17352/2455-5363.000006
001
Silva. (2016)

natural killer cells (NK) are an important component of the innate The role of cytokines
immunity. The dendritic B cells begin the immunologic response by
The immune system is a complex organ with both professional
presenting antigens to the T lymphocytes. The authors resume that
and non-professional cells involved, whose main objective is to
the interaction among the T lymphocytes, B lymphocytes, dendritic
cells and the natural killer cells (NK) constitutes the fundamental allow the most developed organisms to endure in a world where
defensive mechanism of the host. microorganisms try to make use of them to survive. In short; it is a
sophisticated and interconnected system that makes human existence
The mechanism against pathogenic microbes demands different possible; and so communication between its main components is a
responses depending on the characteristic of the pathogen and on major issue. Therefore, the competent cells of the immune system
the attacked tissue. CHAPLIN [3], claimed that the organism of the make use of substances that may be unleashed in the blood stream
host has developed innate and adaptive immune mechanisms of to signalize the need of the cell recruitment or the production of
defense, being the former unspecific, attacking any nonself structure specific substances. It is accomplished by direct cell-cell contacts,
or antigen, and the latter, on the other hand, extremely specific. by contacts with non-self-factors; like pathogen compounds, and
Both types of immune response act together in order to eliminate by soluble proteins. This immune response is obtained partially
pathogenic antigens through the discrimination of what is self and by the synchronized synthesis and function of the small cytokines
what is not. called chemokines (CKs) and their action on their counterparts, the
The changes described in blood flow, increased permeability chemokine receptors (CKRs); without which the cells would never
of blood vessels and escape of cells from the blood into the tissues respond. In fact, CKRs define the subpopulation that will be recruited
(diapedesis) are basically the same whatever the cause and wherever in each step of the immune responses. The name chemokines is
the site of inflammation is. Thermal injuries cause permanent derived from chemoattractant cytokines, and is related to their
occlusion of the blood vessels in a narrow zone of tissue immediately capacity of inducing directed chemo taxis in nearby responsive cells.
surrounding the burned site. Beyond the zone where the injury is
The cytokine family is large with still unanswered questions. It
less intense, blood flow is reestablished after a short initial period of
includes the Interleukins (IL), Interferon (IFN), Tumor Necrosis
vasoconstriction. Immediately after injury, there is transient ischemia
Factor (TNF), Coloning-stimulating Factor (CSF), Chemokines
due to vasoconstriction, particularly of the arterioles. The sequelae of
(CKs), and Growth Factor (GF) [3].
acute inflammation depend upon the type of tissue involved and the
amount of tissue destruction, which depend, in turn, upon the nature Interleukins – ranging from IL1 to IL32 - are different among
of the injurious agent. The possible outcomes of acute inflammation each other, have different functions and are secreted by different
can be either healing or chronic inflammation. Chronic inflammation cells. Interferon is subdivided in IFNα (leukocyte IFN - inhibitor of
is characterized by a dominating presence of macrophages in the viral replication) IFNβ (fibroblast IFN – inhibitor of viral replication)
injured tissue. These cells provide a powerful defensive mechanism and IFNγ (Secreted by lymphocytes – immune regulatory functions).
in the body, but the mediators they release are injurious to the Tumor Necrosis Factor is represented by TNFα (secreted more
organism’s own tissues, as well as invading agents. This is why chronic frequently by monocytes) and TNFβ (secreted by T cells). Colony-
inflammation is almost always accompanied by tissue destruction [4]. stimulating Factor (G-CSF, M-CSF, GM-CSF and others) – able to
Inflammation is referred to, didactically, as acute when it lasts make bone-marrow cells differentiation into specific cell types, like
two days or three weeks and as chronic when more prolonged. The monocytes, macrophages and neutrophils. Chemokines (Eotaxin
typical case of acute inflammation is characterized by vasodilatation, and many others) are very important in controlling the migration of
by exudation of plasma and the emigration of neutrophilic leucocytes cells between and within tissues. Growth Factor (IGF, TGF and many
into the injured tissue. But not all the examples of acute inflammation others) was originally identified because of non-immune-related
exhibit neutrophilic infiltration and, conversely, neutrophils may functions but may have effects on immune cells. Some of them are
be associated with prolonged and therefore chronic inflammation. considered pro-inflammatory and can be induced during an immune
Between acute and chronic there occurs a wide range of overlapping response to promote cells of the immune system to a site of infection,
processes and those at halfway point are sometimes referred to as whereas others are considered homeostatic and are involved in
subacute inflammation. The main events in acute inflammation are controlling the migration of cells during normal processes of tissue
vascular in origin and remarkably consistent for a wide range of maintenance or development. The first cytokine identified to have
stimuli. Nevertheless, the response exhibits considerable differences chemotactic activity was interleukin-8 (IL-8), which proved to be a
that depend, first, on factors related to the injury or infection and, selective neutrophil chemoattractant [6].
second, on the condition of the host and nature of the tissue involved Not only is the inflammatory bone destruction governed by
[5]. On the other hand, inflammation is said to be chronic when its local cytokine production but also the normal bone remodeling
duration is prolonged for months or years, or even indefinitely. Its throughout the lifetime of an individual. Some of the factors which
prolonged course is due to persistence of the causative factor in the
regulate physiologic bone remodeling are prostaglandins (PGs), IL-1,
tissues, whether the factor be infection or inanimate foreign body.
TNF-α and possibly IL-6 [7].
The tissues committed are infiltrated by macrophages, lymphocytes
as well as plasma cells. In addition, there is a varying but often form The production of cytokines at the sites of inflammation in
substantial proliferation of fibroblasts forming collagen, blood vessels the oral tissues is part of the host response which is essentially
and of tissue histiocytes. protective in nature. Both under-activity (hypo-responsiveness)

Citation: Silva L (2016) A Literature Review of Inflammation and Its Relationship with the Oral Cavity. Glob J Infect Dis Clin Res 2(1): 001-007. DOI:
10.17352/2455-5363.000006
002
Silva. (2016)

and over-activity (hyper-responsiveness) of the host response, soluble decoy receptor, osteoprotegerin, by osteoblast/stromal cells
such as unrestricted production of cytokine(s), may result in tissue [19].
destruction. Traditionally, the immune functions have been thought
As for what concerns root resorptions; one study showed that
to be regulated by signals originating within the immune system. It is
only interleukin-1α has a potent capacity, to increase it [20].
now evident that the immune system is regulated in part by the central
nervous system (CNS), acting principally via the hypothalamic- ESSAYAN, 1998 studied the role of the IL-1 cytokine family
pituitary adrenal (HPA) axis and the sympathetic nervous system (interleukin-1), which represents a group of proteins that possesses
(SNS) [8,9]. The pathways between immune system and brain seem synergic and contrasting biological responses. In agreement with
to be bidirectional and the aim is maintenance of homeostasis. The their study, IL-1 and its precursory forms are strongly involved in the
SNS provides a major integrative and regulatory pathway for this establishment of inflammation and host defense [21]. The continuous
communication. The sympathetic innervation of lymphoid tissue, exposure too many sorts of biological, physical and chemical agents
the presence of adrenergic receptors on immune cells (B and T makes the mouth more prone to inflammation and infections,
lymphocytes, macrophages) and studies of catecholamine interactions mainly caused by bacterial influence. Its main tissues are, in normal
with the immune system [10], provide substantial evidence for the conditions, well adapted to endure; supporting even abrupt thermal
role of SNS in immune regulation. Furthermore, the cellular products changes, but sometimes, as a result of low immunity or high virulence
of an activated immune system, namely cytokines, can signal to the of a determined agent (or even a combination of both), it may develop
brain. The cytokines TNF-α, IL26 1 and IL-6 seem to be involved in an inflamed site elsewhere in the mouth, where varieties of anaerobic
the cross-talk between brain and immune system via corticotropin- gram negative bacteria exist and the LPS (lipopolysaccharide – a
releasing hormone (CRH) secretion and hence, they activate both the bacterial pathogenic element) of such bacteria is thought to be
HPA and the SNS [11,12]. a virulence factor which plays a role in the development of dental
diseases [22-24]. Once inflammation such as pulpitis, gingivitis,
The development of methods for the study of leukocyte migration or periodontitis has been established, an inflammatory infiltrate
in vitro [13], facilitated the discovery of several chemoattractants, such is formed consisting of different cell types such as neutrophils,
as complement fragments C3a and C5a, arachidonic acid derivatives macrophages and lymphocytes which will produce different cytokine
such as leukotriene B4 (LTB4) and 12-hydroxy-eicosanotetraenoic subtypes responsible for the immunopathology of the diseases.
acid (12-HETE), and platelet activating factor (PAF) [14].
Chronic marginal gingivitis is characterized clinically by
Inflammation in the oral cavity gingival redness, edema, bleeding, changes in contour, loss of tissue
The oral cavity is exposed in many ways to a number of potential adaptation to the teeth, and increased flow of gingival crevicular fluid
microbial agents firstly because of its main functions: nourishment and (GCF) [25,26]. Its origins is usually associated with dental plaque
communication. Other than these factors, some treatments applied which irritates the surrounding tissues because of the release of toxins
on the teeth may favor the deposition of dental plaque associated with produced by microorganisms and the natural course of the disease
extra strength applied on the teeth, like orthodontics. Even more, may many times be modified by the action of hormones. Pregnancy
inflammation in orthodontics also comes from the forces applied is accompanied by an increase in the levels of both progesterone and
on the teeth, and the presence of osteoclasts at location of alveolar estrogen which, by the third trimester, reaches levels 10-30 times than
bone remodeling is antecedent to orthodontic tooth movement. Cell seen during the typical menstrual cycle. The changes in the levels of
recruitment and clearance are the mechanisms by which osteoclast hormone lead to the conclusion that female steroid hormones may
population are regulated [15]. During orthodontic force application, have dual effects on the pathogenesis of pyogenic granuloma in
the periodontal ligament (PDL) undergoes hyalinization, a light pregnancy.
microscope term describing the loss of cells from an area of the
Development of gingivitis necessarily requires the presence of
ligament because of necrosis. This tissue damage prevents the tooth
plaque bacteria [27,28] which is believed to cause pathological changes
from moving until the adjacent bone and the necrotic tissue are
in the tissues by both direct and indirect means [29]. Histopathologic
removed by osteoclasts. As a result, the tooth movement reaches a
observations have led to the subdivision of gingivitis into 3 stages,
plateau which lasts about 10 to 20 days in humans [16,17].
which are divided didactically for the understanding of the process.
Periodontitis and pulpitis are the most common infections in The first stage usually begins with an initial lesion which appears
odontology and are indeed commonly found in the daily practice 2 or 4 days after initial injury, where there is a transitory period of
in surgery offices. Periodontitis shares many pathologic features vasoconstriction followed by vasodilatation and consequent increase
with other inflammatory diseases with concomitant bone resorption of blood flow that brings along neutrophils (PMNs), progressively
such as rheumatoid arthritis (RA), with accumulative evidence that adhering to the endothelial walls getting ready for diapedesis.
both conditions manifest as a result of an imbalance between pro- Vascular changes and collagen degradation represent the initial
inflammatory and anti-inflammatory cytokines [18]. The increased changes probably due to chemotactic attraction of neutrophils to the
local production of pro-inflammatory cytokines either directly contaminated area by direct vasodilatory effects of bacterial products,
enhances the proliferation and/or activity of cells in the osteoclast as well as activation of host systems such as the complement and
lineage or indirectly affects the production of the essential osteoclast kinin systems and arachidonic acid pathways [30]. The second stage
differentiation factor, receptor activator of NF-κB ligand, and/or its is a continuation of the process represented by the persistence of the

Citation: Silva L (2016) A Literature Review of Inflammation and Its Relationship with the Oral Cavity. Glob J Infect Dis Clin Res 2(1): 001-007. DOI:
10.17352/2455-5363.000006
003
Silva. (2016)

acute inflammatory response. Capillaries engorge and proliferate as a but also allergic and neoplasic diseases have been attributed to
result of blood congestion, which increases the permeability and the the imbalance between pro-inflammatory and anti-inflammatory
inflow of plasma and the diapedesis, with a mixture of the first lineage cytokines and therefore, the regulation of pro/anti-inflammatory
of immune cells, which is unspecific, and the adaptive immunity, with cytokines has attracted considerable interest [46]. Components of the
the lymphocytes as their main representatives, preparing the area for innate immunity such as antigen presenting cells (APCs), dendritic
a transition from acute to chronic. And finally the third stage would cells, and monocytes/macrophages, as well as components of the
be the establishment of chronic gingivitis characterized by slow acquired (adaptive) immunity such as T helper (Th) lymphocytes, are
venous return and color change from red to blue hue and the intense all involved in immunoregulation.
population of lymphocytes B and the formation of granulation tissue
To mediate an effective response, leukocytes must find their way
rather than collagen bundles [31].
to sites of infection or inflammation. Leukocyte invasion of tissues
In situ production of pro-inflammatory cytokines is generally seen can be induced by chemotactic activity of several substances—
in inflamed pulp and/or gingiva as part of the inflammatory response including interleukin-1 (IL-1), tumor necrosis factor- (TNF-α),
[32,33]. The clinical signs and the discomfort of gingivitis have been and bacterial lipopolysaccharide (LPS)—that cause leukocyte
attributed to pathological tissue changes which commit gingival emigration when injected in vivo [47]. All such compounds induce
microcirculation [34], a mechanism which involves capillaries and the production of chemoattractants, which in turn cause leukocyte
small venules right at the site of injury and the adjacent arterioles. migration. Therefore, chemotactic activity includes the receptor-
Bacterial LPS and cytokines have only been implicated in the vascular mediated gradient perception and must be measured by the ability
component of edema formation [35], however their possible effect on of a chemoattractant to induce directed leukocyte migration in vitro
the interstitium has not yet been explored. Following the expectable [47].
path of untreated gingivitis, it can progress to a more severe stage The antigen presenting cells (APC) are those that express high
when the inflammatory process extends to the periodontal ligament levels of class II MHC molecules; with internalizing ability to process
and alveolar bone, compromising directly the anchoring apparatus of and expose foreign antigens in the fitting MHC. Therefore, the immune
the teeth [36]. response comes mainly from the action of four cellular types: T cells
On the other hand, in periodontitis, bone resorption is mediated (fundamental in the elimination of intracellular pathogens such as
largely by the increased local production of pro-inflammatory virus and bacteria) through the generation of cytotoxic T cells. B cells,
cytokines, such as IL-1α, IL-1β, and TNF-α. The LPS released from which defend the organism against extracellular pathogens by the
the periodontopathic bacteria triggers the synthesis of IL-1 and production of antibodies. Natural killer cells (NK), which constitute
TNF-α from macrophages. IL-1 and TNF-α stimulate the production a subseries of positive cytotoxic lymphocytes CD56, which, in spite
of a variety of other inflammatory mediators (cytokines, nitric of belonging to the innate immunologic system for not presenting
oxide and PGE2), matrix-degrading enzymes (metalloproteinases), surface receptors, are fundamental for the recognition of pathogens,
and decrease the synthesis of glycosaminoglycans, enhancing bone and Dendritic cells (DC), cells, which activate the immunologic
destruction [37,38]. response by the exhibition and consequent presentation of foreign
antigens to the T cells [48,49].
The degradation and removal of hard tissue are a cellular
event brought about by giant multinucleated cells formed through Th lymphocytes are divided into two subclasses; Th1 and Th2.
asynchronous fusion of mononuclear cells belonging to the Th1 cells primarily secrete IFN-γ, and IL-2 which enhance cellular
macrophage lineage and originating from the hematopoietic system immunity, whereas Th2 cells secrete a different set of cytokines,
[39]. They are called clasts and are easy to identify under the light primarily IL-4, IL-10, IL-13 and IL-9, which enhance humoral
microscope because of their size (50 to 100µm), their multinucleation immunity [50,51]. The antigen –inexperienced (naïve) CD4+ Th0
(2 to 10 nuclei per cell), and their association with the surface of bone cells can differentiate to either Th1 or Th2 and the differentiation is
(occupying shallow depressions known as Howship´s lacunae). Such strongly dependent on the cytokines produced by cells of the innate
cells are also intermediated by cytokines who induce and stimulate immune system [51]. IL-12 produced by activated monocytes/
their recruitment. macrophages, represents a major inducer of Th1 differentiation and
hence cellular immunity. IL-12, together with TNF-α and IFN-γ act
The field of odontology which deals with bone resorption synergistically in inflammation and further promote Th1 responses
and neoformation is orthodontics, for the fact that its basis is and hence considered major pro-inflammatory cytokines [51]. Th1
the application of mechanical forces which produce organized and Th2 responses are mutually inhibitory. Thus IL-12 and IFN-γ
periodontal tissue remodeling generating tooth movement, with inhibit Th2 and vice versa, IL-4 and IL-10 inhibit Th1 responses
forces transmitted from the dental roots to the periodontium where and the production of pro-inflammatory cytokines. IL-4 and IL-10
cells are stimulated to remodel the surrounding matrices. The forces are the major anti-inflammatory cytokines and an increasing body
applied will necessarily cause an inflamed area in the surrounding of evidence suggests that catecholamines inhibit selectively the
tissues of a tooth, causing bone resorption in the pressure sites and Th1 functions and pro-inflammatory cytokines and favor the Th2
bone deposition in the tension sites [40-43]. There seems to be a role responses and anti-inflammatory cytokines [8].
of cytokines such as IL-1α, IL-1β, and TNF-α in the process [44,45].
Cytokines and chemokines are redundant secreted proteins with
As previously mentioned, several infectious, autoimmune, growth, differentiation, and activation functions that regulate and

Citation: Silva L (2016) A Literature Review of Inflammation and Its Relationship with the Oral Cavity. Glob J Infect Dis Clin Res 2(1): 001-007. DOI:
10.17352/2455-5363.000006
004
Silva. (2016)

determine the nature of immune responses and control immune cell interstitial fluid through pores and intercellular clefts in the capillary
trafficking and the cellular arrangement of immune organs. Which endothelium. Under physiologic conditions, the endothelium of the
cytokines are produced in response to an immune insult determines capillaries and proximal portion of the venules forms a semipermeable
initially whether an immune response develops and subsequently membrane that permits free movement of water and small molecules
whether such response is cytotoxic, humoral, cell-mediated, or to and fro across the endothelium but normally restricts the passages
allergic [52]. Cytokines act on cells through transmembranase cell of plasma protein. The capillary wall acts as a filtration “barrier”.
surface receptors. Binding of the cytokine to the receptor elicits its Fluid equilibrium across this endothelial barrier is maintained by
cellular response by activating an intracellular signal transduction the hydrostatic pressure of the capillary blood being balanced by the
pathway that ultimately leads to induction of new gene transcription equal and opposite restraint of the osmotic pressure of the plasma
and systhesis of new cellular proteins. Most cytokine receptors signal proteins. Most of the fluid within the capillaries is retained, but some
using one of the Janus Kinase (Jak) family of proteins. Specific Jak fluid filters normally through pores between the cells, pushed by the
proteins associate with the cytoplasmatic domains of cytokine pressure difference between the capillary blood and the IF. Water and
receptors. When binding the cytokine activates the receptor, the Jak small solutes can pass freely through these pores. The net effect of
phosphorylates its respective STAT protein, causing the STAT to the hydrostatic pressure alone is a net loss of water and solutes from
dimerize and translocate into the nucleus, where it initiates new gene plasma to the IF. The capillary wall is, however, nearly impermeable
transcription [3]. to the plasma proteins and lipids but following inflammation, the
capillary permeability for proteins increases. Because the capillary
Increased vascular permeability can be induced by cytokines such wall is permeable to water, but essentially impermeable to the plasma
as IL-1 and TNF-α acting either directly at the endothelial cells or proteins, these molecules generate a colloid osmotic pressure gradient
indirectly by inducing other inflammatory mediators that affect the that draws water out of the interstitium and into the plasma. This
vascular endothelium [53,54]. In addition, LPS can increase vascular pressure is proportional to the difference in protein concentration
permeability not only through induction of pro-inflammatory between the plasma and the IF.
cytokines, but also affecting directly the endothelial barrier [55,56].
Nevertheless, there is little information available regarding intra-
The periapical lesion represents a product of the body’s immune and extra-vascular fluid volumes in dental tissues (oral mucosa, pulp)
response to bacterial infection of the pulp, with the purpose to wall- during health and disease. The absence of such information from the
off the infection within the confines of the root canal system [57]. In dental pulp is mainly due to the nature of the tissue that does not
many respects this periapical inflammatory response recapitulates the allow easy access to the interstitium. Its inextensible walls creates a
pulpal response to infection, with the additional feature of periapical hermetic cavity inside which blood runs bringing in nutrients and
bone destruction. A mixed infiltrate of T and B lymphocytes, defense cells, while removes metabolic wastes from inside the pulp.
polymorphonuclear leukocytes (PMNs), macrophages, plasma However, attempts have been made to isolate dentinal fluid, which
cells, natural killer (NK) cells, eosinophils and plasma cells has been is a pulpal IF that moves across the dentinal tubules, in order to
characterized [58-63]. NK cells are thought to represent a third lineage measure COP and protein concentration [69-71]. In order to collect
of lymphoid cells which, when activated, have the morphology of a dentinal fluid, it is mandatory to drill a deep cavity in the dentin and
large granular lymphocyte [3]. the consequent removal of the smear layer. These are rather invasive
There are controversial results regarding the predominant procedures that may affect the pulpal blood flow and subsequently
infiltrating cell type in periapical lesions. Such periapical alterations the rate and direction of dentinal fluid flow [72,73]. The radius of the
are didactically postulated as chronic lesions with either lymphocytes exposed tubules [74], and the disruption of the odontoblast layer as a
[64,65], or macrophages [61,63] generally reported to be most result of the preparation trauma [75], may yet influence the dentinal
numerous. T cells consistently outnumber B cells [65,66]. Of the T fluid composition regarding plasma proteins. It is therefore evident
lymphocytes, both Th and T suppressor cells have been identified that there is a need for a less invasive and traumatic method for the
with temporal differences regarding their relative concentration due isolation of pulp IF in order to explore its microenvironment.
[63,66,]. The variety of inflammatory cells reveals that both non- Conclusions
specific and specific immune responses are mediated in the pulp and
periapical tissues in response to infection. Therefore, the periapical Inflammation is a complex process and a necessary defense
lesion provides a suitable model for studying local immune responses. strategy in search of the reestablishment of health. Its classification,
The superior cervical ganglion (SCG) supplies with sympathetic cell types involved, cytokines and chemokines and other substances
innervation the oral tissues [67,68]. By removal of the SCG, the local give us a hint of its nature and importance, although much more is to
control of immune responses by sympathetic nerves can be studied in be discovered, mostly as for what concerns the oral cavity.
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Citation: Silva L (2016) A Literature Review of Inflammation and Its Relationship with the Oral Cavity. Glob J Infect Dis Clin Res 2(1): 001-007. DOI:
10.17352/2455-5363.000006
007