DENTAL CALCULUS

M.HARITHA
PG1ST YR

1
 CONTENTS
 INTRODUCTION
 ETIOLOGIC SIGNIFICANCE
 HISTORY  IATROGENIC FACTORS

 PREVALANCE  DETECTION OF CALCULUS

 CLASSIFICATION  PREVENTIVE ASPECTS

 COMPOSITION  CLINICAL MEASUREMENT

 ATTACHMENT TO TOOTH  REFERENCES

SURFACE

 FORMATION

 THEORIES OF CALCULUS
 MINERALIZATION OF 2
 INTRODUCTION
• Once a tooth erupts, various materials gather on its surface , these
substances are frequently called as tooth accumulated materials/
deposits.
They are classified as –
 Soft deposit
 Hard deposit

SOFT DEPOSIT HARD DEPOSIT

 Acquired pellicle  Calculus
 Material Alba  Stains
 Microbial plaque
 Food Debris
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 CALCULUS

 Calculus is derived from Greek words Calcis-lime stone, Tartar- white

encrustation inside casks.
Dental Calculus consists of mineralized bacterial plaque that forms on
the surfaces of natural teeth and dental prosthesis. [Carranza ]

A hard deposit that forms by mineralization of dental plaque and is

generally covered by a layer of unmineralized plaque (Lindhe)

A deposit of inorganic salts composed primarily of calcium carbonate

and phosphate mixed with food debris bacteria and desquamated
epithelial cells. (Greene 1967)
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 SYNONYMS
• TARTAR
• DISAMIGUATION
• CALCIS
• ODONTOLITHIASIS
• FOSSILIZED PLAQUE
MANDEL ET AL CALCULUS REVESISED A REVIEW
2013

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 HISTORY

Hippocrates Albucasis
Paracelsus 1535
(460-377 BC) (936-1013)

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• In 1683, van leeuwenhoek described microorganism in
tartar, he called them “ANIMALCULES”

• Fauchard, in 1728, termed it tartar or slime, and

referred to it as “a substance which accumulates on
the surface of the teeth and which becomes, when left
there, a stony crust of more or less considerable
volume

1970's, the first studies of ancient dental

calculus took place on archaeological samples
of cattle, sheep, and horse teeth (Armitage,
1975) and revealed the presence of numerous
oral phytoliths (silica content of some plant
cells)
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 PREVALENCE
Many studies have been Longitudinal study was done
conducted on the prevalence by Anerud and coworkers
of calculus and these surveys (1991) among Srilankan tea
revealed a high laborers and Norwegian
prevalence(70-100%) of academicians for 15 years and
calculus in virtually every all periodontal parameters
population studied. were recorded

Two national surveys by O’Brien(1993) and Bhat M.(1991) have provided data on the
prevalence of calculus.

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National Health and Nutrition Examination Survey
(NHANES ΙΙΙ)

They evaluated 9689 adults in United States between 1988

and 1994 out of which
91.8 % of subjects had detectable calculus
55.1% had subgingival calculus.

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CLASSIFICATION
 According to location

- Supragingival calculus
-Subgingival calculus

 According to source of mineralization

-Salivary calculus
-Serumal calculus (Jenkins, Stewart 1966)

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 According to surface

-Exogenous SLIGHT
-Endogenous (Melz 1950)

 According to initiation and rate of

accumulation, calculus former are classified as

-non calculus formers MODERATE

-Slight calculus formers
-moderate calculus formers
-heavy calculus formers
(Muhler and Ennever 1962)
HEAVY

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 In extreme cases calculus may form a bridge-like structure
along adjacent teeth or cover the occlusal surface of teeth
without functional antagonist.

 Found nearly 100% in mandibular anterior teeth, decreasing

posteriorly to 20% of the third molars. In maxilla, 10% of
the anterior teeth and 60% of first molars had supragingival
calculus.

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 SUPRAGINGIVAL CALCULUS
Location–
 On the clinical crown coronal to the margin of the gingiva and visible in the oral
cavity.

Distribution–
 Most frequent sites are on the lingual surfaces of the mandibular anterior teeth
opposite Warton’s duct and on the buccal surfaces of the maxillary molars opposite
Stenson’s duct.

 Crowns of teeth out of occlusion; non-functional; or teeth that are neglected during
daily plaque removal.

 Surfaces of dentures and dental prosthesis.

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 SUBGINGIVAL CALCULUS
Location
 On the clinical crown apical to the margin of the gingiva, usually in periodontal
pockets, not visible upon oral examination.

 Extents to bottom of the pocket and follows contour of soft tissue attachment.

Distribution
 May be generalized or localized on single teeth or a group of teeth.

 Proximal surfaces have heaviest deposits, lightest deposits on facial surfaces.

(Lovdal et al.1958)

 Occurs with or without associated supragingival deposits.

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 Submarginal Calculus

Hematogenetic Calculus

Serumal Calculus

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 DISTRIBUTION OF DENTAL CALCULUS ON
DENTITION

Lingual surfaces Buccal surfaces

of the lower of the upper
anterior teeth. molars
 COMPOS
ITION
Supragingival calculus consists of:

 inorganic (70 to 90 per cent) and

 organic components (20 to 30%)

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 INORGANIC CONTENT
Inorganic portion consist of:

• 76% calcium phosphate

• 3% calcium carbonate
• 4% magnesium phosphate
• 2% carbon dioxide
• Traces of other metals

Trace elements –
sodium tungsten
zinc gold
strontium aluminium
bromine silicon
copper iron
manganese fluorine 22
4 main crystal forms are-

 Hydroxyapatite -58%
 Magnesium whitlockite - 21%
 Octacalcium phosphate – 12%
 Brushite - 9%

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ORGANIC CONTENT

VARIOUS
MICRORGANISM

DESQUAMATED
LEUCOCYTES CALCULUS EPITHELIAL
CELLS

PROTEIN
POLYSACHARI
DE COMPLEX

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  Carbohydrate – 1.9% and 9.1% of organic component, consist of :

• Galactose sometimes: arabinose

• Glucose galacturonic acid

• Mannose glucosamine
• Glucuronic acid
• Galactosamine
 Salivary proteins 5.9% to 8.2% of organic component

 Lipids 0.2% of organic component

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SUBGINGIVAL CALCUUS

 It has composition similar to supragingival calculus,

with some differences.
• More homogenous with equally high density of minerals.
• Same hydroxyapatite content, more magnesium whitlockite
• Less brushite and octacalcium phosphate
• The ratio of calcium to phosphate is higher subgingivally.
• The sodium content increases with the depth of periodontal pockets.
• Salivary protein found in supragingival calculus is not found subgingivally
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MICROBIOLOGY OF DENTAL CALCULUS
 The percentage of gram positive and gram- negative filamentous organisms is
greater within calculus than in the remainder of oral cavity.

 The microorganisms at the periphery are predominantly gram-negative rods and

cocci.

 Most of the organisms within the calculus is nonviable.

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 Friskopp & Hammarstrom (1980) With TEM & SEM found differences in the
nature of the microbial coverings.

On supragingival calculus filamentous organisms,oriented at right angles to the

surface dominated,

Subgingival calculus was covered by cocci, rods and filaments with no distinct
pattern of orientation.

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 Pathogens like A.actenomycetecomitans,
P.gingivalis, T.denticola have found within
the lacunae Of both supragingival and
subgingival calculus

Plaque bacteria have been proposed to actively participate in the mineralization of

calculus by forming phosphatases, changing the plaque pH inducing mineralization
(Emper et al, 1962)

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SUBGINGIVAL CALCULUS

• Superficial layers : gram- negative filaments most numerous

• Deep and middle zones : gram-positive filaments predominant.

SUPRAGINGIVAL CALCULUS

• Predominance of gram-positive filaments.

• Next in frequency; gram-negative filaments and cocci.

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31
ATTACHMENT TO THE TOOTH SURFACE

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CALCULOCEMENTUM
Calculus embedded deeply in cementum may
appear morphologically similar to cementum
and thus has been termed calculocementum

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 ATTACHMENT OF CALCULUS ON IMPLANT

 Attachment to pure titanium is less intimate than to root surfaces

structure.

 Smooth machined implants have less micro porosities for retention.

(This would mean that calculus may be chipped off from implants without
affecting it)
Matarraso et al 1996

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 Acquired pellicle forms on an implant surface when the metal
surface initially comes into contact with tissues (Baier, 1982). 1

 Adsorption of proteins does not occur on the surface of pure

titanium (Ti).

 5-6nm oxide layer composed of TiO2 forms on the surface of Ti

when exposed to air.

 At physiological pH, the TiO2 layer carries net -ve charges,

which enable the TiO2 layer to bind cations like Ca2+
 This makes the surface of an implant +vely charged and,
consequently, attracts the high-weight molecules carrying -ve
charges, notably proteins.

 Some irregularities may also be encountered on oral implant

surfaces,

 The attachment to commercially pure titanium generally is less

intimate than to root surface structures.
 FORMATION
PELLICLE FORMATION

PLAQUE FORMATION

MINERALIZATION

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38
 PELLICLE FORMATION
• All surfaces of the oral cavity are coated with a pellicle. Following tooth eruption or
a dental prophylaxis, a thin, saliva- derived layer, called the acquired pellicle, covers
the tooth surface

Initial adhesion and attachment of bacteria

 Transport to the surface – involves the initial transport of the bacterium to the tooth
surface.

 Initial adhesion – reversible adhesion of the bacterium, initiated by the interaction

between the bacterium and the surface , through long-range and short-range forces

 Attachment – a firm anchorage between bacterium and surface will be established by

specific interactions.
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 Colonization and Plaque Maturation

• When the firmly attached microorganisms start growing and the newly formed
bacterial clusters remain attached, microcolonies or a biofilm can develop.

• Gram- positive coccoidal organisms are the first settlers to adhere to the formed
enamel pellicle, and subsequently, filamentous bacteria gradually dominate the
maturing plaque biofilm (Scheie, 1994).

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 MINERALIZATION

Rate of formation and accumulation

• Formation of plaque consist of amorphous and/ or finely granular organic matrix

containing mass of variety of gram positive and gram negative coccoid bacteria and
filamentous form.

• The matrix is a form of mucopolysaccride derived from either saliva or bacteria or

both.

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 CALCIUM
IONS
CRYSTALLINE
CALCIUM
PHOSPHATE
SALT

CARBOHYDRATE
PROTEIN
COMPLEX

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 RATE OF FORMATION
Calculus is formed by the a l c ul u s f ormation
C
precipitation of mineral salts n t i n u e s u ntil it
co
aximum
which can start between 1st reaches m
to14th day of plaque v e l s i n a bout 10
le
formation k s t o 6 m onths
wee
t ime

ge da il y
ve ra
The a ment in Calcification is reported to occur
incre ormer-
us f in as little as 4-8 hrs. (Tibetts
calcul o 0.15%
t 1970)
0.10% weight
of dry
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 THEORIES OF MINERALISATION OF
CALCULUS
Bact Enz
erial yma
Booster
mechanism
Epitactic Theory Inhibiton Theory
Transformation
Theory

theo tic
theo
ry
ry
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 BOOSTER MECHANISM
• Mineral precipitation results from a local rise in the degree of saturation of calcium and
phosphate ions

• A rise in the pH of the saliva causes the precipitation of calcium phosphate salts by lowering the
precipitation constant

• Colloidal proteins in saliva bind calcium and phosphate ions and maintain a supersaturated
solution with respect to calcium phosphate salts.

• Phosphatase liberated from dental plaque, desquamated epithelial cells, or bacteria precipitates
calcium phosphate by hydrolyzing organic phosphates in saliva, thereby increasing the
concentration of free phosphate ions.

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EPITACTIC CONCEPT / SEEDING
THEORY/HETEROGENOUS
NUCLEATION
(Mandel 1957)
According to this concept, seeding agents induce small foci of calcification, which enlarge
and coalesce to form a calcified mass.

The seeding agent in calculus formation are not known, but it is suspected that the
intercellular marix of plaque plays an active role.

The carbohydrate protein complexes may initiate calcification by removing calcium from
the saliva(chelation) and binding with it to form nuclei that induce subsequent deposition
of minerals.
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 INHIBITION THEORY
 Calcification at specific sites - because of inhibiting mechanism at non-
calcifying sites.

 The site where calcification occur ,the inhibitor is apparently altered or

Removed.

 Alkaline pyrophosphatase enzyme involved in controlling mechanism----

hydrolyzes pyrophosphate to phosphate (Russell and Fleisch 1970).

 Pyrophosphate inhibits calcification - prevents the initial nucleus from

growing, possibly by poisoning the growth centers of the crystals

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 TRANSFORMATION THEORY

• Hypothesis - hydroxyapatite need not arise exclusively via epitaxis or nucleation.

• Amorphous non-crystalline deposits and brushite Transformed into

octacalcium phosphate and then to hydroxyapatite (Eanes et al 1970).

• Controlling mechanism in transformation mechanism can be pyrophosphate

(Fleisch et al 1968).

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 BACTERIOLOGICAL THEORY
• Oral microorganisms are the primary cause of calculus formaton

• Involved in the attachment to the tooth surface.

• Leptotrichia and Actinomyces have been considered most often as the causative
microorganism.

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ENZYMATIC THEORY
Calculus formation

Action of phosphatases derived from either oral tissues

or oral microorganism on some salivary phosphate
complex (phosphoric ester of hexophosphoric group)

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 ROLE OF MICRORGANISM IN THE
MINERALIZATION OF CALCULUS

• Mineralisation of plaque generally starts extracellularly around both

gram positive and gram negative organism, but it may also start
intracellularly.

• Mineralisation spreads until the matrix and bacteria are calcified.

• Bacterial plaque may actively participate in the mineralizaion of

calculus by forming phosphatases, which change the pH of plaque and
induce mineralization.

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 ETIOLOGICAL SIGNIFICANCE
FRENCKEN et al. (59), in a
The incidence of calculus, gingival inflammation longitudinal study of Morogoro
and periodontal disease increases with age.(Greene school children from 1984-1988
et al, 1963; Gregory et al, 1965) in Tanzania, observed that
dental calculus increased with
increasing age while gingival
Calculus does not contribute directly to gingival bleeding remained the same,
inflammation, but it provides a fixed nidus for the suggestive of no correlation
continued accumulation of of plaque and its between calculus and gingival
retentionin close proximity to the gingiva condition.

ENZER reported that only 11%. of examined tooth surfaces

containing calculus (supragingival or subgingival) exhibited
gingivitis, while 75% of the surfaces harbouring plaque exhibited
gingival inflammation
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 IATROGENIC FACTORS
• Margins of restorations
• Over Contoured Crown
• Design Of Removable Partial Dentures
• Restorative And Endodontic Procedures

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 MARGINS OF RESTORATIONS

• Over hanging margins

1) increases plaque formation
retentive areas
2) Changed the ecologic balance
3) Compromises hygiene practice.

Subgingival margins
• Waerhaug - restorations placed in a sub gingival location - detrimental to
periodontal health.
• Increased plaque, severe gingivitis and deeper pockets.
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 OVER CONTOURED CROWN

• Leads to accumulation of plaque and prevent the self-cleaning

mechanisms of oral tissues .
• proximal contacts , contour of the marginal ridges , developmental
grooves - prevent interproximal food impaction – prevent periodontal
disease.

• Hancock et al 1980 – food impaction – periodontal pathosis.

• Jernber G et al 1983 - probing depth , clinical attachment loss –
increased in open contact and food impaction. 57
 DENTAL MATERIALS

• Restorative materials are not in themselves injurious to the periodontal tissues

• Self curing acrylics
• Silicate

• Kourkouta et al – highly glazed porcelain – less plaque than enamel

• Composites – more likely to harbor bacterial plaque.

• Wang et al 1998 – metal pontics – higher amount of periodontal pathogens than

porcelain.

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• Plaque accumulation maintained – finished and polished surfaces.
Zlataric et al

DESIGN OF REMOVABLE PARTIAL DENTURES

• Favor the accumulation of plaque.

• Quantitative and qualitative changes
• Increase in spirochetal microorganisms
• Mobility of abutment teeth, gingival
inflammation, pocket formation increase
• Studies by Zlataric et al

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 RESTORATIVE AND ENDODONTIC PROCEDURES

• Rubber dam clamps, matrix bands, burs – lacerate the

gingiva – inflammation

• Gingival retraction cord – impacted debris – foreign body

reaction.

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 MISCELLANEOUS FACTORS – MALOCCLUSION

• Poorly aligned teeth themselves are not associated with a greater degree of gingivitis
• complicate oral hygiene procedures - increased plaque accumulation - subsequent gingival
inflammation.

• Behfelt et al - direct relationship between tooth displacement and gingival inflammation

• Reduced interproximal spaces – less effective removal of plaque

• Extreme anterior overbite - palatal recession in maxillary incisors. 61
 MISCELLANEOUS FACTORS – VERTICAL ROOT FRACTURE

• Longitudinal , confined to the root of the tooth.

• Mesiodistal, buccolingual plane – occur at any point along the root.

• Narrow, isolated periodontal pocket. Recurrent periodontal

abscesses. 62
 MUCOGINGIVAL DEFORMITIES – ABERRANT FRENAL ATTACHMENT

• Aberrant frenal attachments may be a problem, especially in shallow

vestibules or areas of minimal attached gingiva.

• frenum is stretched - the muscle attachments may pull the marginal tissue
away from the tooth - accumulation and apical migration of bacterial
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plaque – gingival recession
 MISCELLANEOUS FACTORS – ORTHODONTIC THERAPY

Orthodontic therapy affects the periodontium by

• Favouring plaque retention
• Directly injuring the gingiva as a result of
overextended bands
• Creating excessive forces, unfavourable
forces, or both on the tooth and supporting
structures.
• Modify the gingival ecosystem

- Orthodontic band
- Excessive orthodontic forces – necrosis of PDL and
adjacent alveolar bone , apical root resorption.
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 RADIATION THERAPY

• Cytotoxic effects on both normal cells and malignant cells.

• >60 Sv – salivary production impaired – xerostomia – greater

plaque accumulation and reduced buffering capacity by saliva.

• Periodontal attachment loss and tooth loss has been reported to be

greater in cancer patients who were treated with high-dose unilateral
radiation as compared with the non radiated control side of the dentition
65
 TOBACCO SMOKING

• Smoking is strongly related to severity of diseases and to recurrent

and refractory diseases.
• Numerous studies have shown the association of smoking with
periodontitis.

66
 FACTORS AFFECTING THE RATE OF
CALCULUS FORMATION

• Diet and nutrition –the significance of diet in calculus

formation depends more upon its consistency than upon its
content.

• Increased calculus formation has been associated with

deficiencies of vitamin A, niacin, or pyridoxine, and with an
increase in dietary calcium, phosphorus, bicarbonate, protein
and carbohydrate.
• Age – there is an increase in calculus deposition with an
increasing age.(Schroeder et al,1969).5

• This increase, is not only increase in the number of surfaces,

but also the size of calculus deposits.

• This may be due to change in quantity and quality of saliva with

age, favouring the mineralization properties.
• Habits – In populations that practice regular oral hygiene and
with access to regular professional care have low tendency for
calculus formation.

• Smoking- is associated with an elevated risk for

supragingival calculus deposition. Smoking may exert its
influence systemically (elevated levels of salivary calcium
and phosphorus) or locally via a conditioning of tooth
surfaces.
• Salivary pH- increase pH increases the calculus formation.

• When the calcium phosphate crystals in solution are in kinetic

equilibrium, the rate of precipitation is equal to that of
dissolution.

• If pH in solution drops (the concentration of hydrogen ions

increases), OH- and (PO4)3 - tend to be removed by H+ by
forming water and more acidic forms of phosphate, respectively
• Salivary flow rate – increased salivary flow rate decreases the
calculus formation. Salivary flow rate affects calcium phosphate
saturation.

• Salivary calcium concentration- Elevated salivary calcium

concentration, increases the rate of calculus formation.

Higher total salivary lipid levels – is associated with increased

calculus formation
 Emotional status- increased calculus formation has been
associated with disturbed emotional status.
DETECTION OF CALCULUS

(A) VISUAL

 Transillumination
 Airblast
 Color change

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(B) Tactile

 Probe
 explorer

(C) Radiographs

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LATEST METHOD OF DETECTION
OF CALCULUS
COMBINED CALCULUS
DETECTION ONLY DETECTION AND REMOVAL

• Fiberooptic endoscopy-based
technology • Ultrasonic oscillating
system
• Spectro- optical technology
• Laser based technology
• Auto fluorescence based
technology

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FIBEROOPTIC BASED TECHNOLOGY
• Perioscopy involves a modified medical
endoscope exclusively for periodontal
purpose.

• Fiberoptic system permits visualization of

the subgingival root surface, tooth structure
and calculus in real time on a display
monitor.

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 SPECTRO OPTICAL BASED TECHNOLOGY

• Uses a light emitting diode and fiberoptic

technology.

• The characteristic spectral signature of

subgingival calculus which is caused by
absorption, reflection and diffraction when
irradiated by red light is sensed by an
optical fiber and converted into an electrical
signal that is analysed by a computer
processed algorithm

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 AUTO FLUORESCENCE BASED
TECHNOLOGY
• The ability of calculus to emit light
following irradication with light of certain
wavelength enables the detection of
calculus.

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ULTRASONIC TECHNOLOGY
• Ultrasonic calculus detection technology is
based on a conventional piezo – driven
ultrasonic scaleand is similar to the way one
might tr ap on the rim of a glass with a
spoon to identify cracks acoustically.

• The ultrasonic device currently available

(Perioscan) provides a detection mode to
discriminate between calculus deposits and
clean roots, along with a treatment mode
that allows conventional ultrasonic
treatment at different power levels.

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LASER BASED TECHNOLOGY

 Key laser 3 combines calculus detection and

treatment in a feedback controlled manner
for selective removal calculus.

 The device is based on a 655 nm InGaAs

diode laser for autoflourescence based
calculus detection whereas a 2940 nm
ER:YAG LASER is used for treatment.

79
Significance of removal of
calculus

MOMBELLI et al showed that pocket depth reduction w/o calculus

removal altered clinical course of periodontitis

BIAGINI et al demonstrated growth of periodontal ligament

fibroblast on cementum that had attached calculus.

LISTGARTEN and ELLGARD as early as 1973 noted gingival

epithelial reattachment to calculus depoisits sterlized by 2%
chlorhexidine

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 PREVENTIVE ASPECTS

• There are several methods for coping with the problem of calculus. The patient
must understand the importance of individual daily removal & how professional
maintenance appointments on a regular basis can supplement the personal care.

81
PERSONAL PLAQUE CONTROL

Removal of plaque
appropriately by selected
brushing, flossing and
various supplementary
methods is major factor
in the control of dental
calculus formation

82
ANTI CALCULUS AGENT

83
CLASSIFICATION

84
85
 PROPHYLATIC TOOTH PASTE
• Triclosan with pvm /ma copolymer
• Pyrophate and pvm /ma copolymer
• Zinc ions

86
87
 Potassium pyrophosphate,
sodium pyrophosphate in a
combined concentration of 5%.
Also sodium fluoride 0.24%
equivalent to 900 ppm

Zinc citrate in 0.454%

SnF2 multi-benefit
The polypyrophosphate sodium
hexametaphosphate -targets
plaque calcification and has shown
anti-calculus benefits in a dentifrice
as high as 55% greater versus a
regular dentifrice in clinical
investigations.
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89
 CALCULUS INHIBITORS
• CALCIFICATION NUCLEATION INHIBITORS

MAGNESIUM DIPHOSPHONATES
blocks apatite
crystallization Inhibit both apatite and crystal
stabilzes calcium growth
phosphate as
amorphous material
Clinically not used

90
CRYSTAL GROWTH INHIBITORS IN SALIVA

Salivary proteins inhibitory action on crystal growth

Proline rich protien PRPS Margolis et al 1982

STATHERIN
CYSTATINS

91
 PROMOTERS OF CALCULUS FORMATION

• Urea
• Fluorides
• Silicon

92
Calcification promoters –

• Urea is a product from the metabolism of nitrogen -containing

substances. Urea can be secreted in normal saliva at concentrations
of between 5 and 10 mmol/L but can be as high as 30 mmol/L in
patients with renal disease

• Gingival crevicular fluid contains up to 60mmol/L urea.

• Urease is responsible for bacterial urea hydrolysis. At a neutral pH,

urea is hydrolyzed by urease to NH4+ and bicarbonate.
• Fluoride - anti – bacterial action
• Inhibit the acid production by the bacteria
• Potential to increase plaque PH – formation of calculus
• Sodium fluoride – inhibit bacterail enzymes that known to
cause calculus formation
• Silicon – found in drinking water ,
• silicic acid – monoand poly salicylic acids – strong promotors
– calcium phosphates and silica .
• A study done in indonesian and norwegian population – more
calculus formation – consumption of large amount of rice –
enriched in silicon .

94
SCALING AND ROOT PLANING

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LASER

96
CLINICAL MEASUREMENT

 Oral calculus index (Greene and Vermilion 1964)

 Calculus Index ( Ramfjord, 1959)

 Calculus surface severity index(Ennener et al 1961)

 Calculus rating (Volpe and Manhold, 1962)

 Marginal line calculus index (Muhlanann and Villa1967)

97
 CONCLUSION
• Calculus plays an important role in maintaining and
accentuating periodontal disease by keeping plaque in close
contact with the gingival tissues and creating areas where
plaque removal is impossible.

• Therefore the clinician must not only possess the clinical

skills to remove the calculus and other irritants that attach to
teeth .

98
 REFERENCES
• Periodontology 2000; volume 55

• Mandel ID, Gaffar A. Calculus revisited- A review. J Clin Periodontol1986;13: 249-

257

• Newmann, Takei, Klokkevold, Carranza: Clinical periodontology. 10th Edition.

Noida: Elsevier; 2009.

• Glossary of periodontal terms (2001). 4th edn. Chicago: The American academy of
periodontology.

• Greene JC. The Oral Hygiene Index—Development and uses. Journal of

Periodontology. 1967;38(Suppl):37
• Periobasics . 99