PLAQUE AND

CALCULUS

PRESENTER- SANU SUSAN SAM

GUIDED BY-DR. SOWMYA SHETTY
1
PLAQUE:
 INTRODUCTION
 DEFINITION
 CLASSIFICATION
 STRUCTURE AND COMPOSITION
 FEATURES OF BIOFILM
 MICROBIAL COMPOSITION
 FORMATION OF DENTAL PLAQUE
 GROWTH DYNAMICS OF DENTAL PLAQUE
2
 FEATURES OF SUPRA GINGIVAL PLAQUE
FORMATION

 PHYSIOLOGIC PROPERTIES OF DENTAL PLAQUE

 SPECIAL BACTERIAL BEHAVIOUR IN DENTAL

BIOFILM

 PLAQUE AND ITS RELATION TO DENTAL CARIES

 INDICES FOR ASSESSMENT OF PLAQUE & PLAQUE

DISCLOSING AGENTS

3
CALCULUS:
 DEFINITION
 CLASSIFICATION
 COMPOSITION AND STRUCTURE OF DENTAL
CALCULUS
 ATTACHMENT TO TOOTH SURFACE
 FORMATION OF CALCULUS
 THEORIES OF MINERALIZATION
 THE DRIVING FORCE FOR PLAQUE
MINERALIZATION
4
  On the basis of physical & morphologic criteria,
oral cavity can be divided in to 5 major
ecosystems:
1. Intraoral, supragingival, hard surfaces (teeth,
implants, restorations & prosthesis)
2. Periodontal/periimplant pocket (with its
crevicular fluid, root cementum or implant surface,
& the pocket epithelium)
3. Buccal epithelium, palatal epithelium & epithelium
of floor of mouth.
4. Dorsum of tongue
5. Tonsils
 Teeth
•Non shredding surfaces
Cheeks, Lips, Palate •Stagnant sites; food
•Microflora has low impaction possible
diversity •Influenced by GCF &
•Some periodontal saliva
pathogens persist by •Streptococcus,
invading buccal cells. Actinomyces, Veillonella,
•Streptococcus spp. Fusobacteria, Prevotella,
predominate Treponema

Tongue
•Highly papillated surfaces
•Some anaerobic sites.
•Facultative & obligate anaerobes
•Streptococcus, Actinomyces, Rothia,
Neisseria
 Gram Gram
negative positive

cocci cocci

rods rods
8
 Cocci Rods
Abiotrophia Actinobaculum
Enterococcus Actinomyces
Gemella Alloscardovia
Preptostreptococcus Bifidobacterium
Streptococcus Cornybacterium
Finegoldia Eubacterium
Granulicatella Filifactor
Lactobacillus
Propionibacterium
Rothia
solobacterium
9
 Cocci Rods
Anaeroglobu Aggregatibacter
Mega sphaera Campylobacter
Moraxella Cantonella
Neisseria Capnocytophaga
Veillonella Centipeda
Eikenella
Leptotrichia
Prevotella
Porphyromonas
Tanerella
Treponema
wolinella
 Fissure
proximal •Gram positive; Gingival crevice
•Gram positive & •Facultative •Gram positive &
gram negative; anaerobes gram negative &
facultative & 1. Streptococcus obligate
obligate 2. Actinomyces anaerobes:
anaerobes: 1. Streptococcus
1. Neisseria 2. Prevotella
2. Streptococcus 3. Actinomyces
3. Prevotella 4. Treponema
4. Actinomyces Tooth 5. Eubacterium
5. veillonella
Once a tooth erupts, various materials gather on its
surfaces, these substances are frequently called tooth
– accumulated materials/deposits.

They are classified as:

Soft deposits:
 Acquired pellicle
 Microbial plaque
 Materia alba
 Food debris
Hard deposits:
 Calculus
 Stains

12
 The descriptive term gelatinous microbial plaque was first
introduced by J.C William and G.V Black in 1898 to
describe microbial colonies on tooth surfaces.

 Black’s terminology has been shortened to the term

‘Plaque’ by Wild (1941) and its usage has been restricted
to denote only those deposits that are predominantly
microbial in nature.

13
PLAQUE - A French term “PLAQUIER” meaning,
to plate.

 MANDEL- “ A bacterial aspic with millions of

organisms standing shoulder to shoulder.”

 LOE- “Plaque is the soft, mineralized, bacterial deposit

which forms on teeth (and dental prosthesis) that are not
adequately cleaned.”

14
WHO DEFINITION :

Plaque is a specific but highly variable structural entity

resulting from colonization of microorganisms on tooth
surfaces, restorations or other parts of oral cavity,
composed of salivary components like mucin,
desquamated epithelial cells, debris and microorganisms
all embedded in gelatinous extracellular matrix.

15
MAX A. LISTGARTEN –

The non mineralized microbial accumulation that

adheres tenaciously to tooth surface, restorations and
prosthetic appliances, shows structural organization with
predominance of filamentous forms, is composed of an
organic matrix derived from salivary Glyco-proteins and
extracellular microbial products and cannot be removed
by rinsing or water spray.

16
  Dental plaque must be differentiated from other tooth
deposits, like materia alba and calculus.

 Materia Alba refers to soft accumulations

of bacteria and tissue cells that lack
the organized structure of dental plaque.

 Calculus is hard deposits that form by mineralization of

dental plaque and is generally
covered by a layer of un mineralised
plaque.

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18
- SUPRAGINGIVAL PLAQUE
- SUBGINGIVAL PLAQUE
- MARGINAL PLAQUE

19
20
21
CATE- TOOTH DESCRIPITION DERIVATION
GORY DEPOSIT
NON- ACQUIRED Translucent, homogenous, thin, ultra structured film Supra gingival
MINER PELLICLE covering and adherent to the surfaces of the teeth, :saliva
AL- restorations, calculus, and other surfaces of the oral Sub gingival :GCF
IZED cavity
MICRO- Dense organized bacterial system embedded in an inter Colonization of oral
BIAL- microbial matrix that adhere closely to the teeth, calculus, micro-organisms
PLAQUE and other surfaces of the oral cavity

MATERIA Loosely adherent, ultra structured, white or grayish, white Incidental

ALBA mass of oral debris and bacteria that lies over bacterial accumulation
plaque
Vigorous rinsing and water irrigation can remove materia
alba
FOOD Unstructured, loosely attached particulate matter self- Food retention
DEBRIS cleansing activity of tongue and saliva and rinsing following eating
vigorously remove debris

MINE SUPRA- Calcified bacterial plaque: hard tenacious mass that forms Plaque
GINGIVAL on the clinical crown of the natural teeth & on dentures mineralization
RAL- CALCULUS and other appliances
IZED Occurs coronal to the margin of gingiva ; is covered with Source of minerals
bacterial plaque is saliva
SUB- Occurs apical to the margin of gingiva ; is covered with Source of minerals
GINGIVAL bacterial plaque is GCF
CALCULUS

22
 Composed Primarily of Microorganisms
 1gm of plaque = 2 x 1011 bacteria (wet weight)

 More than 500 different bacterial species found

 Non Bacterial Microorganisms-

mycoplasma,yeasts, protozoa and viruses

 Host cells found –

epithelial cells, macrophages and leucocytes

23
CHARACTE SUPRAGINGIVAL SUBGINGIVAL
-RISTICS
LOCATION Coronal MG Apical MG
ORIGIN Salivary down growth bact
glycoprotein from supra gingival
plaque
DISTRIBU- Starts proximal surface Shallow pocket
TION and other protected areas Attached plaque
Heaviest collection on covers calculus
areas not cleaned daily by Unattached
patient plaque extends to
Cervical third , esp. facial the periodontal
and lingual Mandibular attachment
molars
Proximal surfaces
Pits and fissures plaque
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ADHES- Firmly attached to Adhere to
acquired pellicle tooth surface
ION
Surface bacteria subgingival pellicle
(unattached ) loose:  calculus
washed away by saliva
RETEN- Rough surface teeth Pocket hold plaque
restoration , malpositioned against tooth and
TION or carious teeth overhanging margins

SHAPE Friction of tongue lips Molded by pocket

AND cheeks , cervical area wall, follows the form
Thickness: thicker at created by
SIZE
the cervical end and on subgingival calculus
proximal surfaces
Healthy gingival: thin
plaque ,15 to 20 cells thick
Chronic gingivitis: thick
plaque,100 to 300 cells
thick 25
STRUCTURE Densely packed three layers
1. tooth surface attached
plaque: many gram
positive rods and cocci
2. unattached plaque in
middle: many gram
neg, motile forms,
spirochetes,
leukocytes
3. epithelium attached
plaque : gram neg,
motile forms
predominate, many
leukocytes migrate
through epithelium

26
 Composition –
organic and in - organic

27
 80% water
 20% solids, includes cells mainly bacteria making up 35% of
the dry weight and extracellular components making 65% of
the dry weight.
 Other than bacteria, non bacterial organisms include:
• Mycoplasma
• Yeast
• Protozoa
• Viruses
 Host cells in Dental plaque.
 Epithelial cells
 Macrophages
 Leukocytes

28
Intermicrobial Matrix
 the material present between the bacteria in the
dental plaque is called the intermicrobial
matrix.
 accounts for approx 25% of plaque volume.

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 INTERCELLULAR MATRIX OF
DENTAL PLAQUE

Organic constituents

Inorganic constituents

Material from Saliva, GCF and bacteria

 ORGANIC CONSTITUENTS

Poly saccharides - dextran 95% , levan 5%, Sialic

acid and fructose

 Proteins - Albumin

 Glycoproteins - saliva

 Lipid materials - Membrane remnants of bacteria

and host cells.
CARBOHYDRATES:
Fructans (Levans) :
synthesized in plaque from dietary sucrose
provide a storage of energy which may be
utilized by the microorganisms in time of
low sugar supply
Glucans:
also synthesized from sucrose & of two types:
Dextran: serve as energy storage
Mutan: acts primarily as a skeleton in the matrix
in much the same way as collagen stabilizes
the intercellular substances of connective
tissue.

32
INORGANIC CONSTITUENTS

Primarily - Calcium & Phosphate

Traces - Sodium, Potassium and Fluoride
Fluoride - From external sources like
is derived tooth paste, mouth washes
Non bacterial microorganisms that are found in
plaque include
 mycoplasma species

 yeast

 protozoa, and

 viruses

The micro organisms exist with in a intracellular

matrix that also contains
 a few host cells, such as epithelial cells ,

 macrophages and

 leukocytes

34
 The process of plaque formation can be divided
into three phases:-

1. Formation of dental pellicle

2. Initial attachment and Colonization
3. Secondary colonization & plaque
maturation

35
 It is initial phase of plaque development.

 Surfaces of teeth and fixed/removable

restorations coated with glycoprotein pellicle
derived from saliva and GCF. {also from
bacterial and host cells products and debris}.

 Acc to Hanin(1999) pellicle layer is formed on

enamel as early as 1 min after exposure.

36
 Acc to Colla (1983);
Hydroxyapatite surface has a predominance
of –vely charged phosphate components that
interact with +vely charged components.
{derived from salivary and crevicular fuid
macro molecules}.

37
 Thin saliva-derived layer called “accquired
pellicle” covers the tooth surface.

 Pellicle consists of:- mucins, proline-rich

proteins, phosphoproteins (eg:- statherin),
histidine rich proteins, enzymes (eg- α-
amylase); {ACT AS ADHESION SITES FOR BATERIA}

 Although term “accquired pellicle” is misleading.

(Bacteria are found to be attached within seconds after
prophylaxis)

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CHEMICAL COMPOSITION OF ACQUIRED PELLICLE
(Mayhell & Butller 1976, Sonju 1975)
 4.6% amino acids
 2.7% Hexosamine
 14% Total carbohydrates
 Lipids - in small amounts

Amino acids in the pellicle
Hexosamines in the pellicle
Carbohydrates in the pellicle
Salivary Molecules in the pellicle
Pellicle contains more hydrophobic and less neutral
amino acids than whole saliva (ie more leucine,
alamine, tyrosine and sereine than saliva)
Glucosamine - 18%, Galactosamine -18%
Glucose - 20%, Galactose - 27%
Mannose - 9% Fructose - 18%
Acinar cell families
Mucins
Proline rich proteins - statherins
Cystatins, Amylases
Ductal & stromal products
Lactoferrin & Lysozyme
41
 This concept approaches microbial adhesion to
surfaces in aquatic environment as 4 stage
sequence:

Colonization
of surface &
Attachment biofilm
formation

Initial
adhesion

Transport to
surface

42
Clean Molecular Single Sequential
substratum adsorption organisms Multiplication adsorption
(Phase 1) (Phase 2) (Phase 3) of organisms
(Phase 4)

43
Stage I - Attachment (lag - not inert, but metabolically reduced)
Stage II - Growth (log - exponential growth)
Stage III - Maturity (stationary)
Stage IV - Dispersal (death)
44
 Random contacts occur through:

 Brownian motion ( 40 µm/hour)

 Sedimentation of organisms
 Liquid flow
 Active bacterial movement (chemotactic activity)

45
Derjaguin, Landau, Verwey and Overbeek (DLVO)
postulated that,

 above a separation of 1 nm, the summation of

vander wal (attaractive; GA) and electrostatic forces
(repulsive; GE) describes total long range interaction.

 If a particle reaches the primary minimum (<1nm

from the surface), a group of short range forces (eg
hydrogen bonding, ionic pair formation, steric
interaction) dominates the strength of adhesion.

46
 By Reversible adhesion of the bacterium and
the surface
 The proteins and carbohydrates that are
exposed on the bacterial cell surface become
important once the bacterial are in loose contact
with the acquired enamel pellicle.

47
 A firm anchorage between bacterium and
surface will be established by specific
interactions ( ionic, covalent, or hydrogen
bonding)

48
 Adhesins can be subdivided into two major
classes:

Fimbrial adhesins, including fimbriae, pili, curli

and type IV pili,
Nonfimbrial adhesins, such as autotransporter,
outer membrane and secreted adhesins,
Those associated with biofilm formation

Periodontology 2000, Vol. 52, 2010, 12–37

49
 Fimbrial adhesins of gram-negative bacteria are
classified into five major classes –
 Chaperone–usher (CU) pili,
 Curli,
 Type IV pili,
 Type III secretion pili and
 Type IV secretion pili – based on their
biosynthetic pathway

50
 Curli are thin aggregative fimbriae identified
as a new type of fimbrial adhesin expressed on
the outer surfaces of some Enterobacteriaceae,
such as Escherichia and Salmonella spp.
 Curli promote bacterial adhesion to and
invasion of the host, as well as biofilm
formation, and they also function as a potent
promoter of host pro-inflammatory responses.

51
Fimbriae:
• Are proteinaceous hair like appendages
• Composed of protein subunits called fimbrillin
• Fimbriae also carry adhesins

Fimbriae of oral strain are thin, flexible and 2-3nm in

diameter, thus differing from larger more rigid filmbriae
found on other bacteria such as eschericia coli

•Fibrils are also found oral bacterial

species
e.g. S. mitis, Prevotella intermedia,
Prevotella nigrescens and S. mutans.

52
 Other factors that help in attachment of bacteria

• Force generating movement is an important first

step in biofilm formation by G-ve bacteria
• Active motility due to the production of flagella or twitching
mobility due to type IV pili are thought to increase the no of
initial interactions between bacterial cells and solid surfaces
and to help overcome initial repulsive forces between bacteria
and the surface.
• Cell surface proteins of staphylococcus epidermidis and
Caulobacter crescentus are imp in initial attachment.

•Polysaccharide adhesion of S. epidermidis

54
 Selective adsorption of bacteria from oral fluids
to the pellicle.

 Predominantly gram +ve facultative micro

organisms;
Actinomyces, S.sanguis etc.

 S.salivaris prominent on tongue dorsum bind

to slivary components involving the selective
adsorption process.

55
56
 Plaque mass matures through growth of
attached species, colonization and growth of
additional species.

 Transition from early aerobic environment of

gram +ve facultative species to oxygen
deprived gram –ve anaerobic environment.

57
 Undisturbed plaque becomes thicker and
additional bacterial species are detected.

 Flora of plaque changes from predominantly

coccal to mixed filamentous flora.{7-14 days}

 Matrix is formed via adhesion b/w bacteria and

matrix, which involves, bacterial polymer
synthesis or adhesion of salivary components.
58
 Extra cellular glycan synthesis promotes
accumulation of S.mutans but interestingly not
of other glycan synthesizing species(S.sanguis).

 It can be explained by,

-lack of glycan binding sites on the cell
surface.
-inability of cells to bind to GTF.
- differences in nature of the glycan
synthesized.

59
 Gibbons (1980); Houte J. Van (1982):
Their studies suggest that:
- plaque organism unable to produce GTF
(eg veillonella) can bind to these organisms and
then enable them to form plaque

- glycan synthesized by cell free enzymes

promote accumulation of other nearby located
organisms by glycan mediated adhesion.

60
 Aging of plaque is accomapnied by increase in
bacterial density.

 Coaagregation plays more significance during

aging of plaque.

61
 It was described by Gibbsons & Nygaard
 Corncob formation - Streptococci adheres to
filaments of bacterionema matruchotti or
actinomyces species
 Test tube brush – composed of filamentous
bacteria to which gram negative rods adhere.

62
 Corn cob arrangement:
Long standing supra gingival plaque near gingival
margin demonstrates “corncob” arrangement. A
central gram-ve filamentous core that supports outer
coccal cells. Firmly attached by inter bacterial
adherence or coaggregation
63
TO BE CONTINUED

64
GOOD MORNING

65
 FEATURES OF SUPRA GINGIVAL PLAQUE
FORMATION

 PHYSIOLOGIC PROPERTIES OF DENTAL PLAQUE

 SPECIAL BACTERIAL BEHAVIOUR IN DENTAL

BIOFILM

 PLAQUE AND ITS RELATION TO DENTAL CARIES

 INDICES FOR ASSESSMENT OF PLAQUE & PLAQUE

DISCLOSING AGENTS

66
“QUORUM SENSING” Microbial communication.
 Involves the regulation of expression of specific genes
through the accumulation of signaling compounds that
mediate inter-cellular communication.

 Signaling compounds reach a threshold level “Quorum cell

density”, the gene expression can be activated.

 Quorum sensing plays a role in expressing genes for antibiotic

resistance and encourages the growth of beneficial species to
biofilm and discouraging growth of competitors.

68
1. Individual variables
“heavy or fast plaque” former and “light or slow plaque” former-
this depends on various factors as
• diet, chewing fibrous food,
• smoking,
• amalgam restorations,
• tongue and palate brushing,
• the colloidal stability in saliva,
• antimicrobial factors of GCF and saliva
• pellicle composition and
• retention depth of dento-gingival area
69
In general early plaque formation occurs faster
1. In lower jaw compared to upper jaw
2. In molar areas
3. On buccal tooth surfaces compared to other sites
(especially in upper jaw)
4. In the interdental regions compared to buccal or
other surfaces.

70
 Plaque formation is more
rapid on tooth surfaces facing
inflamed gingival margins
than on those adjacent to
healthy gingiva.

 Substances from
GCF as mineral, protein,
carbohydrate favors both
the initial adhesion and
growth of early colonizing
bacteria.

71
 4. Impact of patient’s age
 Developed plaque in older patient , results in
more severe gingival inflammation, this
indicate an increased susceptibility gingivitis
with aging.

72
 First 24 hours, clinically negligent amount of
plaque formation. i.e, <3% coverage of tooth
surface.
 Rapid growth is observed during following days
which slows down grdually.
 After 4 days, 30% of tooth surface is covered.
 Plaque growth is decreased during night time by
50%. {nutrient supply from saliva is important}

73
 2-8 hrs- streptococci saturate salivary pellicle
and thus covers 3%-30% of enamel surface.
 After 1 day biofilm is established.
 Closely packed micro-organism form palisades
while others form pleomorphism.
 During later hours, bacterial densities turn
from
2 to 6 million bacteria/mm2 to 32 million
bacteria/mm2 on the enamel surface.
{due to multiplication of adherent bacteria rather than new
colonizers}.

74
 Plaque thickness increases 20 to 30µm within 3
days.

75
DAY 1 TO 2 gram +ve Cocci, Streptococci (dominate),
Strepto mutans, Strepto sanguis
DAY 2 TO 4 Cocci still dominate , increase gram+ve
filamentous form, slender rods , gradually
filamentous forms replaces cocci.
DAY 4 TO 7 Filaments increases in numbers, and a
more mixed flora begins to appear with
rods, filamentous forms and Fusobacteria .
 Plaque near margin thickens and
develops a more mature flora with gram
neg spirochetes and vibros .
 As plaque spreads coronally, the new
plaque has the characteristic
76 coccal forms
DAY 7 TO 14 Vibros and spirochetes appear. No.
of WBC increases , as plaque
mature and thickens more,gram+ve
anaerbic org appear “during this
period sign of inflammation on
gingiva occurs”
DAY 14 TO 21 Vibros + spirochetes prevalent
along with cocci and filamentous
The densly packed filamentous
organisms arrange themselves
perpendicular to the tooth surface in
a palisade “gingivitis evident
clinically”.
77
Colonies of morphologically Mixture of different
similar organisms Microorganisms

78
 Transition in structural development of plaque is
preceded by physiologic transition.
Increased
Streptococci & Consume the O2, reduce the growth of
actinomyces redox potential of the anaerobic
atmosphere
species in the
plaque.

79
 Gram +ve species use sucrose as their energy
source & saliva as a C source.

 Predominating species of plaque are

ANEROBIC & ASACCHROLYTIC. {utilize
amino acids & small peptides as energy
sources}.

 Lactate and Formate are byproducts of

streptococci & actinomyces and are utilized by
other species as energy source.

80
 Growth of P.gingivalis is enhanced by byproducts of
Capnocytophaga ochraceus (succinate) & Capnocytophaga
rectus.

 Breakdown of host proteins (through bacterial enzymes)

releases Ammonia, provides Nitrogen.

- Host hemoglobin provides Fe; enhances growth of

P.gingivalis.

- Host steroids(hormones) ; increases proportions of

Prevotella intermedia in subgingival plaque
81
82
 two major groups of bacteria, namely the mutans
streptococci and the lactobacilli species, are able to
produce organic acids during metabolism of
fermentable carbohydrates
 The acids produced include lactic, acetic, formic
and propionic, all of which have been shown to
readily dissolve the mineral of the enamel and
dentine
 Bacteria which produce acid as a by-product of
their metabolism are known as acidogenic, and
some, such as the groups named above, are
aciduric and can live in an acid environment

83
 Sucrose has been given special importance due
to its involvement as the sole substrate in the
synthesis of extracellular (water-soluble and
water-insoluble) glucans mediated by microbial
glycosyltransferases
 Glucans can form a major component of the
structural intermicrobial matrix of dental plaque
[Guggenheim, 1970].
 water-insoluble glucans enhance the ability of
mutans streptococci to accumulate on the
smooth surfaces of teeth [Gibbons, 1984].

86
sucrose-mediated synthesis of glucans increases
 the porosity of plaque, permitting deeper
penetration of dietary sugar into the biofilm
 greater acid production immediately adjacent
to the tooth surface

[Dibdin and Shellis, 1988; van Houte et al., 1989;

Zero, 1993].

87
 Bacteria are capable of producing
Polysaccharide more by using sucrose as the
substrate

 The polysaccharides in biofilms can be divided

into two categories:
 (1) extracellular polysaccharides (EPS),
 (2) intracellular polysaccharides (IPS),

88
 EPS are synthesized mostly by bacterial
glucosyltransferases (GTFs) and, to a lesser
extent, by fructosyltransferases (FTFs) using
sucrose as primary substrate.

 The GTFs from S. mutans synthesize a mixture of

α(1→3)-linked insoluble glucans and
α(1→6)-linked soluble glucans,
 whereas FTF produces α(2→6)-linked fructans.

89
 The EPS are largely insoluble, have a complex structure
and promote selective adherence and accumulation of
large numbers of cariogenic streptococci on the teeth.

EPS increase the bulk and porosity of dental plaque

matrix, thereby allowing more substrate to diffuse to the
enamel surface.

They play a role in cell wall permeability, in

enzyme location, in specificity and in
resisting immune responses

90
 Makes upto 10%-20% of volume of the plaque.
 Includes:- Glycans, Fructans, Hetropolysacchrides
and lipoteichoic acid. {Fitzgerald, 1976}.
 Streptococci, Actinomyces and Neisseria can produce
extra cellular polymers- glycan, {Newbrun, 1976}.

Sucrose Bacterial species in presence of Glucan

Glucosyltransferase*

{*Acc to Germaine et al 1976} 91

 IPS are high-molecular-weight metabolizable glycogen-
like storage polymers with α(1→4) and α(1→6) which
provide the micro-organisms with an endogenous
source of carbohydrate during periods of nutrient
limitation in the oral cavity.

IPS can promote the formation of dental caries by prolonging

the exposure of tooth surfaces to organic acids and
maintaining a lower fasting pH in the matrix of the
plaque.

93
 EPS & IPS influence the cariogenicity of dental
biofilms in two pathways:-

1. EPS promote bacterial adherence &

accumulation on the tooth surface.
2. IPS promote lower fasting pH during periods of
nutrition deprivation.

94
1. The rate of sucrose consumption was noticeably
higher in cariogenic plaque

2. The rate of lactic acid formation was considerably

higher in cariogenic plaque

3. Bacteria in cariogenic plaque synthesized more

intra cellular glycogen-amylopectin type
polysaccharides

4. Upto 2% of the sucrose consumed within 15 min

was converted into IPS by cariogenic plaque.
96
5. Cariogenic plaque formed approximately twice as much
extracellular polysaccharides from sucrose as did non
cariogenic plaque

6. Cariogenic plaque contain higher level of S mutan than

non cariogenic plaques

7. Non cariogenic plaques harboured higher level of S

Sanguis and Actinomyces than cariogenic plaques

8. Non cariogenic plaques had significantly higher

proportion of dextranase producing organism

9. Non-cariogenic plaques had higher level of Veillonella

and contained slightly lower concentration of lactic acid
and slightly high concentration of acetic acid and
propionic acids.
97
 Early in the 19th century, it was, like the situation
with diseases such as tuberculosis, a specific bacterial
species was responsible for the disease processes.
 The criteria by which a given bacterial species was
associated with disease historically has been through
the application of Koch's Postulates.

98
These criteria were developed by Robert Koch
in the late 1800's. The criteria are as follows:
 A specific organism can always be found in
association with a given disease.
 The organism can be isolated and grown in pure
culture in the laboratory.
 The pure culture will produce the disease when
inoculated into a susceptible animal.
 It is possible to recover the organism in pure
culture from the experimentally infected animal.

99
the concept that a specific bacterial species was responsible for
periodontal diseases fell out for several reasons.

 First, despite numerous attempts, a specific bacterial agent

was not isolated from diseased individuals. Rather, the
organisms found associated with disease were also found
associated with health.

 Good experimental animal model systems of periodontal

disease were not available to test the pathogenicity of
specific microorganisms

100
 in the mid 1900's, epidemiological studies indicated
that the older an individual was, the more likely they
were to have periodontal disease.

 This led to the concept that the bacterial plaque itself,

irrespective of the specific bacteria found in plaque,
was associated with disease.

 This concept, known as the Non-Specific Plaque

Hypothesis (Loesche, 1976), held that all bacteria were
equally effective in causing disease.

101
organisms that are found as part of the "normal" bacterial flora
may function as pathogens under certain conditions.

 These organisms may be altered, or increase significantly in

numbers relative to other non-pathogenic species, to function
as pathogens.

 This type of bacterial pathogen is referred to as an

endogenous pathogen, in contrast to an organism that is not
normally found in healthy states which is termed an
exogenous pathogen.

102
 Thus, the current concept of the processes involved in the
development of periodontal diseases fall under the Specific
Plaque Hypothesis -Loesche,1976

The Specific Plaque Hypothesis states that disease results

from the action of one or several specific pathogenic
species and is often associated with a relative increase in
the numbers of these organism found in plaque.

103
 Acceptance of this was confirmed by
recognition of A.actinomycetemcomitans as a
pathogen in localized aggressive periodontitis.

104
 Non- specific hypothesis  periodontal disease may
be treated by reducing plaque to an acceptable level &
the maintenance of healthy plaque/ by achievement of
total plaque control

 Specific hypothesis implies that therapy should be

directed at elimination of specific pathogens, antibiotic
therapy

105
 Key features:
 (a) the selection of "pathogenic" bacteria is directly
coupled to changes in the environment

 (b) diseases need not have a specific etiology; any

species with relevant traits can contribute to the
disease process.

107
 It has been proposed for the etiology of periodontal
disease & postulates the following causative process:

The reaction of host to natural plaque accumulation

in the crevice is an inflammatory response.

The ensuing increased GCF flow provides complex

host molecules that can be catabolized by the
proteolytic Gram-ve anaerobes that already exist in
small numbers in normal plaque flora

109
The latter organisms suppress the growth of species
common in healthy crevice( i.e. facultative anaerobic
gram+ve bacteria ) & a population shift occurs in
resident flora.
These periodontopathic flora then produce virulence
factors which overwhelm host defences for a time ,
resulting in episodic tissue destruction & disease
activity

. 

110
 Examination is done with periodontal probe
 Disclosing agent plays a vital role in plaque detection:
 Dye used: “two tone dye”
 Erythrosin + fast green/ brilliant blue
 Pink color indicates new plaque
 Blue color indicates old plaque
 Iodine preparations
 Fluorescin
 Mercurochrome preparations
 Bismark brown
 Basic fuchsin

111
Directions:
Rinse mouth with water or mouthwash.
Chew 1 tablet or use 5 drops of solution.
Swish around for 30 seconds. Do not
swallow. SPIT OUT.
Rinse with water.

112
113
COMMERCIALLY AVAILABLE PLAQUE
DISCLOSING AGENTS

114
115
 The Plaque Detection enables to easily
describe the intraoral status to
patients.
 Features:

 store up to 16 images in its on-board

memory, and with the newly
innovated 405nm LED,
 see plaque ,illuminated in the
intraoral images.

116
 Shick & Ash modification of plaque criteria
1961
 Plaque index by SILNESS P. and LOE H.1964
and modified by Loe H. in 1967
 Turesky- Gilmore – Glickman modifications of
the Quigley-Hein plaque index 1970
 The Navy plaque index by Grossman F.D. &
Fedi P.F. 1970

117
1. PLAQUE INDEX

(Silness and Löe, 1964)

Teeth examined are:-

16, 12, 24, 36, 32, 44
Missing teeth are not substituted.

118
Each of the four surfaces
of the teeth (buccal,
lingual, mesial and
distal) is given a score
from 0-3.

Scores Criteria
0 No plaque
1 A film of plaque adhering to the free gingival margin and
adjacent area of the tooth. The plaque may be seen in situ
only after application of disclosing solution or by using the
probe on the tooth surface.
2 Moderate accumulation of soft deposit s within the gingival
pocket, or the tooth and gingival margin which can be seen
with the naked eye.
3 Abundance of soft matter within the gingival pocket and/or on
the tooth and gingival margin.
119
Inference of Silness and Loe plaque index

INFERENCE SCORE

Excellent O

Good 0.1-0.9

Fair 1.0-1.9

Poor 2.0-3.0
120
2007: A natural anti-plaque compound (purified from a
vegetable) has been elucidated and patented by
Oystershell, the compound was coded RF2

Advantages of RF2 in oral health

 natural and safe compound
 plaque control with respect for normal mouth flora
 biofilm disruption without killing the bacteria
 no need for fluoride in plaque control
 no need for relatively high concentrations of antimicrobial agents
(chlorhexidine, hexitidine, triclosan) in plaque control

121
122
123
“A hard concretion that forms on teeth or
dental prostheses through calcification of
bacterial plaque.”
Glossary of periodontal terms 2001

124
 According to • Supragingival calculus
location • Subgingival calculus

According to • Salivary calculus

source of • Serumal calculus (Jenkins,
mineralization Stewart 1966)

• Exogenous
According to • Endogenous (Melz 1950)
surface • Tooth associated
• Tissue associated

125
Everett and Potter
Further sub classified Subgingival calculus
into:-
Crusty, spiny or nodular
Ring like or ledge like encircling the tooth
Veneer type
Fingerlike or fern like extensions
Individual islands or spots
Combination of the above

126
 • The tightly adherent calcified deposits that form on the
clinical crowns of the teeth above the free gingival
Location margin.(visible in oral cavity)

• usually white-yellow in colour but can darken with age and

exposure to tobacco
Color

• hard clay like consistency

Texture and • Easily detachable from tooth surface
consistenc • Salivary secretions are the main source of mineral salts.
y

127
 Inorganic : 80% of dry weight

Calcium 27 – 29%

Phosphorous 16 – 18%
Organic:
Total Matrix 15-20%
Carbonate 2 – 3% contains 54.9% protein
and 10.2% lipid.
Sodium 1.5 – 2.5%
Magnesium 0.6 – 0.8%
Fluoride 0.003 –.04%
Traces of Na, Zn, St, Cu, Br, Mg, Fe, Al, Si, Tg, Au.
(Little et al 1963 Lundberg et al 1966 Schroeder
1969)

128
 Lipids

Phospholipids
Neutral lipids 61.8% Glycolipids 28%
10.2%

phosphatidylethanolamine,
34.2%
simple glycosphingolipids, diphosphatidylglycerol,
free fatty acids (17.2%) 25.5%
a smaller amount of Neutral and sulfated
triglycerides phosphatidylinositol,
glyceroglucolipids. (82.8% )
2.3% and
phosphatidylserine 1.7%
129
 Octacalcium
phosphate
[Ca8(PO4)4(HPO4)25
HO] (OCP),

ß-tricalcium phosphate or
whitlockite [Ca10(HPO4)(PO4)6]
(WHT) form the inorganic part
Crystals of both supragingival and
subgingival calculus.

Hydroxyapatite
[Ca10(PO4)6(OH)2]
(HAP), Brushite [CaHPO4-2H2O:
dicalcium phosphate dihydrate]
(DCPD) is present only in the
early-stage supragingival
calculus (Rowles, 1964)..

130
 Octacalcium
phosphate was Brushite in
In the middle Supragingival
detected in the calculus is very
Distribution of layer of the calculus adjacent
areas of rare and is found
calcium calculus to the gingival
supragingival only in the
phosphate Hydroxyapatite and subgingival
calculus near the supragingival
compounds was the main calculus contain
superficial layer calculus adjacent
component . Whitlockite.
always in contact to the gingiva.
with saliva

131
Vestibular surfaces.

The mandibular central and lateral incisors have

significantly more supragingival calculus on their
vestibular surfaces than maxillary central and lateral
incisors.

In contrast, maxillary first molars have a significantly

higher mean grade for supragingival calculus on their
vestibular surfaces than mandibular first molars.

132
Lingual surfaces.

The lingual surfaces of the mandibular

anterior teeth have significantly higher
grades of supragingival calculus than the
lingual surfaces of other teeth.
Of these lower anterior teeth, the lingual
surfaces of the central incisors have higher
mean calculus grades than those of the
lateral incisors and both the central and
lateral incisors have significantly greater
amounts of supragingival calculus than the
canines

133
Location-below the crest of marginal gingival

Colour-dark brown or greenish black

Texture and consistency-hard and dense, flint-like, crusty,

spiny or nodular deposits

Firmly attached to tooth surface.

Crevicular fluid and inflammatory exudates are the main

source of mineral salts.

Found on any root surfaces with a periodontal pocket.

134
Inorganic/ Organic

similar to supragingival calculus

except that it contains higher

concentration of calcium, magnesium
and reflecting higher concentration of
ions in GCF than in saliva.

135
Crystals

Octacalcium phosphate
[Ca8(PO4)4(HPO4)25HO] (OCP),

Hydroxyapatite [Ca10(PO4)6(OH)2] (HAP), and

ß-tricalcium phosphate or Whitlockite

[Ca10(HPO4)(PO4)6] (WHT)

The WHT-to-HAP (Jensen and Danø, 1954)

and calcium-to phosphorus ratios (Little and
Hazen, 1964) in supragingival calculus are
lower than those in subgingival calculus

136
 In subgingival
The main
calculus
constituent is Brushite is totally
Octacalcium
Whitlockite and absent
phosphate is
Hydroxyapatite .
scarcely found.

137
 No significant differences
found for subgingival
calculus between right and the vestibular surfaces, the
left sides of the mouth for mandibular anterior teeth
a given site and a given and maxillary molar teeth
tooth. had the greatest amount of
subgingival calculus.
Interdental areas were
most commonly involved

138
Both parotid and submandibular saliva are supersaturated with respect
to various calcium phosphates but show little tendency for spontaneous
precipitation of mineral , during the short time that saliva would be in
contact with plaque on the lingual surfaces of the lower incisors and the
buccal surfaces of the upper molars.

It has been proposed that the lower anterior lingual and upper posterior buccal
surfaces may be most susceptible to calculus formation because of
the low sucrose concentration in saliva in these regions,
the high saliva film velocity, which promotes clearance of salivary sugar and acid
from plaque, and
the higher resting plaque pH because of better access to salivary urea .

139
 Subgingival calculus is found in interproximal
surface and least on buccal surfaces.

 The first teeth to show calculus deposit are

maxillary first molar and mandibular incisor.

 Maxillary incisors and bicuspids are the least

involved.

 Supragingival calculus starts forming within 6 years

of eruption age while,

 Subgingival is least before 20 yrs of age.

140
 Habits eg
Oral hygiene tobacco, betel Systemic
habits nut (Pindborg, disease
1947)

Access to Use of
professional Ethnic origin prescription
care medications

Stress
Diet (Macnill,
Age (Parodneck,
1956)
1937)
141
Soft plaque is hardened by mineralization between 1st and 14th days of
plaque formation.

Calcification is reported to occur in as little as 4-8 hrs.

Calcifying plaque may become 50% mineralized in 2 days and 60% to 90%
mineralization in 12 days.

All plaque does not necessarily undergo calcification.

Plaque that does not develop into calculus reaches a plateau of maximal
mineral content within 2 days.
Calculus is formed in layers which are often separated by a thin cuticle that
becomes embedded in calculus as calcification progresses
Plaque has the ability to concentrate calcium at 2 to 20 times its level in
saliva.

142
 So they are classified as
The initiation of
calcification and the rate heavy,
of calculus accumulation
vary from person to moderate
person for different teeth or slight
and at different times of
same person calculus formers. (Muhlar and
Ennever 1962)

143
 Total protein and total lipid
levels are elevated in Heavy
Early plaque of heavy calculus calculus formers.
former contains more calcium, three
times more phosphorous and less
potassium than that of non-calculus
former

Light calculus formers have
higher levels of parotid
pyrophosphate
Calcification of plaque is
delayed in children. (Turesky,
1961)

144
 The average daily increment in
calculus former is from 0.10% to
0.15% of dry weight. (Lobene et al,
1966)

The time required to reach the

maximal level has been reported
as 10 weeks and 6 months.

The decline for maximal calculus

accumulation, referred to as
reversal phenomenon may be
explained by the vulnerability of
bulky calculus to mechanical wear
from food and from the cheeks, lips
and tongue. 145
 Inhibition Transformation
theory

Epitactic Bacteriological
concept theory

Booster THEORIES OF Enzymatic

mechanism MINERALISATION theory

147
 • According to this theory, calcification will occur
in a particular locus when the local pH,
calcium and phosphorous concentrations are
high enough to allow for precipitation of a
calcium phosphate salt.
Booster • Factors such as loss of CO2 and production of
Mechanis ammonia could account for an elevation in pH;

m • Acid or alkaline phosphatase activity could

result in a higher phosphate concentration;

• Liberation of bound or complexed calcium

from the salivary proteins would produce
higher calcium levels.

148
 • One of the most widely held ,which recognizes that
the concentration of calcium and phosphate ions is
not high enough in tissue fluids and saliva to
precipitate spontaneously, but is sufficient to support
growth of a Hydroxyapatite crystal once an initial seed
or nucleus is formed.
Epitactic • Tissue fluids and saliva are thus called metastable
Concept solutions.

• The formation of the initial crystal or nucleus is called

nucleation and is thought to occur when a proper
organic matrix is available on which the nucleus can
crystallize in exact structural configuration.

(Boskey,
1981) 149
Another approach considers calcification as occurring
only at specific sites because of the existence of an
inhibiting mechanism at non-calcifying sites.

One possible inhibiting substance is thought to be

pyrophosphate and among the controlling
mechanisms is the enzyme alkaline phosphatase,
which can hydrolyze the pyrophosphate to phosphate
(Russsel and Fleisch. 1970).

The pyrophosphate inhibits calcification by preventing

the initial nucleus from growing, possibly by poisoning
the growth centers of the crystal.

150
 The most attractive hypothesis is the idea that Hydroxyapatite
need not arise exclusively via epitaxy and nucleation.
 Amorphous non-crystalline deposits and Brushite can be
transformed to Octacalcium phosphate and then to Hydroxyapatite
(Eanes et al, 1970).
 It has been suggested that the controlling mechanism in the
transformation process may be pyrophosphate (Fleich et al 1968)

151
 Oral microorganisms are Leptotrichia and
the primary cause of Actinomyces have been
calculus, and that they are considered most often as
involved in its attachment to the causative
the tooth surface. microorganism
• (Galippe.V., 1886)

152
 Calculus formation is the resultant of the action of phosphatase
derived from either oral tissues or oral microorganism on some salivary
phosphate containing complex, most probably phosphoric esters of the
hex phosphoric group. (Adamson.K.T, 1929)

154
 Involvement Of Bacteria In Calculus
Formation

• Microbial mineralization occurs even within "acidogenic"

and cariogenic bacteria (Moorer et al., 1993).

• The filamentous micro-organisms (Diphtheroids and

Veillonella sp)are predominant in supragingival calculus
and calculus- associated plaque, whereas micro-
organisms of various morphologies are found in the
plaque adjacent to subgingival calculus (Friskopp and
Hammarström, 1980).

155
 Subgingival calculus deposits appeared to have a significantly
greater percentage of coccoid forms and fewer motile rods (CM
Brown et al., 1991).

 Plaque bacteria actively participate by forming phosphatase,

changing the plaque pH or inducing mineralization

156
 Microbial Mineralization

• Initial deposition of apatite in calcifying bacteria is

associated with membrane or acidic membrane-
associated components (Boyan and Boskey, 1984).
• The functions of acidic phospholipids in calcification
depend upon their ability to bind calcium by their
negatively charged groups.
• Calcium is bound to adjacent phospholipid molecules in
the membrane through a two-point electrostatic
attachment to form a stern layer which facilitates the
interaction of calcium with inorganic phosphate ions in
solution (Hauster et al., 1969).

• v 157
 Inorganic phosphate associates with the bound calcium
to form a Ca-phospholipid-phosphate complex (CPLX).
 Once CPLX has formed, apatite deposition follows
when sufficient calcium and phosphate ions are present
and the concentration of inhibitors is low.
 The availability of CPLX exhibits bacterium-specificity.

 Calcifiable proteolipids in the membrane matrix vesicles

can also initiate the mineralization process in the
calculus matrix.

158
 Nucleation Inhibitors
• It has been demonstrated that magnesium (Mg) prevents apatite
nucleation by C. matruchotii.

• Diphosphonates, such as ethane-1-hydroxy-1, 1-Diphosphonate

(EHDP), inhibit both apatite nucleation (Fleisch et al., 1970) and
crystal growth (Francis, 1969).

• Importantly, nucleation inhibitors should not be used clinically,

because they have been found to interfere with normal mineralization
of hard tissues (Schenk et al., 1973).

159
 Crystal Growth Inhibitors
Negatively charged
salivary proteins,
statherin and PRP are Cystatins in saliva, such
as the acidic cystatin
two representatives of
and the neutral cystatin.
salivary inhibitors of
crystal growth.

Immunoglobulins IgG, It was found that

IgA present in dental albumin could bind to
plaque and calculus may
also have an inhibitory Hydroxyapatite
effect on plaque surfaces and inhibit
mineralization. crystal growth.

In addition to these
salivary proteins,
pyrophosphate and
zinc ions act as
crystal growth
inhibitors. 160
 Calcification Promoters

Urea is a The ureolytic pH

The effect of
Urea product from the
metabolism of urea metabolism response
on plaque pH promotes
nitrogen- calculus
containing formation by
substances. increasing the
Urea can be saturation
secreted in degree of
normal saliva at calcium
concentrations Ammonia
produced from phosphate in
of between 5 ureolysis of plaque fluid.
and 10 mmol/L urea
contributes to
an increased
plaque pH that
is an essential
factor in
natural
calculus
formation.

161
FLUORID
E
Fluoride may promote
the maturation of
spontaneous
precipitated calcium
phosphate at Fluoride not only counteracts demineralization of
physiological pH by hard tissue through the formation of fluorapatite,
reducing the stability of but also contributes to re-mineralization by
OCP (Eanes and Meyer, precipitation of a fluoride-enriched apatite or
1978 calcium fluoride

Fluoride has also been demonstrated to affect the

morphology of the apatite crystals as it converts them from
thin plates to short and slender needles (Eanes and Meyer,
1978).

162
 Silicic acid has been reported as a strong promoter of
Silico both spontaneous precipitation of calcium phosphates
and the growth of seeded crystals (Damen and ten
n Cate, 1989).

Silicic acid was also found to stimulate the

transformation from amorphous calcium phosphate to
HAP (Hidaka et al., 1993).

Silica at a concentration of 0-2 mg/ml was reported to exert

stimulating effects on calcium phosphate precipitation
(Damen and Ten Cate, 1989).

Silica was also reported to increase the rate of calculus

formation 35 days after its incorporation into food

163
Modes of attachment of
calculus

164
First study on modes of Calculus attachment
Calculus Attachment
Zander in 1953, by means of :

1.A secondary cuticle interface between calculus

and tooth surface

2. Attachment of calculus matrix to irregularities of

cementum surface corresponding to previous insertion
locations of Sharpey’s fibers

3. Penetration of microbial organisms of calculus

in cementum

4. Attachment into areas of cementum resorption

via mechanical locking into undercuts.
165
Calculus formation occurs in three basic steps:

Pellicle formation
Plaque formation
Mineralization

In 2 days plaque can be 50% mineralized and 60– 90 % in 12

days.

166
Within 24 to 72 hrs more and more mineralization foci
develop close to the underlying tooth surface. Eventually
they grow to form a unit.

The mineralization starts in centers which arise intracellularly

in bacterial colonies or extracellularly from matrix with
crystallization nuclei.

Filamentous organisms, diphtheroids, and Bacterionema and

Veillonella species have ability to form intracellular apatite
crystals.

167
 Mineralization

Two modes of Type A

mineralization mineralization Type B mineralization
,Type A and centers are centers are apparently
Type B centers formed only in not related to
,have been presence and microorganisms but
distinguished association of have at least one
ultra structurally. microorganisms common border with
, the Type A centers and
included micro
organisms.

The crystals Crystal patters

associated with associated with
Type A have been Type B are
identified as OCP,
Hydroxyapatite Whitlockite and
Brushite.

168
 The plaque that does not develop into calculus
reaches a plateau of maximal mineral content
with in 2 days.
Calculus formation continues until it reaches a
maximum, after which it may be reduce
The time taken to reach the maximal level has
been reported as 10 weeks (conroy 1968) and 6
months (volpe 1969)

169
Diagnostic aids

170
 Advanced

Modified ultrasonic scalers

Perioscope (endoscope)
(CAD CAM)

Fluorescence by
InGaAsHg Diode laser.
Sensitivity of subgingival
calculus detection by laser
induced fluorescence (655 Novel LED probe
nm excitation wavelength) is
significantly higher than the
detection sensitivity of an
explorer 171
ANTI - CALCULUS AGENTS
The major strategies that have been
investigated are to:

(i) dissolve or soften the mature deposit by

removing the inorganic portion
(ii) affect the calculus matrix, i.e., to change
the ‘skeleton’ around which calculus is
deposited
(iii) alter the attachment of the calculus to
the tooth surface

(iv) prevent plaque from forming

(v) inhibit crystal growth and thereby

prevent the development of mineralized 172
plaque
 2nd GENERATION
Anti- Calculus Agents

Inhibition of crystal growth

Vitamin C (By crystal poisoning
mechanism )
Classification Pyrophosphatase
Pyrophosphatase + Sodium
fluoride
1st GENERATION Zinc salts
Biphosphonates
Polymers & Co Polymers

1)DISSOLUTION
2)ALTERING CALCULUS 3.PLAQUE INHIBITION
Ethylene diamine tetra ATTACHMENTS Antibiotics Example :
acetate Silicones Nidamycin Antiseptics 4.MATRIX
- Chelating Agents Ion exchange resins. Example :Chloramines DISRUPTION
Sodium Hexa Enzymes Example
Metaphosphate : Mucinase,
- Acids –Aromatic Trypsin,
sulphuric acid
chymotrypsin
Nitro-muriatic Acid Carboxypeptidase,
20% Trichloroacetic Acid lipase, amylase,
Spring Salts 30% UREA(
Sodium Ricinolate solvent action on
Alkalies protein)
173
 Agents for softening the mature
calculus deposit
• Acids
• Sulphuric acid (Barker 1872).
• Nitro muriatic acid, Niles
(1881)
• 20% trichloroacetic acid,
• Bifluoride of mercury and
• 10% sulphuric acid
problems are… caustic to soft
tissues and decalcify tooth
structure.
 Alkalis
 Badanes (1929) noted the
beneficial effect of natural
mineral water on the removal
of calculus - mild alkalis
contained in the water that
dissolved the 3 principal
organic constituents globulin,
mucin and calcium oxalate.
174
175
 Chlorhexidine

Chlorhexidine is a Although
cationic bis- chlorhexidine is a
biguanide which acts potent anti-plaque
by being adsorbed agent, it has the
onto the bacterial disadvantage of
cell wall, leading to actually increasing
damage of the calculus levels
permeability barriers

Also dead bacteria

Was postulated that,
release
dead bacteria
pyrophosphatase
accumulates on the
leading to decreased
tooth surfaces,
natural
acting as sites for
pyrophosphate
calculus deposition
levels

176
 Niddamycin (CC10232)
Ithad no known
medical uses, was not
significantly absorbed
orally or systemically,
was tested as a and no in vivo
potential anti-calculus bacterial resistance
agent because it had been reported
possessed many (Stallard et al.1969).
desirable Plaque studies (Volpe
characteristics for use et al. 1969b) showed
in mouth rinses and that mouth rinses
dentifrices. containing C10232
(0.01% and 0.005%),
were equally effective
in preventing plaque
accumulation.

177
179
Score Criteria
0 No calculus present
-Supra gingival calculus covering
1 more tha 1/3rd of exposed tooth
surface.
-Supra gingival calculus covering
more than 1/3rd but not more
2/3rd of exposed tooth surface.
2
- presence of individual flecks of
subgingival calculus cervical
portion of tooth or both.
- supragingival calculus covering
more than 2/3rd of exposed tooth
surface
3
- continuous heavy band of
subgingival calculus around the
cervical portion of tooth or both
180
 Calculation:-
total score
no. of surfaces examined.

 Interpretation:-

Score Inference

0.0-0.6 Good

0.7-1.8 Fair

1.9-3.0 Poor
181
Score Criteria
0 -nce of calculus

Supragingival calculus
extending only slightly below
1
the free gingival margin (not
more than 1 mm)

Moderate amount of supra and

2 subgingival calculus or sub
gingival calculus alone

An abundance of supra and sub

3
gingival calculus.
182
 CONCLUSION
 Despite tremendous increases in our understanding of the
pathogenic properties of specific plaque microorganisms and
the role of specific microorganisms in the disease process,
current therapy in periodontics is largely non-specific.

 The treatments that we utilize (e.g., oral hygiene measures,

debridement by scaling and root planning, or even the
currently available mouthwashes) are oriented towards
reducing the accumulation of plaque on the teeth.

 Future developments in periodontics will involve the

development of therapies which prevent the colonization or
growth of specific microorganisms that are known to
function as pathogens in this environment
183
 Newman MG, Takei HH, Klokkevold PR, Carranza FA: Carranza’s
Clinical Periodontology: Role of dental calculus and other
predisposing factors: Hinrichs JE: 170-192
 Mandel ID And Gaffar A: Calculus Revisited: J. Clin Periodontol
1986: 249-257
 Jin Y And Yip HK: Supragingival Calculus: Formation And
Control: Crit Rev Oral Biol Med 2002: 13(5):426-441
 Dental Calculus: Recent Insights Into Occurrence, Formation,
Prevention, Removal And Oral Health Effects Of Supragingival
And Subgingival Deposits: Eur J Oral Sci. 1997 Oct;105(5 Pt
2):508-22
 J Friskopp: Ultra Structure Of Non-decalcified Supragingival And
Subgingival Calculus: J Of Periodontol 1983; 54(9):542-550
184
 Carranzza”s Clinical Periodontology 9th Edition.
 Understanding Dental Caries; Vol 1. Etiology Mechanisms Basic
And Clinical Aspects- Gordon Nikiforuk.
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