Periodontology

Dr. Rawand Samy Mohamed Abu Nahla

Oral Medicine, periodontology& oral Radiology Department.
Dr. Haydar. A. Shafy Faculty Of Dentistry.
El Azhar University.
 lecture 5
Pathogenesis Of Periodontal
Diseases
• Periodontal disease and dental caries are the most prevalent
infections affecting the human dentition.

• Periodontal disease is a chronic bacterial infection

characterized by persistent inflammation, connective tissue
breakdown and alveolar bone destruction.

• The term periodontal disease refers to gingivitis and

periodontitis as well.

• Gingivitis is a reversible dental plaque induced

• Periodontitis, which is bacterially induced, can be defined
as a chronic inflammatory disease initiated by dental plaque
biofilm and perpetuated by a deregulated immune response
usually accompanied by gingivitis resulting in irreversible
destruction of the supporting tissues surrounding the tooth,
including the alveolar bone
• Nowadays, there is a high prevalence of periodontal disease
worldwide, and knowing the etiology and pathogenesis is
basic for its control.

• Biofilms that colonize the oral cavity are among the most
complex of nature.

• Besides pathogenic microorganisms, genetic and

environmental factors contribute to the development of this
disease.
• Periodontal disease can be increased by several risk factors
such as smoking, systemic diseases, medications such as
steroids, antiepileptic, drugs for cancer therapy, poor
placement of dental bridges, dental crowding, lack of teeth,
pregnancy and contraceptive use.
Microbiology Of Periodontal Disease

• Infectious diseases have in common, the fact that they are

necessarily associated with the presence of bacteria that
colonize.

• The mouth facilitates the growth of a characteristic resident

microbiota.

• The composition of the oral microbiota is influenced by

temperature, pH and atmosphere, as well as by the host
defenses and host genetics .
• Recently, published studies show the association between certain
families of virus and periodontal disease. some virus like Epstein-
Barr type 1, cytomegalovirus and human herpes in crevicular fluid
of Nigerian children with necrotizing ulcerative gingivitis.

• This pathogenicity is attributed to the degradation of the host

defense mechanisms due to viral infection of the gingiva, favoring
the bacteria colonization.
• Biofilms that colonize the oral cavity are among the most
complex of nature, as in the mouth, there are 4 different
types: masticatory mucosa, tongue dorsum, saliva and hard
surfaces such as tooth surfaces and restorative materials .

• Bacteria that cause periodontal disease can be classified

according to their function in the associations between them
when colonizing the gingival sulcus. In Table , the
Socransky classification is shown.
• There are three that are particularly relevant in the
initiation and progression of periodontal disease:
Aggregatibacter actinomycetemcomitans (Aa),
Porphyromonas gingivalis (Pg) and Tannerella
forsythensis
 Table .Current Classification System Of Bacteria Responsible
Of Periodontal Disease (Socransky And Haffajee, 2002).

Complex Bacteria Role in periodontal disease

Yellow Streptococcus sanguis

Streptococcus gordonii
Streptococcus intermedius Early
colonizers

Green Capnocytophaga gingivalis

Capnocytophaga ochracea
Capnocytophaga sputigena
Campylobacter concisus Secondary
colonizers
Orange Fusobacterium nucleatum
Prevotella intermedia
Prevotella nigrescens
Peptostreptococcus micros
Streptococcus constellatus
Eubacterium nodatum
Campylobacter showae
Campylobacter gracilis
Campylobacter rectus
Secondary colonizers Precede
colonization by bacteria of the “Red
complex”

Purple Veillonella párvula

Actinomyces odontolyticus
Bridge species between “Orange
complex” and “Red complex”
Red Tannerella forsythia
Porphyromona gingivalis
Treponema denticola

Secondary colonizers

Main pathogens, associated with

bleeding on probing
• Periodontal health is a state of balance in which the
bacterial population coexists with the host.

• Disruption of this balance causes alterations in both the

host and bacteria and results in the destruction of the
periodontium

• In one mm³ of dental plaque weighing approximately 1

mg , more than 108 bacteria are present.
 Periodontal Health
Gram-positive
•facultative species mainly of Streptococcus and
Actinomyces.

•Streptococcus sanguis

•Streptococcus mitis

•Actinomyces viscosus

•Actinomyces naeslundii
Some gram-negative organisms:

•Fusobacterium nucleatum

•Prevotella intermedia

•Capnocytophaga

•Neisseria Veillonella

•Very few spirochetes and motile rods

Gingivitis
Equal in gram-positive and gram-negative

Gram-Positive
•Streptococcus sanguis

•Streptococcus mitis

•Actinomyces viscosus

•Actinomyces naeslundii

•Peptostreptococcus micros
Gram-Negative
•Fusobacterium nucleatum

•Prevotella intermedia

•Campylobacter

•Haemophilus

•Varicella parvula

Pregnancy Gingivitis
Increases in levels of Prevotella intermedia
Acute Necrotizing Ulcerative Gingivitis
•Fusobacterium nucleatum

•Prevotella intermedia

•Treponema vincetii

•Small spirochetes
Chronic Periodontitis
•Bacteroides forsythus

•Porphyromonas gingivalis

•Treponema denticola

Red complex
Aggressive periodontitis

•Aggregatibacter actinomycetemcomitans 90%

•Porphyromonas gingivalis
• Infection refers to the presence and multiplication of a microorganism in
body tissues

• Endogenous infections result when indigenous microbes thrust from their

normal habitats into unusual anatomic regions .

• Infections caused by endogenous microbes are called opportunistic infections

if they occur at the usual habitat of the microorganisms , such infections
may be the result of changing ecologic conditions or due to a decrease of host
resistance
Mechanisms Of Host Tissue Damage
1) Bacteria inhibit growth or alter the metabolism of host tissue cells

2) Enzymes produced by perio pathogens can destroy host tissue

3) Bacterial enzymes facilitate tissue destruction and invasion of bacteria

into host tissue

4) Bacteria degrade host tissues and release biologically active substances

from host tissue cells
Tissue Destruction
•Exotoxins
•Endotoxins
•Enzymes
•Cytotoxicity
•Toxic metabolites
•Evasion of the host immune system
 Bacteria
•Colonization
•Invasion
•Destruction

Environmental Host
•Smoking Susceptibility
•Genetic
•Acquired

Periodontal Diseases
Gingival Inflammation

• Microorganisms – produce products that cause

damage to cells.

• Sequence of events occurs in three different

stages
Stage I Gingivitis: The Initial Lesion (clinically
healthy gingiva):

• Dilation of capillaries Increased blood flow

• PMN’s are main defense cell - this correlates with

increase in flow of gingival fluid

• PMN’s present in JE, CT, and sulcus

• Host response determines if the lesions resolves or

becomes chronic.
 Stage II Gingivitis: The Early Lesion (clinical
gingivitis):
• Clinical erythema due to proliferation of capillaries and increased
formation of capillary loops between rete pegs

• Bleeding on probing

• 70% of collagen is destroyed

• Main defense cell is lymphocytes Neutrophils, macrophages, plasma

cells, and mast cells

• JE is infiltrated with neutrophils

• While the early lesion is not entirely distinct from the initial lesion, it is said to
encompass the inflammatory changes that occur from days four to seven after
plaque accumulation has commenced. 

• It is characterized by a matured leukocytic infiltrate that features

mainly lymphocytes. 

• Plasma cells, if present, are only at the edges of the area. The early lesion can
occupy up to 15% of the connective tissue of the marginal gingiva and up to
60-70% of collagen may be dissolved.
• Fibroblasts appear altered, exhibiting abnormal nuclei,
swollen mitochondria, vacuolization of the rough
endoplasmic reticulum and rupture of their cell membranes,
appearing up to three times the size of normal fibroblasts
are found in association with moderately-sized
lymphocytes.
• The early lesion displays acute exudative inflammation;
exudative components and crevicular lymphocytes reach their
maximum levels between days 6-12 after plaque accumulates and
gingival inflammation commences with the quantity of crevicular
fluid being proportional to the size of the reaction site within the
underlying connective tissue.

• The junctional epithelium may even become infiltrated with

enough leukocytes so that it resembles a microabscess[
Features of the Early Lesion:

•Accentuation of features of the initial lesion, such as

the considerably greater loss of collagen
Accumulation of lymphocytes subjacent to junctional
epithelium

•Cytopathic alterations in resident fibroblasts

•Preliminary proliferation of basal cells of junctional

epithelium
 Stage III Gingivitis: The Established
Lesion(chronic gingivitis)
• Blood vessels engorged and venous return is impaired

• RBC’s get into CT and breakdown of hemoglobin deepens color of

gingiva

• Main defense cell is plasma cell

• JE produces rete pegs which protrude into CT

• Basal lamina is destroyed in some areas

• Collagen destruction is increased

• The hallmark of the established lesion is the
overwhelming presence of plasma cells  in relation
to the prior stages of inflammation.

• Beginning two to three weeks after first plaque

formation, the established lesion is widespread in
both human and animals populations.
• Similar to the initial and early lesions, the established lesion features an
inflammatory reaction confined to the area near the base of the gingival
sulcus, but unlike prior stages, displays plasma cells clustered around
blood vessels and between collagen fibers outside the immediate area of
the reaction site. 

• While most of the plasma cells produce IgG, a significant number do

produce IgA (and rarely, some produce IgM). 

• The presence of complement and antigen-antibody complexes is evident

throughout the connective and epithelial tissue.

• It is in the established lesion that epithelial proliferation and apical migration
begin.

• In health, the junctional epithelium creates the most coronal attachment of the

gum tissue to the tooth at or near the cement enamel junction.

• In the established lesion of periodontal disease, the connective tissue lying

subjacent to the junctional epithelium is nearly destroyed, failing to properly
support the epithelium and buttress it against the tooth surface.
• In response to this, the junctional epithelium proliferates and grows
into the vacant underlying spaces, effectively causing the level of its
attachment to migrate towards apically, revealing more tooth
structure than is normally evident supragingivally (above the level of
the gum line) in health.

• While many established lesions continue to the advanced lesion most

either remain as established lesions for decades or indefinitely; the
mechanisms behind this phenomenon are not well understood.
Features of the Established Lesion:
•Predominance of plasma cells without bone loss

•Presence of extravascular immunoglobulins in the connective

tissue and junctional epithelium

•Continuing loss of collagen

•Proliferation, apical migration and lateral extension of the

junctional epithelium, with or without pocket formation
Advanced Lesion(marginal periodontitis):
• Many of the features of the advanced lesion are
described clinically rather than histologically.

• Periodontal pocket formation

• Gingival ulceration and suppuration

• Destruction of the alveolar bone and periodontal ligament

• Tooth mobility, drifting and eventual loss

• Because bone loss makes its first appearance in the advanced
lesion, it is equated with periodontitis while the first three
lesions are classified as gingivitis  in levels of increasing
severity.

• The advanced lesion is no longer localized to the area around

the gingival sulcus  but spreads apically as well as laterally
around a tooth and perhaps even deep into the gum tissue
papilla.
• There is a dense infiltrate of plasma cells,
other lymphocytes and macrophages.

• The clusters of perivascular plasma cells still

appears from the established lesion.

• Bone is resorbed, producing scarring and fibrous

change.
Features of the Advanced Lesion:
•Extension of the lesion into alveolar bone,  periodontal
ligament with significant bone loss

•Continued loss of collagen

•Cytopathic alterations in plasma cells in the absence of altered

fibroblasts

•Formation of periodontal pocketing

•Conversion of bone marrow into fibrous connective tissue

Pathogenic Process:

• The innate immune system, also known as

the non-specific immune system or in-born immunity system,
is an important subsystem of the overall immune system that
comprises the cells and mechanisms that defend the host from
infection by other organisms.

• The cells of the innate system recognize and respond

to pathogens in a generic way, but, unlike the adaptive immune
system, the system does not provide long-lasting immunity to the
host
The major functions of the innate immune system
include:

•Recruiting immune cells to sites of infection, through the

production of chemical factors, including specialized chemical
mediators, called cytokines

•Activation of the complement cascade to identify bacteria,

activate cells, and promote clearance of antibody complexes or
dead cells
• Identification and removal of foreign substances present in
organs, tissues, blood and lymph, by specialized white blood cells

• Activation of the adaptive immune system through a process

known as antigen presentation

• Acting as a physical and chemical barrier to infectious agents

Inflammation is one of the first responses of the immune
system to infection or irritation.

Inflammation is stimulated by chemical factors released by

injured cells and serves to establish a physical barrier against
the spread of infection, and to promote healing of any damaged
tissue following the clearance of pathogens.
• The process of acute inflammation is initiated by cells already
present in all tissues, mainly resident macrophages, dendritic
cells, histocytes.

• At the onset of an infection, burn, or other injuries, these cells

undergo activation and release inflammatory
mediators responsible for the clinical signs of inflammation.
Inflammatory Mediators:

1-Histamine 
•is an organic nitrogenous compound involved in local immune responses as well
as regulating physiological function in the gut and acting as a neurotransmitter

•As part of an immune response to foreign pathogens, histamine is produced

by basophils and by mast cells found in nearby connective tissues.

•Histamine increases the permeability of the capillaries to white blood cells and
some proteins, to allow them to engage pathogens in the infected tissues
2-The kinin–kallikrein system 
•or simply kinin system . It consists of blood proteins that play
a role in inflammation, blood
pressure control, coagulation and pain. Its important
mediators bradykinin and kallidin are vasodilators and act on
many cell types.
3-Serotonin
• secreted from the enterochromaffin cells eventually finds its way

out of tissues into the blood. There, it is actively taken up by

blood platelets, which store it.

•When the platelets bind to a clot, they release serotonin, where it

serves as a vasoconstrictor and helps to regulate hemostasis and
blood clotting.

• Serotonin also is a growth factor for some types of cells, which

may give it a role in wound healing.
4-Prostaglandins:
• have two derivatives: prostacyclins and thromboxanes.

•Prostacyclins are powerful locally acting vasodilators and inhibit the aggregation

of blood platelets.

•Through their role in vasodilation, prostacyclins are also involved

in inflammation. They are synthesized in the walls of blood vessels and serve the
physiological function of preventing needless clot formation, as well as
regulating the contraction of smooth muscle tissue.

•Conversely, thromboxanes (produced by platelet cells) are vasoconstrictors and

facilitate platelet aggregation.
5-Leukotrienes

• are a family of inflammatory mediators produced in leukocytes by

the oxidation of arachidonic acid (AA) .

•Leukotrienes use lipid signaling to convey information to either the cell

producing them (autocrine signaling) or neighboring cells (paracrine
signaling) in order to regulate immune responses. 

•Leukotriene production is usually accompanied by the production

of histamine and prostaglandins, which also act as inflammatory mediators.
6-Platelet-activating factor
•also known as PAF, AGEPC (acetyl-glyceryl-ether-
phosphorylcholine), is a potent phospholipid activator and
mediator of many leukocyte functions, platelet aggregation and
degranulation, inflammation, and anaphylaxis.
•It is also involved in changes to vascular permeability, the
oxidative burst, chemotaxis of leukocytes, as well as
augmentation of arachidonic acid metabolism in phagocytes.
PAF is produced by a variety of cells, but especially
those involved in host defense, such
as platelets, endothelial cells, neutrophils, monocyts,
and macrophages.
7-Complement System
• The complement system is a biochemical cascade of the
immune system that helps, or “complements”, the ability of
antibodies to clear pathogens or mark them for destruction
by other cells.

• The cascade is composed of many plasma proteins,

synthesized in the liver, primarily by hepatocytes. The
proteins work together to:

• trigger the recruitment of inflammatory cells

• "tag" pathogens for destruction by other cells by opsonizing,
or coating, the surface of the pathogen

• form holes in the plasma membrane of the pathogen,

resulting in cytolysis of the pathogen cell, causing the death
of the pathogen

• rid the body of neutralised antigen-antibody complexes

8-C-reactive protein (CRP)
Its physiological role is to bind to the surface of dead or dying cells
(and some types of bacteria) in order to activate the complement
system via the C1Q complex

•CRP is synthesized by the liver in response to factors released

by macrophages and fat cells (adipocytes). 
9-Fibronectin 

•is a high-molecular weight glycoprotein of the extracellular

matrix that binds to membrane-spanning receptor
proteins called integrins.

•Similar to integrins, fibronectin binds extracellular matrix

components such as collagen and fibrin.
• Fibronectin plays a major role in cell
adhesion, growth, migration, and differentiation, and it is
important for processes such as wound
healing and embryonic development. 

• Altered fibronectin expression, degradation, and

organization has been associated with a number
of pathologies, including cancer and fibrosis.
10-Lysozymes
• These are enzymes that damage bacterial cell walls.

•Lysozyme is abundant in a number of secretions, such

as tears, saliva, human milk, and mucus.

• It is also present in cytoplasmic granules of

the macrophages and the polymorphonuclear
neutrophils (PMNs)
Cellular Reaction:
• All white blood cells (WBCs) are known as leukocytes.

• Leukocytes differ from other cells of the body in that they are not tightly
associated with a particular organ or tissue; thus, their function is similar to
that of independent, single-cell organisms.

• Leukocytes are able to move freely and interact with and capture cellular
debris, foreign particles, and invading microorganisms. Unlike many other
cells in the body, most innate immune leukocytes cannot divide or
reproduce on their own, but are the products of multipotent hematopoietic
stem cells present in the bone marrow
• The innate leukocytes include: Natural killer
cells, mast cells, eosinophils, basophils; and
the phagocytic cells include macrophages, neutrophils,
and dendritic cells, and function within the immune
system by identifying and eliminating pathogens that
might cause infection
1-MAST CELLS
• Mast cells are a type of innate immune cell that reside in connective tissue
and in the mucous membranes. They are intimately associated with wound
healing and defense against pathogens, but are also often associated
with allergy and anaphylaxis.

•  When activated, mast cells rapidly release characteristic granules, rich

in histamine and heparin, along with various hormonal mediators
and chemokines, or chemotactic cytokines into the environment. Histamine
dilates blood vessels, causing the characteristic signs of inflammation, and
recruits neutrophils and macrophages.
 2-Macrophages
• These are immune cells that engulf, or 'phagocytose', pathogens or particles. To
engulf a particle or pathogen, a phagocyte extends portions of its plasma
membrane, wrapping the membrane around the particle until it is enveloped .
Once inside the cell, the invading pathogen is contained inside an endosome,
which merges with a lysosome.

•  The lysosome contains enzymes and acids that kill and digest the particle or
organism. In general, phagocytes patrol the body searching for pathogens, but are
also able to react to a group of highly specialized molecular signals produced by
other cells, called cytokines.

• The phagocytic cells of the immune system include macrophages, neutrophils,

and dendritic cells.
3-Neutrophils

• Neutrophils, along with two other cell types (eosinophils and basophils), are

known as granulocytes due to the presence of granules in their cytoplasm,
or as polymorphonuclear cells (PMNs) due to their distinctive lobed nuclei.

• Neutrophil granules contain a variety of toxic substances that kill or inhibit

growth of bacteria and fungi. Similar to macrophages, neutrophils attack
pathogens by activating a respiratory burst.
• The main products of the neutrophil respiratory burst are
strong oxidizing agents including hydrogen peroxide, free
oxygen radicals and hypochlorite. Neutrophils are the most
abundant type of phagocyte, normally representing 50-60%
of the total circulating leukocytes, and are usually the first
cells to arrive at the site of an infection.
Interleukins 
•are a group of cytokines (secreted proteins and signal molecules) that were first seen to be expressed
by white blood cells (leukocytes).

•The function of the immune system depends in a large part on interleukins, and rare deficiencies of a

number of them have been described, all featuring autoimmune diseases or immune deficiency. The
majority of interleukins are synthesized by helper CD4 T lymphocytes, as well as
through monocytes, macrophages, and endothelial cells.

•They promote the development and differentiation of T and B lymphocytes, and hematopoietic cells.

Interleukin 1

• Interleukin 1 alpha and interleukin 1 beta (IL1 alpha and IL1

beta) are cytokines that participate in the regulation of immune
responses, inflammatory reactions, and hematopoiesis.

• It include osteoclast activating factor (OAF) and lymphocyte

activating factors(LAF), it is also stimulate the release of matrix
metalloproteinase enzyme which degrade proteins.
• It is secreted by monocytes macrophages, B cells and fibroblasts.
Interleukin 2
• T lymphocytes regulate the growth and differentiation of T
cells and certain B cells through the release of secreted
protein factors.

• IL2 is a lymphokine that induces the proliferation of

responsive T cells. In addition, it acts on some B cells, via
receptor-specific binding, as a growth factor and antibody
production stimulant.
 Interleukin 6
• Interleukin 6 (IL6), also referred to as B-cell stimulatory
factor-2 (BSF-2) and interferon beta-2, is a cytokine
involved in a wide variety of biological functions.

• It plays an essential role in the final differentiation of B

cells into immunoglobulin-secreting cells, as well as
inducing myeloma/plasmacytoma growth, nerve cell
differentiation, and, in hepatocytes, acute-phase reactants
 Interleukin 8

• Interleukin 8  is a chemokine produced
by macrophages and other cell types such as epithelial cells,
airway smooth muscle cells and endothelial
cells. Endothelial cells store IL-8 in their storage vesicles

• It appear selectively stimulate matrix metalloproteinase

(MMR) activity which is very important for collagen
destruction and periodontitis.
 Tumor Necrosis Factor
• Tumor necrosis factor  is a cell signaling protein (cytokine) involved in
systemic inflammation and is one of the cytokines that make up the acute
phase reaction. It is produced chiefly by activated macrophages, although it
can be produced by many other cell types such as CD4+ lymphocytes, NK
cells, neutrophils, mast cells, eosinophils, and neurons.

• The primary role of TNF is in the regulation of immune cells. It play a role in
activation of osteoclast and so in bone resorption.
4-Lymphocyte
• A lymphocyte is one of the subtypes of white blood cell in the immune
system. Lymphocytes include natural killer cells (NK cells) (which
function in cell-mediated, cytotoxic innate immunity), T cells (for cell-
mediated, cytotoxic adaptive immunity), and B
cells (for humoral, antibody-driven adaptive immunity). They are the
main type of cell found in lymph, which prompted the name

"lymphocyte".
• The adaptive immune system, also known as
the acquired immune system or, more rarely, as
the specific immune system, is a subsystem of the
overall immune system that is composed of highly
specialized, systemic cells and processes that
eliminate pathogens or prevent their growth.
• Humoral immunity or humoural
immunity is the aspect of immunity that is
mediated by macromolecules found in extracellular
fluids such as secreted antibodies, complement
proteins, and certain antimicrobial peptides. Its
aspects involving antibodies are often
called antibody-mediated immunity.
• Humoral immunity refers to antibody production and the
accessory processes that accompany it, including: Th2 activation
and cytokine production, germinal center formation
and isotype switching, affinity maturation and memory
cell generation. It also refers to the effector functions of
antibodies, which include pathogen and toxin neutralization,
classical complement activation, and opsonin promotion
of phagocytosis and pathogen elimination
• Cell-mediated immunity is an immune
response that does not involve antibodies, but
rather involves the activation
of phagocytes, antigen-specific cytotoxic T-
lymphocytes, and the release of
various cytokines in response to an antigen.
• Activated Effector T cells can be placed into three functioning
classes, detecting peptide antigens originating from various types
of pathogen: The first class being Cytotoxic T cells, which kill
infected target cells by apoptosis without using cytokines, the second
class being TH1 cells, which primarily function to activate
macrophages, and the third class being TH2 cells, which primarily
function to stimulate B cells into producing antibodies.

• The innate immune system and the adaptive immune system each

comprise both humoral and cell-mediated components.
Gingival Bleeding
• Earliest signs of gingival inflammation bleeding on
probing

• increase in gingival fluid

• Gingival bleeding on probing is easily detectable

clinically and therefore is of great value for the early
diagnosis and prevention of more advanced gingivitis
Bleeding On Probing

Detection of bleeding is more

reliable than color changes to
identify early gingivitis
Histologic Exam Of Gingival Bleeding
Sites

*dilation and engorgement of capillaries

*thinning or ulceration of sulcular epithelium

*stimuli that are ordinarily innocuous cause rupture of

capillaries

•Severity of bleeding and ease of provocation depend on degree

of Inflammation

•Bleeding is considered a sign of active tissue destruction

Color Changes In Chronic Gingivitis

Related to vascularity and keratinization

― Vascular proliferation in inflammation - increases redness

― Venous stasis - causes bluish hue

 Changes begin in interdental papillae and gingival margin

and spread to attached

 Color changes vary with the intensity of inflammation

― Initial bright red erythema

Changes In Consistency Of Gingiva

• Destructive changes - edematous tissue

• Reparative changes - fibrotic tissue

• Calcified masses in tissue - root remnants,

cementum fragments, or cementicles
Changes In Surface Texture

• Loss of stippling

• Fibrotic changes - over stippling

Indices
 Plaque Index
 Gingival Index
Plaque Index

 PI of Silness and Löe (1964)

 Records the plaque thickness on the gingival 1/3 of the

tooth

 Complementary index to GI
Criteria
0 = No plaque in the gingival area
1 = A film of plaque adhering to the free gingival margin and
adjacent area of the tooth. The plaque may be recognized only
by running a probe across the tooth surface
2 = Moderate accumulation of soft deposits within the gingival
pocket and on the gingival margin and/or adjacent tooth surface,
which can be seen by the naked eye.
3 = Abundance of soft deposits within the gingival pocket
and/or on the gingival margin and/or adjacent tooth surface
Gingival Index Of Löe and Silness (1963)
THANK YOU