1. The document discusses the host defense mechanisms in the gingiva and periodontium. It describes the roles of saliva, gingival epithelium, gingival crevicular fluid, complement system, and inflammatory cells like neutrophils, macrophages, and lymphocytes in the defense against bacteria. 2. The key inflammatory cells - neutrophils, macrophages, and lymphocytes - work together to detect bacteria via chemotaxis, phagocytose and kill them using various mechanisms, and induce adaptive immune responses through cytokine signaling. 3. The complement system aids in this process through opsonization, chemotaxis, and cytolysis of bacteria. Together these host defenses maintain homeostasis against the bacterial challenge in the

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Host Responces Basic Concepts
Health
“dynamic state in which the living and functioning organism or tissue remains
in balance with a constantly changing environment.”
Thisconstant process of readjustment to maintain a functional integrity is
known as “Homeostasis”.

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ROLE OF SALIVA IN THE HOST DEFENCE
1. A vehicle for swallowing bacteria.
2. Inhibition of attachment
3. Bactericidal action by the
4. Bactericidal action by lysozyme
ROLE OF SALIVA IN THE HOST DEFENCE
bacteria.
of bacteria.
3. Bactericidal action by the peroxidase system.
lysozyme, lactoferrin and other factors.
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factors.

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GINGIVAL EPITHELIUM
Gingival epithelium has three functions:
1. Epithelial cells are tightly attached to each other.
2. Keratinization to resist trauma.
3. Presence of permeability barriers

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GINGIVAL CREVICULAR FLUID
Gingival crevicular fluid functions are:
1. Washing nonadherent bacteria and their products out of the crevice.
2. Reducing the diffusion of plaque products into the tissues.
3. It also carries a steady supply of inflammatory mediators, protease
inhibitors and host defence agents such as complement and antibody, into the
crevice

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COMPLEMENT
The functions of complement are:
a. Chemotaxis cellular activation: Complement products released in this
reaction attracts phagocytes to the site of infection, e.g. C3a and C5a.
b. Opsonization: Once they arrive at the site of infection the complement
components coat the bacterial surface and allow the phagocytes to recognize
the bacteria and thereby facilitating the bacterial phagocytosis, e.g. C3b.
c. Cytolysis: Damage to the plasma membranes of the cells can lead to lysis of
the cell, e.g. C1-C9.

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THE INFLAMMATORY CELL RESPONSE
Is by
Neutrophils
Macrophages
And lymphocytes

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Neutrophils
They are the initial leukocytes seen in the gingiva. They exit the circulation and
migrate into the junctional epithelium and gingival crevice, where they provide
the first cellular host mechanism to control periodontopathic bacteria
Entothelium lumen  Adherence (Rolling and margination) Dipedesis and
interendothelial transmigration
two phases of leukocyte endothelium adherence.
a. The selectin-dependent phase (primarily in rolling and margination).
b. The integrin-dependent phase (primarily in diapedesis)

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L-Selectin  Expressed on surface of leuckocyte
P-Selectin  On endothelial cells in granules
E-Selectin  Expressed by endothelial cells
Functions of Neutrophils
Emigration and Chemotaxis:
Expressed on surface of leuckocyte
On endothelial cells in granules
Expressed by endothelial cells
Chemotaxis:
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Stages in neutrophil chemotaxis
Stage I: Soluble products diffuse forming a concentration
Stage II: Resting neutrophils detect chemotaxins using
Stage III: Receptors move to front of neutrophils, which
Stage IV: Neutrophils crawl up to the concentration gradient.
Stage V: When concentration is constan
Stages in neutrophil chemotaxis
diffuse forming a concentration gradient.
ophils detect chemotaxins using surface receptors.
to front of neutrophils, which becomes polarized.
Stage IV: Neutrophils crawl up to the concentration gradient.
Stage V: When concentration is constant, directional migration ceases.
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gradient.
surface receptors.
becomes polarized.
migration ceases.

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Phagocytosis
Arrival  recognize  attach through receptors
Lysozyme + phagosome  phagolysozyme and finally killing
attach through receptors  engulf by pseudopodia
phagolysozyme and finally killing
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engulf by pseudopodia

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Opsonins  IgG and C3b
Various killing mechanisms are activated after phagolysozyme formation
A. Nonoxygen-dependent killing mechanisms.
B. Oxygen-dependent killing mechanisms.

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Functions of Macrophages in the Gingiva,
Macrophages develop from blood
from the blood and are triggered
cytokines, other inflammatory mediators, bacterial products such as
endotoxins.
Functions of Macrophages in the Gingiva, Crevice and Pocket
lop from blood monocytes, which emigrate into the tissues
from the blood and are triggered to develop into mature macrophages
inflammatory mediators, bacterial products such as
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emigrate into the tissues
develop into mature macrophages by
inflammatory mediators, bacterial products such as

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Functions of macrophages
1. Phagocytose and kill bacteria.
2. Remove damaged host tissue during inflammation.
3. And also trap and present antigens to lymphocytes for induction of immune
responses.
Most of the above mentioned functions are carried out through the secretion
of inflammatory mediators, including cytokines, prostaglandins, leukotrienes
and complement components

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The most significant cytokine in inflammation is interlenkin-1 (IL-1), which is a
key mediator both in inflammation and immunity-induced by bacteria. Tumor
necrosis factor (TNF) is also produced by macrophages. Both TNF and IL-1 have
similar functions
They increase inflammation by, releasing histamine from mast cells, attracting
neutrophils and more macrophages into the tissues and by causing many other
cells to release prostaglandins
In excess amounts IL-1 and TNF can have several damaging effects such as
stimulation of bone resorption and tissue fibrosis

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Other cells such as mast cells, fibroblasts, endothelial cells, plasma cells and
epithelial cells are also seen in gingival connective tissue during inflammatory
response

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Lymphocytes
3 types
1.. T-Cells  derived from Thymus  cell mediated immunity
2.. B-Cells  derived from liver, spleen, bone marrow  humoral immunity
3.. NK
T-Cells
 TH cells (CD4)
Differentiate B-cells into plasma cells  and then AB  release IL-2 & INF
 TS cells (CD8)
Stimulate cytotoxic and microbicidal aactivity of immune cells  release
IL-4 and IL-5

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Humoral Response
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Cellular Response
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