Transcript Tissue of the teeth

Pre-clinical Periodontics
Defense mechanisms of
the periodontium
Dr Jamal Naim
PhD in Orthodontics
Initiation of periodontal disease

Microorganisms which form the dental biofilm contain
or release components which induce gingivitis.

The inflammatory changes may remain confined to the
gingival area for several years but at some sites
gingivitis eventually shifts to destructive periodontal
disease.
Why lesions remain localized to the
marginal portion of the gingival tissues,
while in others they progress to involve
the loss of connective tissue attachment
and supporting alveolar bone?
Imbalance of the host-microbial
relationship is occurring in the
destructive lesions!
Normal gingiva vs. clinical healthy
gingiva

Pink color, firm consistency and scalloped outline for
gingival margin.

The interdental papillae are firm, do not bleed on
gentle probing and fill the space below the contact
areas.

Can only be established
experimentally after supervised meticulous daily plaque
control for several weeks.
Normal gingiva vs. clinical healthy
gingiva

the gingivae we would routinely classify as "clinically
healthy gingivae" are not as histological perfect as
the "normal gingivae“

Clinically healthy gingivae would be typically that
level of health which could be
attained by patients regularly
practicing a good standard of
plaque control.
The oral surface of clinically
healthy gingiva
consists of keratinized oral
epithelium continuous with the
JE.
Below the JE is a vascular
network which supplies
the epithelium with nutrients
and defense cells.
Neutrophils and macrophages
can be seen in the junctional
epithelium of the clinically
healthy gingiva
Defence mechanisms of the periodontium
Clinically the gingival tissue is able to deal with
external challenges without progressing to a
diseased state, probably due to several
defensive factors:
Host defense processes
Host-parasite reactions can be divided into:

Innate (non-specific) response include the
inflammatory response

Adaptive (specific) response include immunological
responses
Innate (non-specific) response
Innate immune mechanisms operate without any
previous contact with the disease-causing
microorganism.
These mechanisms include:

the physical barriers of the oral mucosal epithelial
surfaces and

vascular and cellular aspects of the inflammatory
responses.
Innate (non-specific) response

Regular shedding of epithelial cells into the oral
cavity

Positive fluid flow of the gingival crevice (GCF) which
may remove non-attached microorganisms and
noxious products

Antimicrobial effect of antibodies

Phagocytic function of neutrophils and macrophages

Detrimental effect of complements on microbes
Innate (non-specific) response
1.
Gingival epithelial cells may form the first barriers of
defense against oral bacteria in periodontal tissues.
(KE)
2.
Prevention of attachment and colonization:
1.
2.
the washing effect of the saliva and gingival crevicular fluid
(GCF),
the constituents of these fluids
(antibodies, proteases, complement
and lactoferrin) can be bactericidal.
3 types
of gingival
epithelium
1. Turnover time of JE

JE has a high turnover (5 days) compared to oral
gingival epithelium (8-10 days)

The shedding rate is very high for JE 50-100 > than
OGE.

JE-cells that are degenerating and covered by
bacteria and or their products are expelled at a fast
rate

This also may explain why gingivitis can be a
reversible condition, which is considered a defensive
mechanism of this tissue`
Tooth surface
JE has a rapid turnover
rate
 JE cells at the base of the
Sulcus are covered by
microbes and constantly shed
into the Sulcus.
 Replacement rate of the JE
is 5 days (vs 8-10 days for
oral gingival epithelium)
JE has impressive antimicrobial
systems
 Enzyme-rich lysosomes
(packages of enzymes in the
JE cytoplasm)
 e. g. Defensins
Tooth surface
3. JE behaves like a semipermeable membrane
 Small molecules injected
intravenously can be detected
in sulcus after 1-5 minutes.
 Large molecules (eg
immunoglobins) take 30-120
minutes to get into sulcus.
blood vessels
in gingiva
3. JE behaves like a semipermeable membrane
 Bacteria in the sulcus release
large quantities of metabolites
which diffuse through the JE:
 Butyric & propionic acids
(toxic to tissues)
 Peptides
 Lipopolysaccharides (LPS)
Bacteria
4. JE is part of the immune
system
JE has a sensory function
detecting chemical excreted
from the bacteria
HELP!!!!!
we’re
under
attack
Bacteria
4. JE is part of the immune
system
JE produces cytokines (IL8) which recruit PMN from
underlying blood vessels in
connective tissue, through
JE and out into sulcus
blood vessels
in gingiva
Bacteria
4. JE is part of the immune
system
JE produces other cytokines
which switch on the
inflammatory response in
the gingiva.
blood vessels
in gingiva
5. Neutrophils (PMN)
Different
names for
the same
cell
• Polymorphonuclear leucocytes
• Polymorphs
• PMN
• Neutrophils
PMN = primary
periodontal defensive cell
 Produced in the bone marrow from
stem cells; live for about 4-5 days.
 PMN have a rapid turnover rate.
 Engulf microbes in sulcus
(phagocytosis).
 Digest microbes by powerful
enzymes contained in cytoplasm.
PMN = primary
periodontal defensive cell
May blow up in the gingival
tissues, releasing destructive
enzymes and pro-inflammatory
mediators which exacerbates
the inflammatory response.
Biofilm
Tooth surface
PMN form a dense layer
(pallisade) over plaque
& engulf bacteria in
sulcus
Bacterial product
stimulates JE cells to
produce concentration
gradient of chemoattractant (IL-8) for
PMN.
blood vessels
in gingiva
Transendothelial
migration
 Defects of the PMN function can reduce host defense
capability.
 PMN function may be blocked at various sites:
 Chemotactic defects
 Inadequate adherence
 Defective phagocytosis
 Impaired ability to digest
Transendothelial
migration
 Systemic diseases characterized by granulocyte defects
are usually accompanied by severe periodontal disease
(diabetes mellitus, crohn's disease, down syndrome)
 Granulocytes in most patients with LJP or RPP exhibit more
or less comprised functions
6. Gingival crevicular fluid
 Gingival Crevicular Fluid
transports PMN, antibodies,
Tooth surface
host enzymes and helps flush
out the sulcus
 Positive pressure from gingival
blood vessels, through JE into
sulcus.
blood vessels
will be discussed later
7. Non specific antibodies
Non-specific: from circulation
Specific: against bacteria localized in the gingival
tissues
This topic will be discussed in more
details later
8. Immune system interactions
 PMN
 Complement
 Antibody interaction
8. Immune system interactions
 The complement system is a series of 25 proteins
manufactured in the liver and are are activated by, and
work with, (i.e. complement) antibodies
Function of complement:
 lysing (bursting) of cells and signal to phagocytes
that a cell have to be removed. Complement coated
bacterial cells are easier for PMN to phagocytose
 binding to bacteria, and when activated, can directly
kill them.
Defensive factors
All of these factors may operate at the
same time to reduce the bacterial
load and thus prevent an overresponse of the tissue defense
systems which could result in the
formation of a lesion.
Summary of primary periodontal defenses
 Physical barrier
 High turnover rate
 Large inter-cellular spaces permit PMN progress
to sulcus
 JE produces cytokines which call to PMN
 Crevicular fluid, flushing carries cells +
antibodies
 Immune system interactions