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Lectures in periodontics – 4th stage
Host – microbial interaction
Assist. Lec. Fahad M. al Dabbagh
The host response functions in a protective capacity, preventing the local
infection from progressing to a systemic, life-threatening infection.
MICROBIOLOGIC ASPECTS OF THE MICROBIAL-HOST INTERACTION:
- In general, gram-negative facultative or anaerobic bacteria appear to
represent the predominant microorganisms associated with disease.
(Predominant bacterial species that have been implicated in the disease
processes
include
Porphyromona
sgingivalis,
Actinobacillus
actinomycetemcomitans, Treponemadenticola, Bacteroidesforsythus,
Fusobacteriumnucleatum, Prevotellaintermedia, Campylobacter rectus,
Peptostreptococcus micros and Eikenellacorrodens).
- to function as a pathogen, a bacterium must:
1- Colonize the appropriate host tissue site (periodontium) and then
cause destruction of the host tissues.
2- Has the ability to evade host defense mechanisms aimed at
eliminating the bacterium from the periodontal environment.
- Thus virulence properties can be broadly categorized into two groups:
1- Factors that enable a bacterial species to colonize and invade host
tissues,
2- Factors that enable a bacterial species, directly or indirectly, to cause
host tissue damage.
A- Bacterial Adherence in the Periodontal Environment:
- The surfaces available for attachment include the tooth or root, tissues,
and preexisting plaque mass.
- Bacteria that initially colonize the periodontal environment most likely
attach to the pellicle- or saliva coated tooth surface.
B- Host Tissue Invasion (microbial colonization and proliferation within the
tissues):
1- Bacteria may enter host tissues through ulcerations in the epithelium of
the gingival sulcus or pocket and have been observed in intercellular
spaces of the gingival tissues.
Lectures in periodontics – 4th stage
Host – microbial interaction
Assist. Lec. Fahad M. al Dabbagh
2-
Direct penetration of bacteria into host epithelial or connective tissue
cells (as A. actinomycetemcomitans, P gingivalis, nucleatum and
Treponemadenticola).
- "bursts of disease activity" observed in periodontitis may be related to
phases of bacterial invasion of the tissues."' An additional possibility is
that bacteria in the tissues may enable persistence of that species in the
periodontal pocket by providing a reservoir for recolonization.
Consistent with this hypothesis is the observation that mechanical
debridement alone is insufficient, and that systemic antibiotics in
combination with surgical therapy are required, to eliminate A.
actinomycetemcomitans from lesions in patients with localized
aggressive periodontitis.
C- Bacterial Evasion of Host Defense Mechanisms.
- To survive in the periodontal environment, bacteria must neutralize or
evade the host mechanisms involved in bacterial clearance and killing.
- Periodontal bacteria neutralize or evade host defenses via numerous
other mechanisms:
Lectures in periodontics – 4th stage
Host – microbial interaction
Assist. Lec. Fahad M. al Dabbagh
Bacterial Species
Biologic Effect
Bacterial
Property
Host Defense
Mechanism
P. gingivalis
P intermedia
Degradation of specific antibody
P. melaninogenica
IgA and IgG
degrading
Specific antibody
proteases
Capnocytophaga sp.
Leukotoxin
Inhibition of PNM function
F. nucleatum
Heat-sensitive
surface
Apoptosis (programmed cell death) of
protein
PMN
P. gingivalis
Inhibition of phagocytosis
P. gingivalis
Decreased bacterial killing
A. actinomycetemcomitons
T. denticola
Killing of mature B and T cells;
nonlethal suppression of activity
Impairment of function by
A. actinomycetemcomitans
arresting of lymphocyte cell
A. actinomycetemcomitans
Inhibition of Polymorphonuclear
superoxide
production
leukocytes
Leukotoxin
Cytolethal
distending
toxin
Lymphocytes
Impairment of PMN response
P. gingivalis
Capsule
to bacteria
Inhibition of
IL-8
production by
epithelial
cells
Release of IL-8
D- Microbial Mechanisms of Host Tissue Damage:
- Some bacterial products inhibit the growth or alter the metabolism of
host tissue cells; these include
1- A number of metabolic by-products such as ammonia; volatile sulfur
compounds; and fatty acids, peptides, and indole.
Lectures in periodontics – 4th stage
Host – microbial interaction
Assist. Lec. Fahad M. al Dabbagh
2-
3-
A variety of enzymes produced by periodontal microorganisms. These
enzymes appear to be capable of degrading essentially all host tissue
and intercellular matrix molecules (proteolytic enzymes).These
soluble enzymes may digest extracellular host proteins and other
molecules and thereby produce nutrients for bacterial growth.
Bacteria may indirectly cause tissue damage is by induction of host
tissue proteinases such as elastase and matrix metalloproteinases.
- Well-characterized interactions involve the release of interleukin-1 (IL-1),
tumor necrosis factor (TNF), and prostaglandins from monocytes,
macrophages, and PMNs exposed to bacterial endotoxin
(lipopolysaccharide). These host-derived mediators have the potential to
stimulate bone resorption and activate or inhibit other host immune
cells.
Important aspects of host defense processes:
Inflammatory processes:
- Host responses may either result in
1- a rapid resolution of the lesion (e.g. a staphylococcal abscess which
heals)
2- No lesion at all develops in the affected tissue (e.g. smallpox infection
in a successfully vaccinated host).
3- An ineffective response may result in a chronic lesion that does not
resolve (e.g. tuberculosis)
4- A lesion in which the host responses contribute significantly to tissue
destruction (e.g. rheumatoid arthritis or asthma).
A-
- In the classical description of inflammation, tissue is presented that
appears macroscopically:
1- Redness and heat which due to vasodilatation and increased blood
flow.
2- Swelling is a result of increased vascular permeability and leakage of
plasma proteins that create an osmotic potential that draws fluid into
the inflamed tissues. Related to the vascular changes there is an
accumulation of inflammatory cells infiltrating the lesion.
Lectures in periodontics – 4th stage
Host – microbial interaction
Assist. Lec. Fahad M. al Dabbagh
3- Pain is rarely experienced in aggressive and chronic periodontal
disease, but could theoretically occur due to stimulation of afferent
nerves by chemical mediators of inflammation in necrotizing
periodontal disease.
4- Possible loss of function in specific sites.
B-
-
-
-
Leukocyte in dentogingival region:
Leukocytes (predominantly PMNs) are present in sulci even when
histologic sections of adjacent tissue are free of inflammatory infiltrate.
Leukocytes are attracted by different plaque bacteria
The majority of these cells is viable and has been found to have
phagocytic and killing capacity; therefore they constitute a major
protective mechanism against the extension of plaque into the gingival
sulcus.
Leukocytes are also found in saliva. The main port of entry of leukocytes
into the oral cavity is the gingival sulcus.
The number of PMNs varies from person to person at different times of
the day and is increased in gingivitis.
PMNs reach the oral cavity by migrating through the lining of the gingival
sulcus.
Living PMNs in saliva are sometimes referred to as orogranulocytes, and
their rate of migration into the oral cavity is termed the orogranulocytic
migratory rate.
Some investigators think that the rate of migration is correlated with the
severity of gingival inflammation and is therefore a reliable index for
assessing gingivitis.
Saliva:
- Secretions are protective in nature because they maintain the oral
tissues in a physiologic state.
- Saliva exerts a major influence on plaque by mechanically cleansing the
exposed oral surfaces, by buffering acids produced by bacteria, and by
controlling bacterial activity.
- Saliva contains numerous inorganic and organic factors :
1- Inorganic factors include ions and gases, bicarbonate, sodium,
potassium, phosphates, calcium, fluorides, ammonium, and carbon
dioxide.
C-
Lectures in periodontics – 4th stage
Host – microbial interaction
Assist. Lec. Fahad M. al Dabbagh
2- Organic factors include lysozyme, lactoferrin, myeloperoxidase,
lactoperoxidase, and agglutinins such as glycoproteins, mucins, ß2macroglobulins, fibronectins, and antibodies.
a- Lysozymeis a hydrolytic enzyme that cleaves the linkage between
structural components of the glycopeptidemuramic acidcontaining region of the cell wall of certain bacteria in vitro.
Lysozyme works on both gram negative and gram-positive
organisms.
b- The lactoperoxidase-thiocyanate system in saliva has been shown
to be bactericidal to some strains of Lactobacillus and
Streptococcus by preventing the accumulation of lysine and
glutamic acid, both of which are essential for bacterial growth.
c- Myeloperoxidase, an enzyme similar to salivary peroxidase, is
released by leukocytes and is bactericidal for Actinobacillus" but
has the added effect of inhibiting the attachment of Actinomyces
strains to hydroxyapatite.
Salivary Buffers and Coagulation Factors
- The maintenance of physiologic hydrogen ion concentration (pH) at the
mucosal epithelial cell surface and the tooth surface is an important
function of salivary buffers
- In saliva the most important salivary buffer is the bicarbonate-carbonic
acid system.
- Saliva also contains coagulation factors (factors VIII, IX, and X; plasma
thromboplastin antecedent [PTA]; and the Hageman factor) that hasten
blood coagulation and protect wounds from bacterial invasion. The
presence of an active fibrinolytic enzyme has also been suggested.
Leukocytes
- Saliva contains all forms of leukocytes (PMNs).
Role in Periodontal Pathology
- Saliva exerts a major influence on plaque initiation, maturation, and
metabolism.
- Salivary flow and composition also influence calculus formation,
periodontal disease, and caries.
D-
Proteinases (proteases):
Periodontal disease results in tissue degradation, and thus proteases,
derived both from the host and from bacteria, are central to the
Lectures in periodontics – 4th stage
Host – microbial interaction
Assist. Lec. Fahad M. al Dabbagh
disease processes. Proteinases (collagenase, elastase-like and trypsinlike, as well as serine and cysteine proteinases) cleave proteins by
hydrolyzing peptide bonds and may be classified into two major
classes, endopeptidases and exopeptidases, depending on the
location of activity of the enzyme on its substrate.