Immune system - Specifics of
children's immunity
Oral immunity and
immunopathological processes in
the mouth
• Microorganisms are in the air we breathe and in/on the
food we eat;
• Thus our epithelial surfaces are continuously exposed
to microorganisms;
• Disease occurs when microorganisms invade epithelial
• However, we have a long infection-free periods and that
infections are the exception rather than the rule;
• This resistance (immunity) of epithelial surfaces to
invasion, is a characteristic which is present from birth,
and is therefore called innate (natural) immunity.
• A complex of physiological processes whose
function is to store the constancy of the internal
environment of the body;
• Protects the body from all foreign endogenous
and exogenous factors.
Innate Immunity
• This prevents entry of microorganisms into
tissues or, once they have gained entry,
eliminates them prior to the occurrence of
• Present from birth;
• Non-specific - acts on many organisms and does
not show specificity;
• Does not become more efficient on subsequent
exposure to same organisms.
Prevention of entry of organisms
• Mechanical barriers at body surfaces, skin,
mucous membranes - disruption leads to
• Antibacterial substances in secretions, lysozyme,
lactoferrin, low pH of stomach contents.
The immune system is composed of
two main categories:
• Nonspecific immunity - provides general
▫ First line of defense;
▫ Second line of defense;
• Specific immunity - the body recognizes specific
▫ Third line of defense.
Nonspecific immunity
• First line of defense:
▫ mechanical barriers;
 Skin;
 Mucosa;
▫ Chemical barriers:
 Saliva:
 Enzymes;
 Secretory immunity.
Second line of defense
• Nonspecific inflammation;
• Phagocytosis:
▫ Neutrophils;
▫ Macrophages;
▫ Histiocytes;
• Natural "killer" cells:
▫ Kill tumor cells;
▫ Kill infected cells.
Nonspecific protective factors
• Tissue factors;
• Cellular factors;
• Humoral – mediators.
Tissue factors
• Skin;
• Mucosa;
• In the mouth - continuous oral mucosa.
Cellular factors
Act after overcoming tissue barrier;
Vascular cell phenomenon – inflammation;
Sensitized cells;
From the stem cells of the bone marrow;
Hematopoietic - neoplastic cells;
Cells of specific immunity.
Protection`s cells
• Macrophages;
• Microphages;
▫ PMNs;
▫ Three cell populations;
▫ Mature cells:
Mast cells;
Killer cells.
The light micrograph
shows the multilobed nucleus,
because of which these cells are also
called polymorphonuclear
leukocytes, and the faint cytoplasmic
• Mononuclear phagocytes;
• Derived from monocytes;
• They are:
▫ Histiocytes;
▫ Fixed macrophages (in the lymph nodes and
▫ Osteoclasts;
▫ Kupffer cells;
▫ Microglial cells;
▫ Langerhans cells.
Characteristics of the macrophages
• They have receptors for:
• Cause "oxidative burst“:
Released superoxide anion;
It turns into H2O2;
Kill pathogenic factor;
Digest it intracellularly.
The next steps are:
They transfer antigens to lymphocytes;
lymphocytes are sensitized;
Induce a specific immune response;
Separate bioactive substances;
Regulate the immune response.
Microphages (granulocyte) - PMNs
• Neutrophils:
Involved in inflammation;
Separate membrane oxidases;
Include object within the cell;
Forming phagosomes;
• Eosinophils:
▫ Regulate allergic reactions:
Growth factors.
• Basophils
Anaphylactic degranulation;
Mediated by IgE antibodies;
Receptors binding;
Mast cells
Involved in non-specific inflammation;
In allergic reactions of immediate-type;
In degranulation;
Released histamine:
Hyaluronic acid.
• They are nuclear-free cytoplasmic fragments;
• They are derived from bone marrow
• They have haemostatic function;
• Involved in coagulation.
Killer cells
They represent a third population lymphocytes;
They are located in the circulating blood;
They have a cytotoxic effect;
Participate in the second line of defense.
Mediators of inflammatory response
• Bioactive substances:
▫ From the plasma;
▫ From different cells;
• Their production is stimulated by:
▫ Microorganisms;
▫ Own proteins;
Mediators effect of the inflammatory
By binding to the receptors;
By target cells;
Direct enzyme activity;
Or oxidative degradation;
The mediators of the the inflammatory
response are:
• Vasoactive amines;
• Plasma proteins;
• Interferons.
Vasoactive amines
• Histamine:
▫ Released from mast cells;
▫ Influences:
 Smooth muscle fibers;
 Small blood vessels;
▫ Inflammatory action:
 Inhibits lysosomal enzyme;
 Inhibits chemotaxis.
Synthesized in nerve endings;
Shortens the smooth muscle fibers;
Dilates blood vessels;
Increased permeability.
Plasma proteins
• Complement system;
▫ It consists of 20 serum proteins;
▫ They react with the cascade of reactions;
▫ The enzyme catalyzes the reaction of a following:
 They are involved in specific
 and nonspecific protection.
Kinin system
• Plasma proteins of the beginning of the reaction;
• Bradykinin:
Increases vascular permeability;
Causes contraction of smooth muscle fibers;
Follows vascular dilatation;
Causes a pain.
Coagulation system
• Activated by various substances in the tissue
• Stops the movement of microorganisms;
• Makes them available for phagocytosis;
• Stops bleeding;
• Decreased neutrophil chemotaxis;
• Reduces permeability.
Other mediators - interferons
• They are low molecular weight proteins:
▫ Leukocytes - α-interferon;
▫ Fibroblasts - β-interferon;
▫ Lymphocytes - immune interferon;
• Their action is to block:
▫ Replication of the viral RNA;
▫ The reproduction of the tumor cells;
▫ Regulate the immune system.
Arachidonic acid
lipid mediator;
Formed quickly;
Acts locally;
It produces:
▫ Prostaglandins;
▫ Leukotrienes;
▫ Hypoxines.
Nonspecific defense mechanisms
Inflammatory reaction
Major defense mechanism;
Is a sequence of vascular and cellular reactions;
They provide counteraction of the pathogens;
The basic phenomenon of the inflammation is
Types of inflammation
• Nonspecific inflammatory response:
▫ Before the formation of antibody;
• Specific inflammatory reaction:
▫ At the second meeting with the pathogen antigens;
▫ Or at a later stage of the initial meeting;
• Sensitization occurs of the immunocompetent
• It include specific immune responses.
The process of the inflammation
• Starting with local hypoxia;
• Starting release of the vasoactive substances;
• Separated the histamine, serotonin, prostaglandins,
• They cause vasodilation;
• This leads to congestive hyperemia;
• Follows hypoxia;
• The next result is acidosis;
• Began massive migration of the microphages and
• Performed phagocytosis.
Phagocytosis is mediated
by macrophages and polymorphonuclear
• Phagocytosis involves the ingestion and
digestion of the following:
Insoluble particles;
Damaged or dead host cells;
Cell debris;
Activated clotting factors.
1.Phagocytosis -
ingestion and killing of
microorganisms by specialised cells (phagocytes)
• Phagocytes - polymorphonuclear leukocytes
• Mononuclear phagocytes (monocytes,
• 2. Opsonisation - the process of coating microorganisms with some of the proteins found in
plasma, to make them more easily
• Complement and phagocytes exist mainly in
blood so a mechanism is required to recruit
these elements to the site of tissue invasion.
Inflammation involves:
• a) opening up of junctions
between endothelial cells in
post-capillary venule to allow
plasma proteins to escape;
b) adhesion of leukocytes to
endothelial cells of postcapillary venule, followed by
emigration of phagocytes
into tissues.
• Inflammation is localised to
area of infection or tissue
injury by release of
substances from microorganisms or chemicals
(chemical mediators)
released from cells in tissues,
e.g. histamine from MAST
CELLS. Once organisms
destroyed inflammation
settles down (RESOLVES).
There are several stages of
1. Chemotaxis;
2. Adherence;
3. Pseudopodium formation;
4. Phagosome formation;
5. Phago-lysosome formation.
1. Chemotaxis
• This is the movement of cells up a gradient of
chemotactic factors;
• It may be directly induced by a substance,
produced as a result of complement activation;
• It can also be indirectly induced as a
consequence of release of preformed mediators
within mast cells by the action of eosinophil
chemotactic factor, or neutrophil chemotactic
• Leukotrienes, produced by the metabolism of
mast cell arachidonic acid, are also chemotactic.
2. Adherence
• This works reasonably well for whole bacteria or
viruses, but less so for proteins or encapsulated
• In order to deal more effectively with
encapsulated bacteria, antibodies directed
against the capsule enable the phagocytic cells to
ingest the organisms, using their Fc receptors.
• Performed by serum opsonins;
• Some objects have receptors for antibodies and
• Their presence facilitates adhesion.
3. Pseudopodium formation
• This is the protrusion of membranes to flow
round the "prey".
4. Phagosome formation
• Fusion of the pseudopodium with a
membrane enclosing the "prey" leads to the
formation of a structure termed a phagosome.
5. Phago-lysosome formation
• The phagosome moves deeper into the cell, and fuses
with a lysosome, forming a phago-lysosome;
• These contain hydrogen peroxide, active oxygen species
(free radicals), peroxidase, lysozyme and hydrolytic
• This is known as the oxidative burst, and leads to
digestion of the phagolysosomal contents, after which
they are eliminated by exocytosis;
• Some peptides however, undergo a very important
separate process at this stage;
• Instead of being eliminated, they attach to a host
molecule and end up being expressed on the surface of
the cell within a groove on the molecule (antigen
The speed of phagocytosis can be increased
markedly by bringing into action two attachment
devices present on the surface of phagocytic
• Fc receptor: which binds the Fc portion of antibody
molecules, chiefly IgG. The IgG will have attached the
organism via its Fab site.
• Complement receptor: the third component
of complement (C3) also binds to organisms and then
attaches to the complement receptor.
• This coating of the organisms by molecules that speed up
phagocytosis, is termed 'opsonization', and the Fc
portion of antibody, and C3 are termed 'opsonins'.
Invagination of the cell wall;
Coverage of the site;
Formation of phagosomes;
Fusion with the lysosome;
Phagolysosome formation;
Follows hexose-monophosphate cycle;
Release of superoxide anion;
Superoxide explosion;
Digestion - enzymatic digestion
• Phagocytosis graduated with digestion;
• At incomplete phagocytosis part of the
pathogenic properties of the particles are
• Microphages digest them completely;
• Macrophages digest them partially.
Specific immunity - the third
line of defense
Specific immune responses after
primary inflammation - acquired
Acquired Immunity (adaptive
Immunity/specific Immunity)
• This type of immunity occurs in response to
infection called ADAPTIVE as the immune system
must adapt itself to previously unseen molecules;
• Following recovery from certain infections with a
particular microorganism, individuals will never
again develop infection with the same organism, but
can become infected with other microorganisms;
• This form of protection is called IMMUNITY and
an individual is said to be IMMUNISED against
that organism;
• The induction of immunity by infection or with a
vaccine is called ACTIVE IMMUNITY.
• Historically it has been shown that a nonimmune individual can be made immune by
transferring serum or lymphocytes from an
immune individual - PASSIVE IMMUNITY ;
• In passive immunity are involved:
▫ Serum constituents (antibodies);
▫ Lymphocytes.
Immune system responds to microorganisms but not to its
own cells and that the system knows that the body has
been infected previously with a particular organism
• This implies:
Immunity is mediated by the IMMUNE SYSTEM,
which responds to infection by mounting an
• An immune response must:
▫ RECOGNISE a microorganism as foreign (nonself) as distinct from self (AFFERENT LIMB);
▫ RESPOND to a micro-organism by production of
specific antibodies and specific lymphocytes;
▫ MEDIATE the elimination of micro-organisms
• An agent which evokes an immune response is
called an IMMUNOGEN.
• The term ANTIGEN is applied to a substance
which reacts with antibody.
Cellular Basis Of Immune Response
• Key cells are lymphocytes - have capacity to
recognise microorganisms;
• There are two types which develop in bone
marrow from a common precursor:
▫ T-cells - mature in thymus;
▫ B-cells - mature in bone marrow;
• These two types of lymphocyte are used in 3
ways to fight infection.
Strategy One: elimination of
extracellular microorganisms
• In response to infection B-cells mature into
PLASMA cells which secrete soluble recognition
molecules (ANTIBODIES);
• B-cells recognise microbes because they express
membrane bound antibody which acts as an antigen
• At time of first infection there is no antibody in
blood and level does not begin to increase until
between 7-10 days afterwards;
• The level of antibody rises slowly to a low peak and
then gradually declines towards baseline PRIMARY RESPONSE.
• On subsequent exposure to same microorganisms the level of antibody begins to
increase within 24 hours and reaches a high
level which is sustained.
Epitope or Antigenic determinant
• Antibody recognises structures on surface of
bacteria - proteins, carbohydrates, lipids;
• When we have an infection we produce antibodies
which recognise many different types of structure on
bacterial surface;
• Thus serum from an immune individual contains
many different types of antibodies each of which
recognise different structures on surface of
• Each of these structures is called an epitope
or antigenic determinant.
Effector mechanisms
• Antibody is soluble and diffuses through tissues
to target extracellular microorganisms;
• Binding of antibody to microorganisms activate
two effector mechanisms to eliminate microorganisms;
▫ Activation of complement system - bacterial lysis
or opsonisation;
▫ Phagocytosis by neutrophils and macrophages
with intracellular killing.
Strategy Two: Elimination of microorganisms which normally survive for
long periods in macrophages
• Even when antibody and complement opsonise certain
bacteria and phagocytosis occurs, they are not killed but
survive and multiply in macrophages (e.g.
Mycobacterium tuberculosis);
• Elimination occurs by use of a subpopulation of cells
called Helper T-cells;
• These cells recognise macrophages containing
intracellular bacteria by means of T-cells antigen
receptor, which is not an antibody;
• They help macrophages to kill bacteria by synthesising
soluble molecules (cytokines) which stimulate bacterial
killing mechanisms of macrophages.
Strategy Three -
Elimination of microorganisms
which infect cells without an endogenous
antimicrobial defence system
• Viruses are obligate intracellular pathogens, can
infect any type of cells, and most cells do not
possess antimicrobial mechanisms;
• During intracellular replication virus proteins
appear on the surface of the infected cell;
• A second subset of T-cells - cytotoxic T-cells recognises these viruses (foreign) antigens and
secretes cytotoxic molecules which kill the
infected cells.
Acquired immunity is characterized
• Specificity:
▫ Immune responses are specific to each agent
acting as an antigen;
• Memory:
▫ At repeated meeting with antigen the body
recognizes it;
▫ It acts to store their information.
Specific immune responses
• Humoral immune responses:
• Cellular immune responses.
Specific protective factors
• Antigens;
• Antibodies;
• Immune cells:
▫ T-lymphocytes;
▫ B-lymphocytes;
▫ Mediators.
• All substances carrying foreign genetic
information and which are inducing a specific
immune response.
Types of antigens
• According to the effect:
▫ Strong;
▫ Weak;
▫ Haptens – They do not form antibodies, but is connected to
• According to its specificity:
▫ Heteroantigens - of a different kind;
▫ Antigens of the same type but of another individual;
▫ Autoantigens - These antigens should, under normal
conditions, not be the target of the immune system, but,
due to mainly genetic and environmental factors, the
normal immunological tolerance for such an antigen has
been lost in autoimmune disease.
Characteristics of the antigens
Extrinsic - other than those of the host;
Antigenicity - develop antibodies;
Immunogenicity - create immunity;
Specificity - sets of sites in a protein chain called
antigenic determinants;
• High molecular weight proteins;
• Soluble and absorbable colloidal
Antigen-Antibody Interaction
• The specific association of
antigens and antibodies is
dependent on hydrogen bonds,
hydrophobic interactions,
electrostatic forces, and van
der Waals forces
• Substances that enhance the immunogenicity;
• They are in a dental plaque.
Proteins to different immunoglobulins;
Are formed at the entry of the antigen;
They are constructed from a sensitized plasma cells;
Antibodies according to the type of
Blocking monovalent antibodies.
• Proteins with a common structure and activity of
Construction of the immunoglobulin
1 – light chains;
2 – heavy chains;
3 – constant region;
4 – changing area Binding antigen.
Immunoglobulin G - dimmer
Represents 75-80% of all Immunoglobulins;
Synthesized in utero;
Cross the placental barrier;
Activates complement;
Immunoglobulin A - monomer
10-15% of the total immunoglobulin;
Do not synthesized in utero;
Do not cross the placenta;
Activates complement by alternative pathway;
There are anti-adhesive and opsonized effect;
Increases in chronic inflammation.
Immunoglobulin A - S (secretory)
• Dimer possessing a fragment of secretory
component and connecting chain;
• In the mouth is secreted from the salivary
• Participated in the first line of defense of the
enamel and lining mucosa;
• The main factor of local immunity.
immunoglobulin M
Represents 6-9% of the total immunoglobulins;
Represents a pentamer with ten active centers;
When sensitization it occurs a first;
Its synthesis begins in early childhood or first
meeting with antigens.
immunoglobulin D
• Receptor immunoglobulins of the mature betalymphocytes.
immunoglobulin E
• Antibodies of the allergic reactions;
• In the blood they are in low concentrations;
• Adsorbed to the surface of:
▫ mast cells
▫ basophil leukocytes
▫ Platelets
• Cause hypersensitivity
Action of the antibodies
Adsorption to microbial surface;
Prevent its adhesion;
Opsonized bacterial cells;
Receptor binding between phagocytic cell and the
particular antibody fragment;
Agglutinate microorganisms;
Precipitate molecular antigens;
Defense and neutralize cell;
Make them available to complement;
Neutralize viruses;
Cause hypersensitivity;
Protective or pathological inflammation.
Cytokines - common name of a group
of proteins
• Small protein molecules;
• Mediators and regulators of:
They are produced in at immune stimulus.
Types of cytokines
Lymphokines - by lymphocytes;
Monokines - from the monocytes;
Chemokines – with chemotaxis activity;
Interleukins - from one leukocyte and acting on
• Interferons.
Cytokines, due to the action
• Antiinflammatory - activate macrophages and
cellular immune response;
▫ IL 1
▫ IL 6
• Antiinflammatory - suppress cellular immune
responses and stimulate antibody-dependent
IL 4
IL 5
IL 10
IL 13
Specific immunity cells - lymphocytes
• Immunocompetent cells;
• Start development in:
Bone marrow;
lymph nodes;
There are two classes lymphocytes
• B-lymphocytes
▫ Produce antibodies;
▫ They attack the antigens;
▫ Perform antibody-dependent immunity;
• T-lymphocytes
▫ Directly attack pathogens;
▫ Mediate cell dependent immunity.
B lymphocytes and humoral immunity
• First stage of development
▫ Precursors of the B-lymphocytes the first months after
• Second stage
▫ After antigenic stimulation;
▫ Development of sensitized B-lymphocytes in the
spleen and lymph nodes;
▫ They form clonal cell lines;
▫ Produce antibodies;
▫ Connect with antigens;
▫ Antigen-antibody reaction.
Humoral immune responses - with the
participation of antibodies
• Formed antigen-antibody complexes are more
vulnerable to phagocytosis;
• Nutralization;
• Precipitation;
• Agglutination + complement;
• Improving imunoadhezion;
• Cytolysis;
• Release of mediators;
• Stimulation of immune responses.
T-cell and cell-dependent
T-lymphocytes mediate cell
immune responses
Development of T-lymphocytes
• First stage:
▫ Development of precursor Tcells (thymocytes);
▫ Derived from the bone
▫ Differentiate in the thymus;
• Second stage:
By the blood;
To T-dependent areas;
In lymph nodes and spleen;
Antigen by macrophages;
Activated surface receptors;
Repeated divisions of Tlymphocytes;
▫ A branch of the Tlymphocytes to antibody;
▫ Connect with them;
▫ Release lymphokines.
Types T-lymphocytes
• Tk - killer cells:
▫ Released lymphotoxins;
▫ Kill the target cell;
• Th - helper cells:
▫ Regulate the function of B-lymphocytes;
• Ts - suppressor cells:
▫ Inhibit the differentiation of plasma cells to Blymphocytes;
• Tm - memory cells were performed
immunological memory.
Cellular immune responses
Direct cytolysis;
Release of mediators;
TM creates immunological memory;
This Immunity is against:
The invasion tissues;
Malignant cells.
Immune tolerance
• Tolerance to the resident microflora;
• In the mouth - "adaptive immunity" or "immune
• Regulatory system and integrated processes for
maintaining immune homeostasis.
Development of the immune
system in childhood
Intrauterine development
• Passive immunity from mother
• Developing own immunoreactivity
• Protection of the fetus from congenital infections
• Rejected zero immunity;
• Presence of the phagocytic activity of:
▫ Complement;
▫ Interferon;
▫ Other factors of nonspecific immunity;
• Congenital and acquired infections occur:
▫ Undifferentiated clinic;
▫ Tendency to generalization.
Maternal antibodies
• From the second month of the infant began to
• Within six months disappear;
• When breast-fed infants are retained longer.
Oral immunity of the newborn
• Oral mucosa adapts as a barrier;
• Supported by the emergence of
immunoregulatory network;
• Depend on microbial colonization;
• Of food allergens;
• Breastfeeding is the best way to shape the
immune phenotype.
Contains immune cells;
Growth factors;
Immunoglobulin A;
Provides early postnatal development of the
secretory imunity.
Secretory IgA till 8 months is obtained
from the mother - secretion begins
Surface colonization of microorganisms;
Prevents penetration of harmful factors;
Neonatal period is critical for infections and
Between the ages of 3 and 6 months
Immune reactions are more subdued;
More difficult recovery from infections;
Low productivity of lymphoid tissue;
Homeostasis is easily broken by:
▫ Malnutrition;
▫ Antibiotics.
Between the ages of 6 and 12 months
The child is creeping;
He is started walking;
In contact with the environment;
First viral infections:
• Disease is more severe.
Aged 1 to 3 years
• Close contact with adults;
• Child is exposed to a variety of infections;
• Cross-bacterial viral, mycoplasma, viral and
▫ Immunological reactivity is better - organ
development on immune
• Serum reactions are weak
• The antibody concentration is low
• In the re-encounter with antigen antibody titer
After three years
• Viral infections occur more easily;
• Often subclinical and asymptomatic;
• In school and adolescence incidence is close to
that in adults.
immunopathological reactions
Protection and adaptation of body
Types of immunopathological reactions
• Allergic;
• Autoimmune;
• Immunodeficiencies.
Allergic reactions
• Upon re-entry of the antigen immune system
responds in three ways:
▫ A protective immune response;
▫ With increased sensitivity - an allergic reaction;
▫ No reaction – anergy.
Allergic reactions can be four
An antigen that causes an allergic
response is called an
First type - allergic immediate
Hypersensitivity by humoral type;
Called anaphylactic or atopic;
Rapid immune response involving IgE;
It binds to mast cells;
Exempt mediators.
The second type - the cytotoxic
Toxic effects on cells;
Cytolysis involving IgM, IgD and complement;
Target cells are erythrocytes, leukocytes and
Third type - the antigen-antibody
• Immediate reactions;
• Toxic effect of antigen-antibody complex.
Fourth type - cell-mediated delayed
Similar to cellular immune reactions;
Affects allergy;
Autoimmune reactions
• The immune system is tolerant to its own tissues
and antigens;
• Breach of this tolerance;
• Autoimmune reactions;
• The body produces antibodies against its own
cells and antigens.
Adaptive immunity in the mouth may
be impaired
• Commensal microorganisms have similar
• They bind to the molecules of macroorganism;
• Macroorganism did not perceive them now as
• Or develop cross-immune response;
• The body perceives its own cells as foreign.
Common autoimmune diseases
• Manifestation in the oral mucosa;
• Dermato Bullous:
▫ Pemphigus;
▫ lupus erythematodes;
▫ Epidermolysis bullosa.
Immunodeficiency states
• Deficits in the humoral immunity or in the
cellular immunity;
• Susceptibility to infections.
Congenital immunodeficiency
Heritage, most often recessive;
Rare syndromes;
Appear in childhood;
Patients do not survive long;
Infections are fatal;
Affect the oral mucosa, gingiva and
Acquired immunodeficiency conditions
Viruses and bacteria;
Prolonged cytostatics treatment ;
Corticosteroids and antibiotics.
Oral immunity - defense mechanisms
• A combination of local and systemic immune
responses and mechanisms;
• The basic function – protecting;
• Preventing the entry of foreign antigens;
• Tolerance to the resident microflora;
• Food.
Protective mechanisms of the oral
mucosa - the first line of defense
• Barrier;
• Physiological exfoliation;
• The degree of keratinization - nonspecific
• Protection, regardless of age;
• Masticatory act;
• Washout effect of saliva;
• Mucin and secretory immunoglobulin A.
Protective role of oral lymphoid tissue
• Oral immune response is carried out by:
▫ Intraoral lymphoid formations:
Palatal tonsils;
Submucosal lymphoid aggregations:
soft palate;
Floor of the mouth;
▫ Extraoral lymph nodes.
Protective role of saliva
Mechanical action;
Salivary enzymes;
Buffer systems:
▫ Bicarbonate;
▫ Phosphate;
▫ Protein;
• Secretory immunity.
Protective role of gingival fluid
• Transudate of gingival capillary network
• Dependent is:
▫ The composition of the blood serum;
▫ Permeability of the gingival epithelium;
• Permanent presence of:
▫ Phagocytic cells;
▫ Monocytes.

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