2. Once a tooth erupts, various materials gather on its
surfaces, these substances are frequently called tooth –
accumulated materials/deposits.1
They are classified as:
Soft deposits:
Acquired pellicle
Microbial plaque
Materia alba
Food debris
Hard deposits:
Calculus
Stains
3. Acquired Pellicle : Following tooth eruption or a dental
prophylaxis, a thin, saliva- derived layer, called the acquired
pellicle, covers the tooth surface.1
Dental Plaque is defined as a specific but highly variable
structural entity resulting from sequential colonization and
growth of micro organisms on the surfaces of teeth and
restoration consisting of micro organisms of various strains and
species are embedded in the extra cellular matrix, composed
of bacterial metabolic products and substance from serum,
saliva and blood. (WHO-1978)1
Materia Alba refers to soft accumulations of bacteria and
tissue cells that lack the organized structure of dental plaque.1
4.
5. Calculus:
*Dental calculus can be considered as an ectopic
mineralized structure.2
Dental Calculus consists of mineralized bacterial
plaque that forms on the surfaces of natural teeth and
dental prosthesis. [Carranza ]2
6. *Calculus can be defined as a hard concretion that forms on
teeth or dental prostheses through calcification of bacterial
plaque [GPT 4th
ed.].3
A deposit of inorganic salts composed primarily of calcium
carbonate and phosphate mixed with food debris bacteria and
desquamated epithelial cells. (Greene 1967)4
Mineralized dental plaque that is permeated with crystals of
various calcium phosphates (Schroeder,1969)5
Calculus is also known as odontolithiasis or tartar. It is also
called fossilized plaque.1
7. *Calculus was recognized as a clinical entity in some way related
to periodontal disease as far back as the tenth century.1
*In 1683 Van Leeuwenhoek described microorganisms in tartar.
He called them ‘animalcules’.1
*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.1
8.
9. *Dental calculus is classified by its location on a tooth surface
as related to the adjacent free gingival margin:
10. 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.6
Crowns of teeth out of occlusion; non-functional; or teeth that
are neglected during daily plaque removal.
Surfaces of dentures and dental prosthesis.
11.
12. *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.7
14. 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.
15.
16. 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)1
Occurs with or without associated supragingival deposits.
19. Characteristic
SUPRAGINGIVAL
CALCULUS
SUBGINGIVAL
CALCULUS
COLOR
White creamy–yellow, Or Gray
May be stained by tobacco,
food,
Light to dark brown, dark green
or black stains .
SHAPE
Amorphous, bulky
Gross deposits may form
interproximal bridge between
adjacent teeth.
Extend over the margin of the
gingiva.
Shape of the calculus is
determined by the anatomy of
the teeth.
Flattened to conform with
pressure from the pocket wall.
Combination of the following
calculus forms occur:
1.crusty, spiny, or nodular
2.Ledge or ring like forms
20. CONSISTENCY
AND TEXTURE
Moderately hard newer
deposits- less dense and hard
and porous.
Surface covered with
nonmineralized plaque
Brittle, flint-like.
Hardens and more dense than
supragingival calculus.
Newest deposits near bottom
of pocket are less dense and
hard.
Surface covered with plaque
SIZE AND
QUANTITY
Quantity has direct relationship
to
1. Personal oral care procedures
and plaque control measures.
2. Physical character of diet.
3. Individual tendencies.
4. Function and use
Increased amount in tobacco
smokers.
Related to pocket depth
Increased amount with age
because of accumulation
Subgingival is primarily related
to the development and
progression of periodontal
disease.
21.
22. Supragingival calculus consists of
*inorganic (70 to 90 per cent) and
*organic components (20 to 30%)
INORGANIC CONTENT-
Inorganic portion consist of:
75.9% calcium phosphate, Ca(PO4)2
3.1% calcium carbonate, CaCO3.
Traces of magnesium phosphate,Mg3(PO4)2
Traces of other metals.( Monetite & calcite)
24. FLOURIDE IN CALCULUS-
*Concentration of fluoride in calculus varies and is
influenced by the amount of fluoride, received from
fluoride in the drinking water, topical application,
dentifrices, or any form that is received by contact
with the external surface of calculus.7
*Fluoride concentrations were highest in or near the
outermost regions of the calculus.
25. CRYSTALS-
At least two thirds of the inorganic component is crystalline in
structure.
Electron microscopy & x-ray diffraction studies,4 distinct
phosphate crystals :
*Hydroxyapatite Ca10(OH)2(PO4)6 – approximately 58%
*Magnesium whitlockite Ca9(PO4)6XPO4 - 21%
*Octacalcium phosphate Ca4H(PO4)3.2H2O - 12%
*Brushite CaHPO4.2H2O - 9%
26. *Generally, two or more crystal forms are typically
found in a sample of calculus.
*Hydroxyapatite and octacalcium phosphate are
detected most frequently (in 97-100% of all
supragingival calculus) and constitute the bulk of
the specimen.
*Brucite is more common in the mandibular anterior
region.
*Magnesium whitlockite is common in the posterior
areas and sublingually.
27.
28. ORGANIC CONTENT
*Consist of mixture of protein- polysaccharide complexes,
desquamated epithelial cells, leukocytes, and various types
of microorganisms.
*Carbohydrate – 1.9% and 9.1% of organic component,
consist of :
Galactose sometimes: arabinose
Glucose galacturonic acid
Mannose glucosamine
Glucuronic acid
Galactosamine
29. Salivary proteins
5.9% to 8.2% of organic component, include most amino acids.
Lipids-
0.2% of organic component, in the form of:
Neutral fats
Free fatty acids
Cholesterol
Cholesterol esters
Phospholipids
30. Subgingival calculus-
has composition similar to supragingival calculus, with some
differences.
*More homogenous with equally high density of minerals.
*Same hydroxyapatite content, more magnesium
*Less brucite and octacalcium phosphate
31. *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
32. BACTERIAL CONTENT-
*The percentage of gram positive and gram- negative
filamentous organisms is greater within calculus than in the
remainder of oral cavity.7
*The microorganisms at the periphery are predominantly
gram-negative rods and cocci.
*Most of the organisms within the calculus is nonviable.
33. *SUPRAGINGIVAL CALCULUS
Predominance of gram-positive filaments.
Next in frequency; gram-negative filaments and
cocci.
Gram-positive cocci seen in calculus about which
suppuration had taken place.
36. Calculus is dental plaque which has undergone mineralization.
*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.
37.
38.
39. *Calculus formation continues until it reaches a
maximum from which it may be reduced in
amount.
*The time required to reach the maximum level
has been reported as 10 weeks, 18 weeks, and 6
months.7
40. SOURCES OF MINERALS
*Supragingival calculus – the source of elements for
supragingival calculus is saliva.
*Subgingival calculus – the gingival sulcus fluid and
inflammatory exudate supply the minerals for the
subgingival deposits.
*Because the amount of sulcus fluid and exudate
increases in inflammation, more minerals are
available for mineralization of subgingival plaque
41. *As calcification progresses, Number of filamentous bacteria
increases.
*Foci of calcification changes from basophilic to eosinophilic.
*Calculus is formed in layers, which are often separated by a thin
cuticle that becomes embedded in the calculus as calcification
progresses.
42.
43. In 1878, Magitot was of the opinion that tartar
consisted mainly of mineral matter formed by
the precipitation of earthy carbonates and
phosphates from the saliva.
These mineral salts were united with organic
matter, epithelial cells, fatty globules, and
leukocytes.
44. *BOOSTER CONCEPT1
according to this concept mineral
precipitation results from a local rise in the degree of
saturation of calcium and phosphate ions which may be
brought about in several ways:
*Salivary pH theory – Hodge & Leung1
1950
A rise in the pH of saliva causes precipitation of calcium
phosphate salts by lowering the precipitation constant.
The pH may be elevated by the loss of carbon dioxide, by
the formation of ammonia by dental plaque and bacteria,
or by protein degradation during stagnation.
45.
46.
47. *Another enzyme esterase, present in the cocci,
filamentous organisms, leukocytes, macrophages and
desquamated epithelial cells of dental plaque, may initiate
calcification by hydrolysing fatty esters into free fatty
acids.
*The fatty acids forms soaps with calcium and magnesium
that are converted later into the less soluble calcium
phosphate salts
49. III. Inhibition theory
Calcification is considered to occur only at specific sites because of the
existence of an inhibiting mechanism at non calcifying sites, where
calcification occurs, the inhibitor is altered / removed.
One possible inhibiting substance is pyrophosphate and among the
controlling mechanisms is the enzyme alkaline pyrophosphatase which
can hydrolyse pyrophosphate to phosphate (Russell ad Fleisch, 1970).
Pyrophosphate decrease calcification by preventing the initial nucleus
from growing, possibly by ‘poisoning’ the growth centers of the crystal.
50. IV. Transformation
*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.
*Controlling mechanism in the transformation process may be
pyrophosphate.
51. V. Miscellaneous theories
*It was suggested that calculus deposition might be due to some systemic
factor / pathological condition of the person (Berka et al, 1935; Black et al
1915).
*Emotional states increased the amount of calculus formed (Badanes et al,
1927), that calculus formation was a symptom of an error in the patients
nutritional state that should be corrected (Kirk et al, 1906) as that the
consumption of excessive amounts of food seemed to increase the quantity
of calculus deposits formed (Black et al, 1915).
*Some factor in the saliva of people that do not form calculus that inhibits
the precipitation of calcium salts.
* This was demonstrated by Wasserman et al (1958) in an in vivo study in
which testicular hyaluronidase inhibited calcification of deposits that had
started to form in the mouth
52. ETIOLOGIC SIGNIFICANCE
*There is a positive correlation between the presence of calculus and
the prevalence of gingivitis (Ramfjord, 1961), but this correlation is
not as great as that between plaque and gingivitis (Greene et al,
1963).
*In young persons, periodontal condition is more closely related to
plaque accumulation than to calculus, but the situation is reversed
with age (Greene et al, 1963; Gregory et al, 1965).
53. *The incidence of calculus, gingivitis and periodontal disease
increases with age.
*The non-mineralized plaque on the calculus surface is the
principal irritant, but the underlying calcified portion may
be a significant contributing factor, it provides a fixed nidus
for the continued accumulation of plaque and holds it
against the gingiva.
* Thus calculus is a significant pathogenic factor in
periodontal disease.
54. CLINICAL IMPLICATIONS OF DENTAL
CALCULUS
*Strong association by calculus deposits and periodontitis has been
demonstrated in experimental (Waerhaug, 1952) and epidemiologic
studies (Lovdal et al, 1958).
55. STUDIES
*If calculus surface has been disinfected with chlorhexidine in
monkeys – a normal epithelial attachment with junctional epithelial
cells forming hemidesmosones and a basement membrane on calculus
could be established (Listgarten, 1973).
*Autoclaved calculus may be encapsulated in connective tissue
without inducing marked inflammation / abscess formation (Allen and
Kerr, 1965).
*These studies exclude the possibility of dental calculus being a
primary cause of periodontal disease.
*The effect of calculus seems to be secondary by providing an ideal
surface configuration conducive to further plaque accumulation and
56. *Calculus deposits may have developed in areas of difficult access
for oral hygiene.
*Calculus may amplify the effects of bacterial plaque by keeping
the bacterial deposits in close contact with tissue surface
(Friskopp, 1980)
*Well controlled animal (Nyman et al, 1986) and clinical (Nyman et
al, 1988) studies have shown that removal of subgingival plaque on
top of subgingival calculus will result in healing of periodontal
lesions, provided supragingival deposits are removed on a regular
basis.
*Mombelli et al (1995) demonstrated that diligent and complete
removal of subgingival plaque on top of mineralized deposits after
chipping off gross amounts of calculus showed almost identical
results in the composition of microbiota.
57. *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.
58. *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.
59. *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.
60. *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
61. *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
62. Emotional status- increased calculus
formation has been associated with disturbed
emotional status.
Nucleation inhibitors - Mg blocks apatite
crystallization and stabilizes calcium
phosphate as amorphous mineral (Ennever and
Vogel, 1981)
63. *ULTRASTRUCTURE OF
CALCULUS
*LAYERS – calculus forms in layers that are more or less
parallel with the tooth surface.6
*The layers are separated by a line that appear to be a
pellicle that was deposited over previously formed calculus,
and as mineralization progressed, the pellicle became
embedded.
*The lines between the layers of calculus can be called
incremental lines. The lines are evidence that calculus
grows, or increases by apposition of new layers.
64. *LIGHT MICROSCOPY-
Young supragingival calculus- the interface with tooth
surface is fairly smooth where as the external
mineralized surface is generally irregular and covered by
a layer of plaque.
There are large areas within the calculus that are non-
mineralized plaque layer of variable thickness
65. *Mature supragingival calculus- fewer non- mineralized lacunae, and
in some sections, the lacunae formed a continuous connection with
the external bacterial plaque.
*The presence of areas of non-mineralization matrix was a frequent
finding at all levels within the body of supragingival calculus. two
possible explanations have been suggested(Friskopp 1983) :1
*Filamentous bacteria that are predominant in supragingival
plaque could have properties that inhibit mineralization,
resulting in non-mineralized regions within the calculus.
*Differences in calcification capability between different bacterial
colonies located in different parts of supragingival plaque.
66. *Subgingival calculus- uniform mineralized component.
Unlike supragingival calculus, lacunae are not seen within
the body of subgingival calculus.
67. *ATTACHMENT OF CALCULUS TO
TOOTH SURFACE
*Differences in the manner in which calculus is attached to the
tooth surface affect the relative ease or difficulty encountered
in its removal.
*Several modes of attachment has been observed by
conventional histological techniques and by electron
microscopy.
*On any one tooth and in any one area, more than one mode of
attachment may be found.
68. Attachment by means of an organic pellicle on enamel-
*Calculus attachment is superficial because no interlocking
or penetration occurs.
*Pellicle attachment occur most frequently on enamel and
newly scaled and planned root surfaces
*Calculus can be readily removed because of smooth
attachment
69. Mechanical locking into surface irregularities.
*Enamel irregularities include cracks, lamellae, and
carious defects.
*Cemental irregularities include resorption lacunae ,
cemental tears.
*Close adaptation of calculus undersurface depressions
to the gentle sloping moulds of the unaltered
cementum surface.
70. *Attachment of organic matrix of calculus into
minute irregularities that were previously
insertion locations of sharpey’s fibres.
*Calculus embedded deeply in cementum may
appear morphologically similar to cementum
and thus has been termed calculocementum
71.
72. 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
+
73. 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.
74.
75. SUPRAGINGIVAL EXAMINATION :
Direct Examination – supragingival calculus can be seen
directly or indirectly.
Using a mouth mirror with a combination of retraction, light
and drying with air, small deposits can be seen.
76. SUBGINGIVAL EXAMINATION:
Visual Examination – dark edge of calculus may be seen at or
just beneath the gingival margin.gentle air blast can deflect
the margin from the tooth for observation into the pocket.
Gingival tissue colour change – dark calculus may reflect
through a thin margin and suggest its presence.
Tactile examination- Clerehugh 1996 used WHO # 621
probe and a fine subgingival explorer is also used.
77. *Simplified calculus index (Green & Vermillion ’64 )
*Calculus component of periodontal disease index
(Ramfjord 1959 )
*Calculus surface index (Ennever J,, Sturzenberger &
Radike 1961)
*Marginal line calculus index (Muhleman & Villa ’67)
*Volpe- Manhold index (Volpe A R & Manhold J H ’62)
80. *Perioscopy involves a modified medical endoscope
exclusively for periodontal purpose.
*This was developed in year 2000.
*It consists of a fiberoptic bundle surrounded by multiple
illumination fibres, a light source and irrigation system.
81. *Its miniature nature causes minimal tissue trauma.
*Fiberoptic system permits visualization of the subgingival
root surface, tooth structure and calculus in real time on
a display monitor.8
82.
83. *DetecTar™ uses a Spectro-optical approach in order to
detect subgingival calculus by utilizing a light emitting
diode and fiberoptic technology.
*This involves an optical fibre which recognizes the
characteristic spectral signature of calculus caused by
absorption, reflection and diffraction of red light.8
84.
85. *Calculus and tooth structure differ in composition.
*This structural difference gives a typical fluorescence to
both these structures.
*Calculus contains various non-metal as well as metal
porphyrins and chromatophores which make it able to emit
fluorescent light when irradiated with a light of certain
wavelength.
86. *Diagnodent™ makes use of this property of calculus
to detect its presence.
*Calculus and teeth fluoresce at different
wavelength region of 628-685nm & 477-497nm
respectively.
*Diagnodent™ involves use of an indium gallium
arsenide phosphate (InGaAsP) based red laser diode
which emits a wavelength of 655nm through an
optical fibre causing fluorescence of tooth surface
and calculus.8
89. *Keylaser3™ combines a 655nm InGaAsP diode for detection of
calculus and a 2940nm Er: YAG laser for treatment.
*Previous versions of this system (i.e. Keylaser 1 and 2) can be
used for removal of calculus only.
*A scale of 0-99 is used for detection of calculus.
*Values exceeding 40 indicate definite presence of
mineralized deposits.
90. *Er: YAG laser is activated as a certain threshold is reached.
*As soon as the value fall below threshold level Er: YAG laser
is switched off.
*Studies done to assess the efficacy of this device have shown
that it produces tooth surface comparable to hand and
ultrasonic instruments. Cost factor can be a limiting aspect for
using lasers for detection and treatment.8
91.
92. *Perioscan™ can differentiate between calculus and healthy
root surfaces.
*It also has a treatment option that can be used to remove
these calculus deposits immediately.
*This combination of detection and removal mechanism is
advantageous since calculus can be removed just by
switching the mode from detection to removal.
93. *Perioscan™ is an ultrasonic device that works on
acoustic principles.
*It is similar to tapping on a glass surface with a hard
substance and analysing the sound produced to find
out the cracks that are present on glass.
*Tip of the ultrasonic insert is oscillating
continuously.
94.
95. *Different voltages are produced due to changes in
oscillations depending on the hardness of the
surface.
*Hardness of the calculus differs from the hardness
of the tooth surface.
*This difference in hardness can be used to generate
the information of the surface that is being touched
by the device.8
96. *This instrument is used in two different modes.
*Whenever ultrasonic tip touches the tooth surface a light
signal is displayed on hand-piece and actual unit.
*Light signal is also accompanied by an acoustic signal.
*During calculus detection mode, the instrument shows a blue
light when calculus is present. (Fig.2)
97.
98. *Once a healthy root surface is attained, green
light is displayed when the ultrasonic tip
touches healthy cementum. (fig.3)
* Different power settings aid the clinician in
removing tenacious calculus
99.
100. 1.Mandel ID, Gaffar A. Calculus revisited- A review. J Clin Periodontol1986;13: 249-
257
2.Newmann, Takei, Klokkevold, Carranza: Clinical periodontology. 10th Edition.
Noida: Elsevier; 2009.
3.Glossary of periodontal terms (2001). 4th edn. Chicago: The American academy of
periodontology.
4.Greene JC. The Oral Hygiene Index—Development and uses. Journal of
Periodontology. 1967;38(Suppl):37.
5.Schroeder HE (1969) Formation and inhibition of dental calculus. Vienna: Hans
Huber
6.Ten Cate's Oral Histology, Nanci, Elsevier, 2013, page 255
101. 7. Jepsen S, Deschner J, Braun A, Schwarz F, Eberhard J. Calculus removal
and the prevention of its formation. Periodontol 2000 (2011);55: 167-188
8. Meissner G, Kocher T. Calculus detection technologies and their clinical
application. Periodontol 2000 2011;55:189-204
