Defense Mechanisms of

the Gingiva
 Health is not a static condition.
 It is a dynamic state in which the living and
functioning organism or tissue remains in balance
with a constantly changing environment.
 This constant process of readjustment to maintain a
functional integrity is known as “Homeostasis”.
 The tissues of the periodontium are exposed to various
environmental factors in the oral cavity.

 Over 300 species of bacteria have been isolated in the oral

cavity.

 The periodontal tissues remain in a state of partnership

(symbiosis) with most of the bacteria and only under certain

circumstances do we suffer from their attack because, host

defence system strikes a balance between the two.

 GINGIVAL EPITHELIUM

Gingival epithelium has three functions:

 1.
Epithelial cells are tightly attached to each
other (barrier).
 2. Keratinization to resist trauma.
 3. surface shedding .
 Furthermore, the cells of the epithelium can respond
to the bacteria by:
(1) producing antimicrobials, including beta-defensin
etc., that kill the microbes.

(2) releasing other molecules, such as IL-1 Beta,

capable of inducing or enhancing the local inflammatory
reaction.

(3) releasing IL-8, a chemokine which attracts host

defense cells such as neutrophils and macrophages to
reduce the microbial insult.
Gingival Crevicular Fluid
 a fluid that emerges between the surface of the
tooth and the epithelial wall (sulcus or pocket).

 it is a complex mixture of substances derived

from serum, leukocytes, cells of the
periodontium and oral bacteria.

 the exact nature of the fluid, its origins and

composition, has been the subject of
controversy.
The principal questions are:

 whether the initial fluid produced represents a

transudate or is an exudate.

 and whether any GCF may be found at a clinically

healthy site.
 Exudate

 It is an inflammatory extra-vascular fluid that has

high protein concentration , much cellular debris
which leaks from the vessel into the interstitial
spaces due to icreased vascular permeability.
 transudate

 Itis an ultrafiltrate of blood plasma with low

protein content resulting from increased
vascular hydrostatic pressure , endothelium
permeability is normal.
 Osmosis

Movement of water molecules across a semi-permeable

membrane from a region of low concentration of a solute
to a region of high concentration of the solute.
 Fluid exchange

 There are 4 primary forces that control fluid exchange

between plasma and interstitium.

Starling forces include:

 Capillary hydrostatic pressure : it tends to escape the
fluid out the vessel.
 Osmotic pressure of plasma protein : it tends to hold
the fluid in side the vessels.
 Osmotic pressure and hydrostatic pressure in
interstitial spaces.
 ISF hydrostatic and oncotic pressures are of low magnitude,
they cancel each other; therefore they are negligible in the
balanced phsiological status.

During inflammation fluid exudation occurs due to :

 Increased capillary hydrostatic pressure due to enhanced

blood flow.

 Increased vascular permeability allowing plasma protein to

enter the interstatial space where they exert osmotic
pressure and draw more fluid from blood vessels.
 (a) Absence of inflammation:
low vascular permeability and
low permeability of the
basement membrane results in
low GCF flow and high % uptake
by lymph vessels.

(b) Macromolecules of plaque

result in an osmotic gradient,
increased vascular permeability
, resulting in increased passage
of fluid into the tissues and
increased GCF production.
 Recent work on GCF protein concentration suggested that
inflamed gingivae had a protein concentration similar to that
of serum.

 Suggesting that GCF represents an inflammatory exudate of

serum.

 However, the small volumes of fluid collected from healthy

gingival crevices had a protein concentration similar to
interstitial fluid.
 This would be consistent with the hypothesis of
Alfano that the initial fluid accumulation represents
a transudate of interstitial fluid produced by an
osmotic gradient and that the later fluid represents
a true exudate.
Methods of collection

 Several techniques have been employed for the

collection of GCF and the technique chosen will
depend upon the objectives of the study as
each technique has advantages and
disadvantages.

 techniques can be divided into four basic

strategies
Methods of collection

 Gingival washing methods.

 Capillary tubing or micropipettes.
 Absorbent filter paper strips.
 Pre- weighted twisted threads.
Composition
 The components of GCF can be characterized
according to individual proteins, specific antibodies,
antigens, and enzymes of several specificities.

 The GCF also contains cellular elements.

 Many researches have been attempted to use GCF

components to detect or diagnose active disease or to
predict patients at risk for periodontal disease.
Composition

 The components of GCF can be characterized

according to individual proteins, specific antibodies,
antigens , and enzymes of several specificities.

 The GCF also contains cellular elements.

 Cellular Elements

 Cellular elements found in GCF include:

 bacteria,
 desquamated epithelial cells,
 leukocytes (PMNs, lymphocytes, monocytes/macrophages),
which migrate through the sulcular epithelium.

.
Electrolytes

 Potassium, sodium, and calcium.

 Organic Compounds

 Bothcarbohydrates and proteins have been

investigated.

 glucose levels do not correlate with GCF glucose

levels, glucose concentration in GCF is three to
four times greater than that in serum.

 Thetotal protein content of GCF is much less

than that of serum
Clinical Significance
 The amount of GCF is greater when inflammation is
present and is sometimes proportional to the severity
of inflammation.

 GCF production is not increased by trauma from

occlusion.

 but is increased by mastication of coarse foods, tooth

brushing and gingival massage, ovulation, hormonal
contraceptives, and smoking.
 Circadian Periodicity

 There is a gradual increase in GCF amount from

6 am to 10 pm and a decrease afterward.
 Sex Hormones

 Female sex hormones increase GCF flow, probably

because they enhance vascular permeability.
 Pregnancy, ovulation, and hormonal contraceptives
all increase gingival fluid production.
 Mechanical Stimulation

 Chewing and vigorous gingival brushing stimulate the

flow of GCF.

 Even the minor stimuli represented by intrasulcular

placement of paper strips increases the production of
fluid.

Smoking
 Smoking produces an immediate transient but
marked increase in GCF flow
 Periodontal Therapy

There is an increase in GCF production

during the healing period after surgery
 Drugs that are excreted through the GCF may be used
advantageously in periodontal therapy.

 Bader and Goldhaber demonstrated in dogs that

tetracyclines are excreted through the GCF; this finding
triggered extensive research that showed a concentration
of tetracyclines in GCF compared with serum.

 Metronidazole is another antibiotic that has been detected

in human GCF.
 GCF function:

 It washes the crevice , carrying out shed epithelial cells ,

leucocyte , bacteria and other debris.

 The plasma protein may influence the epithelial attachment

to the tooth.

 It contains many antimicrobial agent.

 It carries polymorphonuclear leukocytes and macrophage ,

which are capable of phagocytosing bacteria

 Transport of Igs and other factor of the immune system

Leukocytes in the Dentogingival Area

 Leukocytes have been found in clinically healthy

gingival sulci in humans and experimental animals.
The leukocytes found are predominantly PMNs.

 They appear in small numbers extravascularly in the

connective tissue adjacent to the bottom of the
sulcus; from there, they travel across the epithelium
to the gingival sulcus, where they are expelled
 Leukocytes are present in sulci even when
histologic sections of adjacent tissue are free of
inflammatory infiltrate.

 Differential counts of leukocytes from clinically

healthy human gingival sulci have shown 91.2% to
91.5% PMNs and 8.5% to 8.8% mononuclear cells.
 The ratio of T lymphocytes to B lymphocytes was
found to be reversed from the normal ratio of
about 3 : 1 found in peripheral blood to about 1 : 3
in GCF
 Leukocytes are attracted by different plaque bacteria
but can also be found in the dento-gingival region of
germ-free adult animals.

 Leukocytes were reported in the gingival sulcus in

non-mechanically irritated (resting) healthy gingiva,
indicating that their migration may be independent of
an increase in vascular permeability.
 The majority of these cells are viable and have
phagocytic and killing capacity.

 Therefore leukocytes constitute a major protective

mechanism against the extension of plaque into the
gingival sulcus.

 The main port of entry of leukocytes into the oral

cavity is the gingival sulcus.
Saliva
 Salivary 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
 by controlling bacterial activity
ROLE OF SALIVA IN THE HOST DEFENCE

 1. A vehicle for swallowing bacteria.

 2. Inhibition of attachment of bacteria.

 3. Bactericidal action by the peroxidase system.

 4. Bactericidal action by lysozyme, lactoferrin and

other factors.
 Peroxidase is synthesized by salivary gland acini and
secreted into the saliva, where it becomes bound to
bacteria.

 thiocyanate is secreted into saliva by the ductal cells.

 Hydrogen peroxide is constantly secreted in low

concentration by bacteria, neutrophils and other host
cells.

 H2O2 is used by peroxidase to oxidize the thiocyanate

to hypothiocyanous acid, which kills bacteria.
 Lactoferrin: It is secreted by serous salivary gland, which
binds iron, an important growth factor or requirement for
many microorganisms.

 This action is bacteriostatic rather than bactericidal.

 Lysozyme: It is an antimicrobial enzyme in the saliva

secreted mainly by mucous salivary glands and it degrades
mucopeptides in the cell wall of gram-positive bacteria,
weakening the wall and causing lysis.
Salivary Antibodies

 saliva contains antibodies that are reactive with

indigenous oral bacterial species.

 Although immunoglobulins G (IgG) and M (IgM) are

present, the major immunoglobulin found in saliva
is immunoglobulin A (IgA).

 IgG is more prevalent in GCF.

 Many bacteria found in saliva have been shown
to be coated with IgA.

 It has been shown that IgA antibodies present in

parotid saliva can inhibit the attachment of oral
Streptococcus species to epithelial cells.

 Gibbons et al suggested that antibodies in

secretions may impair the ability of bacteria to
attach to mucosal or dental surfaces.
 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.

 Their primary effect has been studied in relationship to

dental caries.

 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]
 Hageman factor that hasten blood coagulation and
protect wounds from bacterial invasion.
 An active fibrinolytic enzyme may also be present.
 Leukocytes
 saliva contains all forms of leukocytes, of which the
principal cells are PMNs.

 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 believe the rate of migration

correlates with the severity of gingival inflammation.
 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.

 The removal of the salivary glands in experimental

animals significantly increases the incidence of dental
caries and periodontal disease and delays wound healing.
 In humans, an increase in inflammatory gingival
diseases, dental caries, and rapid tooth destruction
associated with cervical or cemental caries is partially
a consequence of decreased salivary gland secretion
(xerostomia).

 Xerostomia may result from sialolithiasis, Sjögren's

syndrome, irradiation, surgical removal of the salivary
glands, and other factors
 COMPLEMENT
Complement is an aggregate system composed of serum
proteins that function primarily to control inflammation.
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:
C1-C9 causes cytolytic and cytotoxic damage to the
cell.

 The complement system comprises of nine major

complement proteins which circulate in an inactive
form and which, like the clotting system, are
activated in an enzyme cascade.

 Classical Pathway: antibodies

 Alternative Pathway: bacteria (endotoxins)

 STAGES AND CLINICAL FEATURES OF
GINGIVITIS

Dr Saadou sami khalaf

Msc periodontology at University of
Khartoum
German Board of Oral Implantology (GBOI)
 GINGIVITIS
INFLAMMATION OF GINGIVA

inflammation: The reaction of a part of the body to

injury or infection, characterized by swelling, heat,
redness, and pain.

The process includes increased blood flow with an

influx of white blood cells and other chemical
substances that facilitate healing.
 Loe et al 1967 defined gingivitis as a
bacterially elicited inflammation of the
marginal gingival
 Gingivitis is the inflammation of the
gingiva with no attachment loss or with
previous attachment loss that is stable and
not progressing
 Bacterial products

widening and destruction of the intercellular spaces in the

junctional epithelium

Bacterial products or bacteria it self could gain access into the

connective tissue
 Microbial products activate the local leukocyte
(macrophages , mast cell) to produce vasoactive
substances as
(prostaglandin E2, tumour necrosis factor, interleukin-1)
 Gingivitis is a reversible condition & is the
mildest form of periodontal disease
 STAGES OF GINGIVITIS

 In 1976, Page and Schroeder divided the progressing

lesion in the gingival/periodontal tissues into four
phases:
I) INITIAL STAGE
II) EARLY STAGE
III) ESTABLISHED STAGE
IV) ADVANCED STAGE
 STAGE I GINGIVITIS: THE INITIAL LESION

 The first manifestations of gingival inflammation are vascular

changes consisting of dilation of capillaries and increased blood
flow.

 These initial inflammatory changes occur in response to microbial

activation of resident leukocytes and the subsequent stimulation of
endothelial cells.

 Microscopically, some classic features of acute inflammation can be

seen in the connective tissue beneath the junctional epithelium.
 Changes in blood vessel morphologic features occur within 1 week
and sometimes as early as 2 days after plaque has been allowed to
accumulate .

 Predominant Immune Cells POLYMORPHONUCLEAR

NEUTROPHILS (PMNs)

 Clinically : no visible changes are seen except presence of

exudation of fluid from the gingival sulcus (Gingival Crevicular
Fluid ) for that this condition is called subclinical gingivitis
 Stage II Gingivitis: The Early Lesion

 The early lesion evolves from the initial lesion

within about 1 week after the beginning of plaque
accumulation.
 clinical signs of erythema may appear, mainly
because of the proliferation of capillaries and
increased formation of capillary loops between rete
pegs .
 Bleeding on probing may be evident
 Predominant Immune Cells (lymphocytes 75%, with
the majority T cells)
 STAGE III GINGIVITIS:THE ESTABLISHED LESION

 In chronic gingivitis (stage III), which occures 2 to 3 weeks after

the beginning of plaque accumulation ,the blood vessels
become congested, venous return is impaired, and the
blood flow becomes sluggish.
 The result is localized gingival anoxemia, which superimposes a
somewhat bluish hue on the reddened gingiva.
 Clinically estimated as moderate to severely inflamed
gingiva

 A key feature that differentiates the established lesion is the

increase in the number of plasma cells.
 STAGE IV GINGIVITIS: THE ADVANCED LESION

 Extension of the lesion into alveolar bone characterizes a

fourth stage known as the advanced lesion" or phase of
periodontal breakdown.“

 Gingivitis will progress to periodontitis only in

individuals who are susceptible.
 CLINICAL FEATURES OF GINGIVITIS
 Classification according to COURSE and DISTRIBUTION
 according to course
1. ACUTE GINGIVITIS :
• It is of sudden onset and short duration and can be painful.
• SUBACUTE :A less severe form of acute condition

2. RECURRENT GINGIVITIS :
• Reappears after eliminated by treatment or disappearing
spontaneously.

3. CHRONIC GINGIVITIS :
• Slow in onset and of long duration, and is painless.
Classification According to DISTRIBUTION :

A) LOCALIZED GINGIVITIS :
 is confined to the gingiva of a single tooth or group of teeth,

b) GENERALIZED GINGIVITIS :
 involves the entire mouth or most of the mouth
 According to the area of inflammation , Gingivitis
could be

 Marginal : the inflammation is limited to the marginal

gingiva

 Papillary : the inflammation is limited to the interdental

papilla

 Diffuse :the inflammation involve s marginal , papilla and

attached gingiva
LOCALIZED PAPILLARY GINGIVITIS GENERALIZED MARGINAL AND PAPILLARY
GINGIVITIS.

GENERALIZED DIFFUSE GINGIVITIS INVOLVES

LOCALIZED, DIFFUSE GINGIVITIS THE MARGINAL, PAPILLARY,AND ATTACHED
GINGIVAE.
CLINICAL FINDINGS :
 A systematic clinical approach requires an orderly
examination of the gingiva for:

 Color
 Contour
 consistency
 position
 ease and severity of bleeding
 pain
BLEEDING ON PROBING (BOP) :

SIGNIFICANCE :
1. It is one of the earliest visual signs of inflammation
2. It can appear earlier than color changes or any other
visual signs of inflammation
3. Bleeding on probing is easily detectable clinically and is
of value for the early diagnosis and prevention of more
advanced gingivitis.
4. BOP is an objective sign that requires less sujective
estimation by the examiner
5. BOP also help to determine whether the lesion is in
an active or inactive state
6. the severity and ease of bleeding could indicate the
intensity of the inflammation
 a probe has been introduced to the
bottom of the gingival sulcus.

Bleeding appears after a few second

 HISTOPATHOLOGIC CHANGES ASSOCIATED WITH BOP:
1. Dilation and engorgement of the capillaries.
2. Thinning or ulceration of the sulcular epithelium .
COLOR CHANGES IN CHRONIC GINGIVITIS :

 Changes in color is an important clinical sign of gingival disease.

 The normal gingival color is "coral pink“
Change in colour depends upon :
 tissue's vascularity
 thickness of the epithelium
 degree of epithelial keratinization
 The gingiva becomes more red when there is an increase
in vascularization or the degree of epithelial keratinization
becomes reduced or disappears.
 The color becomes pale when vascularization is reduced
or epithelial keratinization increases.
 chronic inflammation intensifies the red or bluish red
color because of vascular proliferation, reduction of
keratinization and venous stasis.
 The changes start in the interdental papillae and gingival
margin and spread the attached gingiva
MELANIN PIGMENTATION
CHANGES IN THE CONSISTENCY OF THE GINGIVA
:
1. Both chronic and acute inflammation produce changes in
the normal firm, resilient consistency of gingiva.
2. Factors that are responsible are cellular and fluid content
and collagenous nature of lamina propria
3. In chronic gingivitis, both destructive (edematous) and
reparative (fibrotic) changes coexist.
4. The consistency of gingiva is determined by their
relative predominance.

5. It can be soggy and edematous or firm and leathery in

consistency
 Changes in the size of the gingiva

1. Normal size depends on the sum of the bulk of cellular and

intercellular elements and their vascular supply
2. In disease the size is increased which can be termed as
gingival enlargement
3. The factors responsible for this are increase in fibers and
decrease in cells as in non inflammatory type
4. In inflammatory type there will be increase in cells and
decrease in fibres
Surface Texture Changes in Disease
 The surface of normal gingiva usually exhibits
numerous small depressions and elevations =
stippling.

 In chronic inflammation the surface is either

smooth and shiny or firm and nodular
 This depends on whether the dominant changes
are exudative or fibrotic
 LOSS OF SURFACE STIPPLING is an early sign of
gingivitis.
 Stippling is restricted to the attached gingiva, but it
extends to a variable degree into the interdental papilla
Smooth, Shiny Tissue

Fibrotic = firm nodular

CHANGES INTHE POSITION OF THE GINGIVA :

RECESSION :
 The exposure of the root surface by an apical shift in the position
of the gingiva.

 Recession refers to the location of the gingiva, not its condition.

 localized , or generalized
 The prevalence, extent, and severity of gingival recession
increase with age and are more prevalent in males.
A. ACTUAL POSITION OF THE GINGIVA :
 The level of the coronal end of the epithelial attachment on the tooth,.
B. APPARENT POSITION OF THE GINGIVA :
 The level of crest of the gingival margin.
 The severity of recession is determined by actual position of
gingiva, not its apparent position.

The two types of recession are :

a. VISIBLE :
 Clinically observable.
b. HIDDEN :
 Covered by gingiva and can be measured by inserting a probe to the by
the level epithelial attachment.
ETIOLOGIC FACTORS OF RECESSION :

a) Faulty tooth brushing technique (gingival abrasion).

b) Tooth malposition.
c) Friction from soft tissues (gingival ablation).
d) Gingival inflammation.
e) Abnormal frenum attachment.
f) Trauma from occlusion.
CLINICAL SIGNIFICANCE :

1. Exposed root surfaces are susceptible to caries.

2. Abrasion or erosion of the cementum exposed by
recession cause dentinal sensitivity.
3. Hyperemia of the pulp and associated symptoms
results from excessive exposure of root surface.
4. Interproximal recession causes oral hygiene
problems and plaque accumulation.
 Changes in gingival contour

 Marginal gingiva is scalloped and knife edged

 The interdental papilla in the anterior region and posteriolry

tent –shaped

 The factors that maintain normal contour are ,shape of the

teeth and its alignment in the arch , location and size of the
proximal contact and dimensions of facial and lingual gingival
embrasures
 In diseased conditions , the marginal gingiva may
become rounded or rolled whereas interdental
papilla can become blunt and flat
Change in Shape of Margin
Bulbous Papilla
Missing and Blunted Papilla
Cratered Papilla
 Stillman’s cleft
 Apostrophe shaped indentation extending from and in
to the gingival margin
 Common in facial surface /gingival margin blunt
 Resuls from occlusal trauma

McCall’s festoons
 Life preserver shaped enlargement of gingiva
 Occur in canine and premolar on the facial surface
 Accumulation of food leads to secondary inflammatory changes
Thank you
The Immune System
and Host Response
• The only reason that the human
body survives is that it has a
protective defense system that is
very effective at recognizing and
fighting disease - causing
micro-organisms .
 The Immune System
• Immune system is a complex body defense system that
protects the body against bacteria , viruses , fungi , toxins
and parasites
 immune response - prime purpose
• the prime purpose of the immune system is to defend
the life of the individual by identifying foreign
substances in the body and developing a defense against
them .
 Host Response
• The way an individual's body responds to the infection
is known as the host response .
 Host Response ( cont .)
The body responds by
• Sending certain cells to the infection site
• Producing biochemical substances to counteract the
foreign invaders
 Consequences of Loss of Immune Function

• Loss of immune function is deadly to the body .

• E.g., AIDS
• HIV disables a specific group of immune cells .
• HIV + individuals often develop infections from
microorganisms that rarely cause infections in persons
with healthy immune systems .
 Overzealous Immune System
• The immune system can become so intense in its
response that it begins to harm the body that it is
trying to protect .

• This over reaction which harms the body's own cells and
tissues is referred to as an - auto - immune response .

• An overzealous response of the immune system occurs in

periodontitis.
 Recap - Immune System
• Immune system is a complex body defense system that
protects the body .
• The prime purpose of the immune system is to defend
the life of the individual .
• Host response — the way an individual's body responds
to the infection
 Leukocytes ( White Blood Cells )
• Act like independent single - cell organisms
• Can move through tissues and capture microorganisms
on their own
• 2 types that are important in periodontal disease are
—Polymorphonuclear leukocytes ( PMNS )
—Monocytes/macrophages
• Phagocytosis - the process
by which leukocytes engulf
and digest microorganisms
- " cell eating “
 Polymorphonuclear Leukocytes ( PMNs )
• Also called neutrophils
• Rapid responders ,
provide the 1st line of
defense
• Capture and destroy
bacterial invaders
• Short - lived cells ; die when they become
engorged with bacteria
 Polymorphonuclear Leukocytes ( PMNS(
( cont . )
• Attracted to site of injury
or infection by a process
called chemotaxis
• PMN contains many
strong bactericidal and
digestive enzymes , called
lysosomes
• Periodontal pathogens
are most effectively
destroyed by PMNS
 Monocytes / Macrophages
• Called monocytes when in the
bloodstream
• Called macrophages when in the
tissues
• Slower to arrive at the infection site
than the PMNS
• Surround and destroy bacteria
• Long - lived cells seen in chronic
inflammation
SEM of Human Macrophage
 Lymphocytes
• Small leukocytes that help defend
the body
• Two main types are
— B lymphocytes ( B cells )
— Tlymphocytes ( T cells )
 B Lymphocytes ( B Cells(
• Once activated , makes
millions of antibodies and
pours them into the
bloodstream
• Can differentiate into 2
types of B cells
—Plasma B cells
— Memory B cells
 Antibodies
• Y - shaped proteins
• One end of the Y binds to
the outside of the B cell .
• The other end of the Y
binds to a microorganism
and helps to kill it .
 Immunoglobulins
• Antibodies are known collectively as immunoglobulins
• Five major classes of immunoglobulins are
— Immunoglobulin A ( IgA )
— Immunoglobulin D ( IgD )
— Immunoglobulin E ( IGE )
— Immunoglobulin G ( IgG )
— Immunoglobulin M ( IgM )
 T Lymphocytes ( T Cells )
• The main function is to
intensify the response of other
immune cells ( macrophages ,
B lymphocytes ) to the
bacterial invasion .
• T cells produce substances
called cytokines that further
stimulate the immune
response .
• Cytokine - a general
name for any protein that
is secreted by cells and
affects the behavior of
nearby cells.
• Complement system
• a complex series of proteins
circulating in the blood that works to:
— Facilitate phagocytosis of bacteria
— Kill bacteria directly by forming pores in bacterial cell
membranes
• Complement was discovered many years ago as a
component of normal plasma that augments the
opsonization of Bacteria by antibodies and allows
antibodies to kill some bacteria.

• This activity was said to ‘complement’ the antibacterial

activity of antibody , hence the name.

• The complement system comprises of nine major

complement proteins which circulate in an inactive form
and which, like the clotting system, are activated in an
enzyme cascade.
 The functions of complement are:

a. Chemotaxis cellular activation: It is the directed movement

of a cell along a chemical gradient.
• Complement products released in this reaction attracts
phagocytes to the site of infection, e.g. C3a and C5a.

a. 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 there by
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.

• Components of complement can destroy certain

microorganisms directly by forming pores in their cell
membranes

d. Immune Clearance:
The complement system acts as a " housekeeper " for the
body by removing immune complexes from circulation .
Activities of the Complement System
 Recap - Immune System Cells
Immune cells that are important in the control of
periodontal disease are:
• PMNs and macrophages - capture and destroy bacteria
• B lymphocytes - make antibodies
• T lymphocytes - intensify the response of other immune
cells
 Recap - Complement System
• The complement system is a complex series of proteins
circulating in the blood that works to facilitate
phagocytosis or kill bacteria directly .
 Leukocyte Migration to the Tissues
• To fight an infection , leukocytes travel through the
bloodstream .
• The thin layer of epithelial cells that line the interior
surface blood vessels is called the endothelium .
Leukocyte Migration to the Infection Site ( cont . )

• Near the infection site , leukocytes push their way

between the endothelial cells ( extravasation ) and enter
the connective tissue .
• This process is called transendothelial migration .
 Attraction of Leukocytes to the Infection
Site
• Chemotaxis is the process whereby leukocytes
— Enter the connective tissue
— Are attracted to the site of the infection in response
to biochemical compounds released by the invading
bacteria
Leukocyte Migration to Connective Tissue
• Phagocytosis - the process by which leukocytes engulf
( surround ) and digest microorganisms
 Steps in
Phagocytosis
 Recap - Migration , Chemotaxis , and
Phagocytosis
• Migration - leukocytes travel through the bloodstream to
fight an infection
• Transendothelial migration - leukocytes push their
way between the endothelial cells of the blood vessels
and enter the connective tissue
 Recap - Migration , Chemotaxis , and
Phagocytosis ( cont . )
• Chemotaxis is the process whereby leukocytes are attracted
to the site of the infection in response to biochemical
compounds released by the invading bacteria .

• Phagocytosis is the process by which leukocytes engulf and

digest microorganisms .
Inflammation and the

Response
 Inflammation
• Focuses host defense components at the site of an
infection to eliminate microorganisms and heal damaged
tissue.
Inflammatory Response
 Inflammatory Biochemical Mediators
• Biologically active compounds secreted by cells that
activate the body's inflammatory response
• Mediators of importance in periodontitis include
— Cytokines
— Prostaglandins
— Matrix metalloproteinases
 Cytokines
• Leukocytes secrete cytokines that play a major role in
regulating the behavior of immune cells .
• Chemokines - a subgroup of cytokines - cause additional
immune cells to be attracted to the site of an infection or
injury .
Two stages of inflammation
• Acute inflammation
• Chronic inflammation
 Acute Inflammation
• A short - term , normal process that protects and heals
the body
• The acute inflammation process is achieved by the
increased movement of plasma and leukocytes from the
blood into the injured tissues .
Major Events in the Inflammatory
Response
 5 Classic Signs of Acute Inflammation
• Heat - a localized rise in temperature due to an
increased amount of blood at the site
• Redness - the result of increased blood in the area
• Swelling - the result of accumulation of plasma and
leukocytes at the site
• Pain – excess fluid in the tissues puts pressure on sensitive
nerve endings, causing pain.

• Loss of function - the result of swelling and pain

 The Acute Inflammatory Response

• Blood vessels near the infected site become more permeable

• PMNs are the first cells to arrive at the site .
• PMNs release cytokines .
• The liver produces C - reactive protein ( CRP ) .
• If the body succeeds in eliminating all the microorganisms
• the tissue will heal and inflammation will cease .
• If the acute inflammatory responses are not effective
in controlling the invading microorganisms , the
inflammatory response becomes chronic .
 Chronic Inflammation
• Chronic inflammation is a long - lived , out - of – control
inflammatory response that continues for more than a
few weeks .
• It is a pathological condition that can destroy healthy
tissue and cause more damage than the original
problem .
 Chronic Inflammation ( cont . )
• The classic warning signs seen in acute inflammation
usually are absent in chronic inflammation .

• The problem may go unnoticed by the host ( patient ) .

• Clinically , pain is often absent .

 Why does Chronic Inflammation occur ?
• Chronic inflammation occurs because the body is
unable to rid itself of invading organism .

• The invading microorganisms are persistent and

stimulate an exaggerated immune response .
• When inflammation becomes chronic

• the inflammatory response can become so intense that

it does permanent damage to the body tissues .

• This is the case in periodontitis .

Good luck
Periodontal response to the external forces
 Physiologic adaptive capacity of the
periodontium to occlusal forces

The Periodontium tries to

accommodate to the forces
exerted on the tooth, this is
called:
The adaptive capacity of the
periodontium

The adaptive capacity varies

in different persons and in the
same person at different times
Effect of occlusal forces on the
periodontium is influenced by:
(1) Magnitude

(2) Direction

(3) Duration

(4) Frequency

Of forces
 (1) Magnitude of forces
When the magnitude of occlusal forces is
increased the periodontium responds with:

• Increase in the number and

width of the periodontal
ligament fibers

• Widening of the periodontal

ligament space

• Increase in the density of

the alveolar bone
 (2) Direction of forces
Changing the direction of the occlusal forces
causes:
• Reorientation of the stresses and
strains within the periodontium
• Periodontal ligament fibers are
arranged so that they best
accommodate occlusal forces along
are likely to injure the periodontium
 (3) Duration of forces

• Constant pressure on
the bone is more
injurious than
intermittent forces

(no repair)
 (4) Frequency of forces

• The more frequent the

application of an
intermittent force , the
more injurious the forces to
the periodontium
Definition
Trauma from occlusion or occlusal trauma,
is the tissue injury of the supporting
structures of tooth , that occur when the
occlusal forces exceed the adaptive
capacity of the periodontium.
The occlusion that produces forces that
cause an injury is called

Traumatic occlusion
• Thus trauma from occlusion refers to the tissue
injury not the occlusal force.
• An occlusion that produces such an injury is
called a traumatic occlusion.
• Excessive occlusal forces may also disrupt the
function of the masticatory musculature and
cause painful spasms
• injure the temporomandibular joints
• produce excessive tooth wear.
• However, the term trauma from occlusion is
generally used in connection with injury in the
periodontium.
• Traumatic occlusal relationships are referred
to by such terms as occlusal disharmony,
functional imbalance, and occlusal dystrophy.

• These terms refer to the effect of the

occlusion on the periodontium, not to the
position of the teeth.

• Because trauma from occlusion refers to the

tissue injury rather than the occlusion, an
increased occlusal force is not traumatic if the
periodontium can accommodate it.
 Malocclusion:
Does not necessarily produce
periodontal trauma
But
*Trauma from occlusion may
occur when the occlusion
appears normal, with the
dentition anatomically and
aesthetically acceptable.
Etiology
 Etiology of trauma from occlusion
[1]Factors that increase
the magnitude or
frequency of occlusal
forces :

*Parafunctional habits such

as bruxism ,clenching

*Fixed and removable

prosthetic appliances
[2]Factors that change
the direction of occlusal
forces so that they are not
directed along the long axis
of tooth:

* Parafunctional habits
*Restorative and prosthetic
treatment
* Tilting and drifting of teeth
 Etiology of trauma from occlusion
[3]Factors that reduces the
resistance of the periodontium
to the occlusal forces:

*Loss of bone and periodontal

ligament support
*loss of a number of teeth
causing fewer teeth to absorb
the entire occlusal load.
[4]Combination of all factors
Classification
Classification of trauma from occlusion:

{a} Acute or chronic

{b} Primary , secondary or

combined
Classification of trauma from occlusion:

{a} Acute or chronic

{1}Acute trauma from occlusion
- from an abrupt occlusal impact( Biting on hard
object).
-Restorations or prosthetic appliances that
interfere with or alter the direction of occlusal
forces on the teeth may also induce
acute trauma

Signs & symptomes

* Sensitivity to percussion
* Tooth pain
* Tooth mobility
* Cementum tear
{2}Chronic trauma from occlusion
• more common
• greater clinical significance
Gradual changes in occlusion produced
by:
* Tooth wear

* Drifting and extrusion of teeth

* Parafunctional habits
Primary and Secondary Trauma from
Occlusion
Trauma from occlusion may be caused by
• alterations in occlusal forces,
• reduced capacity of the periodontium to withstand
occlusal forces,
• or both

• When trauma from occlusion is the result of

alterations in occlusal forces, it is called primary
trauma from occlusion.
• When it results from reduced ability of the tissues to
resist the occlusal forces, it is known as secondary
trauma from occlusion.
{1}Primary trauma from
occlusion:
It is the injury that occur to the
periodontium as a result of excessive
occlusal forces applied to a tooth or
teeth with normal supporting structures

*So the trauma from occlusion is the primary

etiologic factor in periodontal destruction

Example: High filling

• Examples include periodontal injury produced
around teeth with a previously healthy
periodontium:
• (1) insertion of a “high filling,”
• (2) insertion of a prosthetic replacement that
creates excessive forces on abutment and
antagonistic teeth,
• (3) drifting movement or extrusion of teeth into
spaces created by unreplaced missing teeth
• (4) orthodontic movement of teeth into
functionally unacceptable positions.
{2}Secondary trauma from
occlusion
-It is the injury that occurs to the
periodontium resulting from normal
occlusal forces applied to a tooth or
teeth with inadequate(abnormal)
periodontal support
-The periodontium becomes more
liable to injury and previously well-
tolerable occlusal forces become now
traumatic
 {
{3}Combined trauma from occlusion

Is the injury that occurs to the periodontium

resulting from abnormal occlusal forces
applied to a tooth or teeth with inadequate
(abnormal) periodontal support
{1}Primary trauma from occlusion:
Abnormal occlusal forces applied to normal
supporting structures

{2}Secondary trauma from occlusion

Normal occlusal forces applied to abnormal
periodontal support

{3}Combined trauma from occlusion

Abnormal occlusal forces applied to
abnormal periodontal support
Tissue response to increased
occlusal forces

Stages
of
trauma from occlusion
Tissue response to increased occlusal forces

Stages of trauma from occlusion

Stage (I) Injury

Stage (II) Repair

Stage(III) Adaptive remodeling

of the periodontium
 Stage I: Injury
• Tissue injury is produced by excessive
occlusal forces.
• The body then attempts to repair the injury
and restore the periodontium.
• This can occur if the forces are diminished or
if the tooth drifts away from them.
• If the offending force is chronic,
however, the periodontium is
remodeled to cushion its impact.

• The ligament is widened at the

expense of the bone, resulting in
angular bone defects without
periodontal pockets, and the
tooth becomes loose.
• Under the forces of occlusion, a tooth rotates
around a fulcrum or axis of rotation, which in
single-rooted teeth is located in the junction
between the middle third and the apical third
of the clinical root
• and in multirooted teeth in the middle of the
interradicular bone.
• This creates areas of pressure and tension on
opposite sides of the fulcrum.
• Different lesions are produced by different
degrees of pressure and tension.
• If jiggling forces are exerted, these different
lesions may coexist in the same area
• The areas of the periodontium most
susceptible to injury from excessive occlusal
forces are the furcations.

• Injury to the periodontium produces a

temporary depression in mitotic activity and
the rate of proliferation and differentiation of
fibroblasts, in collagen formation, and in bone
formation.

• These return to normal levels after dissipation

of the forces.
 Stage II: Repair
• Repair is constantly occurring in the normal
periodontium, and trauma from occlusion
stimulates increased reparative activity.
• The damaged tissues are removed, and new
connective tissue cells and fibers, bone, and
cementum are formed in an attempt to
restore the injured periodontium.
• Forces remain traumatic only as long as the
damage produced exceeds the reparative
capacity of the tissues.
• When bone is resorbed by excessive occlusal
forces, the body attempts to reinforce the
thinned bony trabeculae with new bone .

• This attempt to compensate for lost bone is

called buttressing bone formation and is an
important feature of the reparative process
associated with trauma from occlusion.
• Buttressing bone formation occurs within the
jaw (central buttressing) and on the bone
surface (peripheral buttressing).

• In central buttressing the endosteal cells

deposit new bone, which restores the bony
trabeculae and reduces the size of the
marrow spaces.

• Peripheral buttressing occurs on the facial

and lingual surfaces of the alveolar plate.
• Depending on its severity, peripheral
buttressing may produce a shelflike
thickening of the alveolar margin, referred to
as lipping , or a pronounced bulge in the
contour of the facial and lingual bone
• Stage III: Adaptive Remodeling of the
Periodontium
• If the repair process cannot keep pace with
the destruction caused by the occlusion, the
periodontium is remodeled in an effort to
create a structural relationship in which the
forces are no longer injurious to the tissues.
• This results in a widened periodontal
ligament, which is funnel shaped at the crest,
and angular defects in the bone, with no
pocket formation.
• The involved teeth become loose.
• The injury phase shows an increase in areas of
resorption and a decrease in bone formation,
whereas the repair phase demonstrates
decreased resorption and increased bone
formation.

• After adaptive remodeling of the periodontium,

resorption and formation return to normal.
 Effects of Insufficient Occlusal Force
• Insufficient occlusal force may also be
injurious to the supporting periodontal
tissues.
• Insufficient stimulation causes thinning of
the periodontal ligament, atrophy of the
fibers, osteoporosis of the alveolar bone, and
reduction in bone height.
• Hypofunction can result from an open-bite
relationship, an absence of functional
antagonists, or unilateral chewing habits that
neglect one side of the mouth.
 Reversibility of Traumatic Lesions

• Trauma from occlusion is reversible

• The injurious force must be relieved for repair to
occur
• The presence of inflammation in the
periodontium as a result of plaque accumulation
may impair the reversibility of traumatic lesions
• Effects of Excessive Occlusal Forces on
Dental Pulp

• The effects of excessive occlusal forces on

the dental pulp have not been established.

• Some clinicians report the disappearance of

pulpal symptoms after correction of excessive
occlusal forces.
• Influence of Trauma from Occlusion on
Progression of Marginal Periodontitis

• The accumulation of bacterial plaque that

initiates gingivitis and results in periodontal
pocket formation affects the marginal gingiva,
but trauma from occlusion occurs in the
supporting tissues and does not affect the
gingiva.
• It has been repeatedly proved that trauma
from occlusion does not cause pockets or
gingivitis nor does it increase gingival fluid
flow

• mobile teeth in humans harbor significantly

higher proportions of Campylobacter rectus
and Peptostreptococcus micros than
nonmobile teeth.
• As long as inflammation is confined to the
gingiva, the inflammatory process is not affected
by occlusal forces.
• When inflammation extends from the gingiva
into the supporting periodontal tissues (i.e.,
when gingivitis becomes periodontitis), plaque-
induced inflammation enters the zone influenced
by occlusion, which Glickman has called the zone
of co-destruction
 Glickman’s concept

• Glickman (1965, 1967) claimed that the

pathway of the spread of a plaque-associated
gingival lesion can be changed if forces of an
abnormal magnitude are acting on teeth
harboring subgingival plaque
• Instead of an even destruction of the
periodontium and alveolar bone (suprabony
pockets and horizontal bone loss), which,
according to Glickman, occurs at sites with
uncomplicated plaque-associated lesions,
• sites which are also exposed to abnormal
occlusal force will develop angular bony
defects and infrabony pockets.
• The periodontal structures can be divided into
two zones

• 1. The zone of irritation

• 2. The zone of co-destruction.
• The zone of irritation includes the marginal
and interdental gingiva.

• The soft tissue of this zone is not affected by

forces of occlusion
• The plaque-associated lesion at a “non-
traumatized” tooth propagates in the apical
direction by first involving the alveolar bone
and only later the periodontal ligament area.

• The progression of this lesion results in an

even (horizontal) bone destruction.
• The zone of co-destruction includes
• the periodontal ligament,
• the root cementum,
• and the alveolar bone,

• It is coronally demarcated by the trans-septal

(interdental) and the dento-alveolar collagen
fiber bundles
• The fiber bundles which separate the zone of
codestruction from the zone of irritation can
be affected from two different directions:

• 1. From the inflammatory lesion maintained

by plaque in the zone of irritation.

• 2. From trauma-induced changes in the zone

of co-destruction.
• Through this exposure from two different
directions the fiber bundles may become
dissolved and/or orientated in a direction
parallel to the root surface
• The spread of an inflammatory lesion from
the zone of irritation directly down into the
periodontal ligament (i.e. not via the
interdental bone) may hereby be facilitated
• Waerhaug’s concept

• Waerhaug (1979) examined autopsy

specimens similar to Glickman’s, but in
addition measured the distance between the
subgingival plaque and

• (1) the periphery of the associated

inflammatory cell infiltrate in the gingiva, and
• (2) the surface of the adjacent alveolar
bone.
• He concluded from his analysis that angular
bony defects and infrabony pockets occur
equally often at periodontal sites of teeth
which are not affected by trauma from
occlusion as in traumatized teeth.
• The loss of connective attachment and the
resorption of bone around teeth are,
according to Waerhaug, exclusively the result
of inflammatory lesions associated with
subgingival plaque.
• Waerhaug concluded that angular bony
defects and infrabony pockets occur when
the subgingival plaque of one tooth has
reached a more apical level than the
microbiota on the neighboring tooth,

• and when the volume of the alveolar bone

surrounding the roots is comparatively large
• When trauma from occlusion is eliminated, a
substantial reversal of bone loss occurs,
except in the presence of periodontitis.

• This indicates that inflammation inhibits the

potential for bone regeneration

• Thus it is important to eliminate the marginal

inflammatory component in cases of trauma
from occlusion because the presence of
inflammation affects bone regeneration after
the removal of the traumatizing contacts
• Trauma from occlusion also tends to change
the shape of the alveolar crest.

• The change in shape consists of a widening of

the marginal periodontal ligament space.
• a narrowing of the interproximal alveolar
bone.
• a shelflike thickening of the alveolar margin.

• Therefore, although trauma from occlusion

does not alter the inflammatory process, it
changes the architecture of the area around
the inflamed site.
• Thus, in the absence of inflammation, the
response to trauma from occlusion is limited
to adaptation to the increased forces.

• In the presence of inflammation, however,

the changes in the shape of the alveolar crest
may be conducive to angular bone loss, and
existing pockets may become intrabony.
 theories that have been proposed to explain
the interaction of trauma and inflammation
include the following:
• Trauma from occlusion may alter the pathway of
extension of gingival inflammation to the underlying
tissues.
• This may be favored by the reduced collagen density
and increased number of leukocytes, osteoclasts, and
blood vessels in the coronal portion of increasingly
mobile teeth.
• Inflammation then may proceed to the periodontal
ligament rather than to the bone.
• Resulting bone loss would be angular, and pockets
could become intrabony.
• Supragingival plaque can become subgingival if
the tooth is tilted orthodontically or migrates into
an edentulous area.

• Increased mobility of traumatically loosened teeth

may have a pumping effect on plaque
metabolites, increasing their diffusion.
• In summary, trauma from occlusion
does not initiate gingivitis or periodontal
pockets, but it may constitute an
additional risk factor for the progression
and severity of the disease.
Clinical Features
• Clinical and Radiographic Signs of
Trauma from Occlusion
• The most common clinical sign of trauma to
the periodontium is increased tooth mobility.

• In the injury stage of trauma from occlusion,

destruction of periodontal fibers occurs,
which increases tooth mobility.

• In the final stage the accommodation of the

periodontium to increased forces entails a
widening of the periodontal ligament, which
also leads to increased tooth mobility.
• Although this tooth mobility is greater than
the so-called normal mobility, it cannot be
considered pathologic because it is an
adaptation and not a disease process.

• If it does become progressively worse, then

it can be considered pathologic..
Clinical features of TFM
(1)increased mobility of the teeth

(2)Sensitivity of teeth to percussion

and thermal sensitivity

(3)Wear facets
Clinical features of TFM
(7)Fremitus which is the movement
of the teeth during mandibular
movements
Clinical features of TFM

Fremitus
*It is the palpable vibration or movement
*It is an important sign during
examination of occlusion

*Fremitus scale is
N normal
+ vibration felt
1 slight movement felt against finger
2 palpable movement visible
3 movement is very apparent
• Radiographic signs of trauma from occlusion may
include the following:

• Increased width of the periodontal space, often with

thickening of the lamina dura along the lateral aspect
of the root, in the apical region, and in bifurcation
areas.

• A “vertical” rather than “horizontal” destruction of

the interdental septum.

• Root resorption