Calculus is a hard deposit that is formed by mineralization of dental plaque on the surfaces of natural teeth and dental prosthesis, generally covered by a layer of unmineralized plaque.

1. 1

2. Presented By
Dr. Faheem Ahmed
MDS 1st Year
2

3.  Definitions
 History
 Classification
 Composition
 Microbiology
 Supragingival v/s
Sungingival Calculus
 Prevalance
 Rate of formation
 Attachment of calculus
 Role of micro-organisms
in mineralization
 Theories of mineralization
 Diagnostic Aids
 Calculus & Systemic
diseases
 Management
 Anticalculus agents
 Conclusion
 References
3

4.  Calculus is a hard deposit that is formed by mineralization of
dental plaque on the surfaces of natural teeth and dental
prosthesis, generally covered by a layer of unmineralized
plaque.
(Carranza's clinical periodontology 11th ed)
 Calculus is a hard concretion that forms on teeth or dental
prosthesis through calcification of bacterial plaque
(Glossary of periodontal terms(2001),4th edition)
4

5.  Calculus consists of mineralized bacterial plaque that forms on
the surface of natural teeth and dental prosthesis, covered on its
external surface by vital, tightly adherent, non mineralized
plaque
Genco
 When dental plaque calcifies ,the resulting deposit is called
calculus
Grant
5

6.  Tartar
 Disambiguation
 Calcis
 Odontolithiasis
 Fossilized plaque
6

7.  Calculus is derived from Greek words Calcis-lime stone,
Tartar- white encrustation inside casks.
 Hippocrates (460–377 BC) was the foremost person whose
writings showed a relation between dental deposits and oral
diseases. He noted the harmful effects of calculus (pituita) on
gums and teeth.
 Albucasis (936–1013) evidently illustrated the association
between calculus and disease and advocated thorough removal
of deposits.
 Paracelsus a Swiss/German physician and alchemist introduced
the term tartar as a description for a variety of stony concretions
that form in humans.
 For nearly 5,000 years, calculus was considered to be the prime
etiologic agent in periodontal disease. In the past 25 years,
however, calculus has been overthrown by plaque, and the
hardened criminal has come to be viewed as a fossilized
remnant of minor significance. 7

8.  This shift in perception, which became most apparent in the
196O's, was largely a response to two lines of investigation
1. Experimental and electron microscopic studies of developing
plaque and calculus demonstrated that supra and subgingival
calculus was mineralized plaque covered by an unmineralized
bacterial layer (Mandei, et al. 1957, Mandei 1960, Muhleman
& Schroeder 1964, Oshrain et al, 1968)
2. The experimental demonstration in humans that plaque,
allowed to develop in the absence of oral hygiene, results in
a gingivitis which is reversible on the resumption of tooth
cleaning. (Loe et al 1965)
8

9.  It was not until 1969 that Schroder provided a more
appropriate definition of calculus other than a calcified deposit
adhering to the teeth.
 He defined dental calculus as, Mineralized dental plaque
that is permeated with crystals of various calcium
phosphates. (Perio 2000 vol.8 1995)
9

10. ACCORDING TO LOCATION
 Supragingival calculus
 Subgingival calculus
ACCORDING TO SOURCE OF MINERALIZATION
(Jenkins, Stewart 1966)
 Salivary calculus
 Serumal calculus
ACCORDING TO SURFACE (Melz 1950)
 Exogenous
 Endogenous
10

11. ACCORDING TO INITIATION AND RATE OF
ACCUMULATION, CALCULUS FORMERS ARE
CLASSIFIED AS (Muhler and Ennever 1962)
 Non calculus formers
 Slight calculus formers
 Moderate calculus formers
 Heavy calculus formers
11

12. SUBGINGIVAL CALCULUS CAN BE FURTHER
CLASSIFIED ACCORDING TO THE MORPHOLOGY:
 Crusty, spiny nodular
 Ring like or ledge like
 Veneer type
 Fingerlike or fern like extension
 Individual island or spots
 Combination of all
12

13.  Supra gingival 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)
13

14. PRINCIPLE
COMPONENTS
 Calcium - 39%
 Phosphorus - 19%
 Carbon dioxide – 1.9%
 Magnesium – 0.8%
TRACE
ELEMENTS
 Sodium
 Zinc
 Strontium
 Bromine
 Copper
 Manganese
 Tungsten
 Gold
 Aluminium
 Silicon
 Iron
 Fluorine
14

15.  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.
Fluoride concentrations were highest in or near the outermost
regions of the calculus.
15

16.  At least two thirds of the inorganic component is
crystalline in structure.
Electron microscopy & x-ray diffraction studies shows
distinct phosphate crystals :
 Hydroxyapatite Ca10(OH)2(PO4)6 – approximately 58%
 Magnesium whitlockite Ca9(PO4)6XPO4 - 21%
 Octacalcium phosphate Ca4H(PO4)3.2H2O - 12%
 Brucite CaHPO4.2H2O - 9%
16

17. *Hydroxyapatite
detected most frequently (in 97-100% of
and octacalcium phosphate are
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.
17

18. 18

19. Carbohydrate – 1.9% and 9.1% of organic component,
consist of :
Galactose sometimes: arabinose
Glucose galacturonic acid
Mannose glucosamine
Glucuronic acid
Galactosamine
19

20. 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
20

21.  It 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
 The ratio of calcium to phosphate is higher subgingivally.
 The sodium contentincreases with the depth of periodontal
pockets.
 Salivary protein found in supragingival calculus is not found
subgingivally
21

22.  The average microscopic count of bacteria in
unmineralized dental plaque has been calculated to be up
to 2.1 × 10 mg wet weight.
 Lactate dehydrogenase and alkaline and acid phosphatase
activities have been identified in dental plaque suggestive
of a boosted calcification by the plaque enzymes.
 In supragingival calculus, viable aerobic and anaerobic
bacteria have been detected while subgingival calculus
provides an excellent environment for further microbial
adhesion and growth.
 Periopathogens, such as Aggregatibacter
actinomycetemcomitans, Porphyromonas gingivalis, and
Treponema denticola have been found within the lacunae
of both supra- and subgingival calculus.
22

23. Bacteria are not essential for calculus formation, but they
enable its development. Hence, high amount of calculus
indicates that oral hygiene has been poor for months or
even years. (Carranza’s clinical periodontology. 10th ed.)
 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.
23

24.  Calculus tooth interface is smooth
 External mineralized surface is irregular
 Covered by non mineralized plaque
 Contain many non mineralized lacunae
24

25. The mineralized intermicrobial areas of the body of the
calculus contained predominantly small, randomly orientated
needle- shaped/platelet-shaped crystals (a).
Areas containing crystals of larger columnar and roof-tile shapes
were also observed (b)
25

26.  Appeared in one piece with a relatively smooth surface.
 Under low magnification - thin at the incisal/occlusal part and
thickened apically.
 Under high magnification - covered with dense layer of
filament (1micron thick with an estimated length of 25 to 100
microns.)
 Fracture surface of Supragingival calculus generally had a
smooth, crystalline appearance.
26

27.  Lustman et al, (1976) In SEM, noted the presence of calcified
masses having a spongy appearance and containing empty
spaces representing the former sites of degenerated organisms.
 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.
27

28. DISTRIBUTION OF CALCIUM
PHOSPHATE COMPOUNDS
OCP - detected near the superficial
layer always in contact with saliva
HA was the main component - Middle
layer of the calculus .
WL - adjacent to the gingival and
subgingival calculus.
Brushite - very rare ; adjacent to the
gingiva.
28

29. 29

30.  Subgingival calculus - interproximal surface ; least- buccal
surfaces.
 Maxillary incisors and bicuspids - least involved.
 Supragingival calculus starts forming with 6 years of eruption
age while Subgingival at 8 yrs of age ; Subgingival calculus is
least before 20 yrs of age.
 Deposition of supragingival calculus - maximal scores around
25 to 30 yrs. of age; By age 45 only a few teeth ,typically the
premolars were without calculus
 By age 30 - all surfaces of all teeth had subgingival calculus
without any pattern of predilection.
30

31.  Plaque mineralization begins within 24-72 hrs and takes
an average of 12 days to mature.
 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.
(Tibetts 1970)
 Calcifying plaque may become 50% mineralized in 2
days and 60% to 90%mineralization in 12 days
 All plaque does not necessarily undergo calcification.
 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.
31

32. The initiation of calcification and the rate of calculus accumulation
vary from person to person for different teeth and at different times
of same person
According to this they are classified as heavy, moderate or slight
calculus former
(Muhler and Ennever 1962)
slight moderate heavy
32

33.  Early plaque of heavy calculus former - more calcium, three
times more phosphorous and less potassium than that of non-
calculus former
 Total protein and total lipid levels - elevated in Heavy calculus
formers.
 Light calculus formers - higher levels of parotid
pyrophosphate.
 The average daily increment in calculus former- 0.10% to
0.15% of dry weight
 The time required by calculus to reach the maximal level has
been reported as 10 weeks (Conroy 1968) and 6 months.
(Volpe1969)
33

34. Attachment
by means of
organic
pellicle on
enamel
Mechanical
interlocking in
cemental
resorption
lacunae
Close adaptation
of calculus
undersurface
depressions to
gently sloping
mounds on the
unaltered
cementum surface.
Penetration of
calculus
bacteria in
cementum. But
this mode of
attachment
was not
acknowledged
The following 4 modes of attachment has been described:-
34

35. 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
35

36.  Mineralization of plaque starts both extracellulary &
intracellulary by gram +ve and –ve microorganisms,
Filamentous organisms, diptheroids,bacterionema and
vellionella species.
 Bacterial plaque may actively participate in the mineralization
of calculus by forming phosphates, which changes the Ph of
plaque and induces mineralization.
36

37. TWO PRINCIPAL CATEGORIES
a)Mineral precipitation results from local rise in the
degree of saturation of Ca and P ions and may be
due to rise in ph.
b)Seeding agents induces small foci of
calcification that enlarge and coalesce to form
a calcified mass.
37

38. 1. Booster mechanism
2. Epitactic concept
3. Inhibition theory
4. Transformation theory
5. Bacterial theory
6. Enzymatic theory
38

39.  Major salivary ducts secrete saliva at a high CO2 tension,
about 54 to 65 mm Hg; but the pressure of CO2 in atmospheric
air is only about 0.3 mm Hg.
 As a result of large disparity in CO2 tension, saliva emerging
from the salivary ducts loses CO2 to the atmosphere.
39

40.  pH in saliva will increase when CO2 escapes since pH in
saliva depends largely on the ratio between bicarbonates and
free carbonic acid.
 Phosphoric acid dissociation increases with rise in the
alkalinity, thus increasing the concentration of less soluble
secondary and tertiary phosphate ions.
 This boost in phosphate ions concentration leads to a situation
where solubility product of calcium phosphate is exceeded
and crystals form
40

41. UREA
AMMONIA
INCREASE IN pH
PRECIPITATION OF
CALCIUM PHOSPHATE
Mandel and thompson 1967- Rapid calculus producers have a
higher than average urea concentrations in saliva which increases
ammonia levels in plaque 41

42.  In saliva the concentration of certain ions like calcium and
phosphate is not high enough to precipitate but is ample
enough to promote the growth of hydroxyapatite crystals once
an initial seed or nucleus is formed.
 The term epitactic refers to crystal formation through seeding
by another compound which is similar to hydroxyapatite
crystals, leading to precipitation of calcium salts from the
metastable solution of saliva.
 Seeding agents provoke small foci of calcification enlarge and
coalesce to form the calcified mass.
42

43.  Intercellular matrix or plaque plays an important role.
 Calcification will be initiated by a carbohydrate/protein
complex which removes calcium from saliva by chelation
process and binds with the nuclei that stimulates subsequent
deposition of minerals.
 The various nucleating molecules are :
 Some types of collagen and proteoglycans (Boskey 1981).
 Calcium –phospholipid-phosphate complexes are important
nucleators in numerous calcifications including
calculus.(Bosky et al in 1981)
 Bacteria are thought to be important nucleators (Ennever et al
In 1976)
43

44.  This theory assumes about calcification as occurring only at
specific sites because of existence of an inhibiting mechanism
at noncalcifying sites.
 According to this theory, the sites where calcification occurs,
the inhibitor is apparently altered or removed.
 Pyrophosphate is thought to be one possible inhibiting
substance and other possible inhibiting substances include
polyphosphates.
 Alkaline pyrophosphatase is the enzyme involved in
controlling mechanism which hydrolyzes the pyrophosphate
to phosphate (Russell and Fleisch 1970) and this
pyrophosphate prevents the initial nucleus from growing and
inhibits their calcification possibly by poisoning the growth
centers of the crystals. 44

45.  Most noticeable hypothesis states that
hydroxyapatite need not arise exclusively via
epitaxis or nucleation.
 Octa calcium phosphate is formed by the
transformation of amorphous noncrystalline
deposits and brushite and then transformed to
hydroxyapatite (Eanes et al 1970).
 It has been suggested that controlling mechanism
in trans-formation mechanism can be
pyrophosphate (Fleisch et al 1968).
45

46.  According to this theory, the primary cause of
calculus formation is oral microorganisms and
their involvement in attachment to the tooth
surface.
 Leptotrichia and actinomyces have been
considered most often as the causative
microorganisms.
46

47.  According to this theory, calculus formation is
the resultant of the action of phosphatases
derived from either oral tissues or oral
microorganism on some salivary phosphate
containing complex, most probably phospheric
esters of the hexophosphoric group.
47

48.  Cifecioglu et al 2003 & Demir T 2008 stated that
nanobacteria may be present in dental calculus and
may play a role in calcification of dental calculus.
 Nanobacteria may be considered as a risk factor
for the periodontal disease.
 Zang et al found nanobacteria from the crevicular
fluid of patients with chronic periodontitis and
stated that it can be cultured and identified from
dental calculus too.
48

49. Visual examination
 Gentle air blast
 Transillumination
 Gingival tissue color change
Tactile examination
 Probe
 Explorer
Radiographs
49

50.  Good lighting helps us to easily visualize supra- and
subgingival calculus just below the gingival margin.
When light deposits of supragingival calculus are
wet with saliva they are frequently difficult to
visualize.
 Supragingival calculus can be dried using
compressed air until it is readily visible and chalky
white. Air may also be directed into the pocket in
steady stream to visualize the subgingival deposits
by deflection of gingival margin away from the tooth
surface.
50

51. 51

52. Highly calcified interproximal calculus deposits - detectable as
radioopaque projections
However, the sensitivity level of calculus detection by
radiographs is low.
The location of calculus does not indicate the bottom of the
periodontal pocket because the most apical plaque is not
sufficiently calcified to be visible on radiographs.
Hence, conventional oral radiography was a poor diagnostic
method for the detection of calculus (Buchanan et al, 1987).
52

53.  Fine-pointed explorer or probe is used for tactile sensation and is
held with light but stable modified pen grasp. Slight vibrations
are perceived by pads of the thumb and the middle fingers
through the shank.
 Method: First, a stable finger rest is established and then the
instrument tip is inserted to the pocket depth. In a vertical
direction light exploratory strokes are activated. On contact with
the calculus, the tip of probe is advanced more apically till the
termination of calculus is felt on root surface. Generally, 0.2 to
1.0 mm is the distance appreciated between apical edge of
calculus and bottom of the pocket. Proximal surfaces when
explored with an instrument tip, it should be extended at least
halfway across the surface past the contact area.
53

54. Fiberoptic endoscopy-based
technology ie PERIOSCOPE
Spectro optical technology
Novel LED probe ie DETECTAR
Autofluorescence based technology
ie DIAGNODENT
Ultrasound technology ie
PERIOSCAN
Laser based technology ie
KEYLASER
54

55.  Currently, perioscopy is the only available method for
detecting calculus (Perioscopy Inc., Oakland, CA, USA).
Based on the principle of medical endoscopy, perioscopy is a
minimally invasive approach that was introduced in the year
2000. The perioscope is a miniature periodontal endoscope.
When inserted into the periodontal pocket, it images the
subgingival root surface, tooth surface, and calculus.
55

56.  Components of the perioscope
include fiber-optic bundles
bound by multiple
illumination fibers, a light
source, and an irrigation
system.
 Perioscopic images can be
viewed on a monitor in real
time, captured, and saved in
computer files.
 Although it causes minimal
tissue trauma, perioscopy is
not widely used, owing to its
high cost and the need for a
rigorous training period prior
to use.
56

57.  The Detec-Tar (Dentsply
Professional, York, PA, USA)
calculus detection device utilizes
light-emitting diode and fiber-optic
technologies. An optical fiber in
the device recognizes the
characteristic spectral signals of
calculus caused by the absorption,
reflection, and diffraction of red
light (Kasaj et al., 2008).
 Advantages of the device include
its portability and emission of
audible and luminous signals upon
calculus detection.
57

58.  Calculus contains various non-metals and metals, such as
porphyrins and chromatophores. Due to their differences in
composition, calculus and teeth fluoresce at different wavelength
ranges (628–685 nm and 477–497 nm, respectively).
 DIAGNODENT is a commercially available calculus detection
device (Meissner and Kocher, 2011). The InGaAsP-based red laser
diode used in Diagnodent emits a wavelength of 655 nm through an
optical fiber, causing fluorescence of calculus (Hibst et al., 2001).
58

59.  Perioscan (Sirona, Germany) is an ultrasonic device that
works on acoustic principles, similar to tapping a glass
surface with a hard substance and analyzing the resulting
sound to identify cracks in the glass.
 The tip of the ultrasonic insert in Perioscan oscillates
continuously. Different voltages are produced depending on
the oscillation that, in turn, depends on the hardness of the
surface encountered by the device.
 Perioscan can differentiate calculus from healthy root surfaces
according to the inherent difference in hardness between the
materials. It provides the option of immediate calculus
removal, simply by switching the mode from ‘‘detection’’ to
‘‘removal,’’ a technique that makes it unnecessary to relocate
previously located calculus.
59

60.  The Perioscan instrument is used in two different modes.
When the ultrasonic tip touches the tooth surface, a light
signal is displayed on the hand-piece and on the actual unit.
The light signal is accompanied by an acoustic signal. A blue
light is shown during calculus detection mode, and a green
light is shown when the ultrasonic tip touches healthy
cementum. Different power settings aid the clinician in
removing tenacious calculus. The only clinical study available
for this device reported a sensitivity of 91% and specificity of
82% (Meissner et al., 2008).
60

61.  Keylaser combines a 655-nm InGaAsP diode
for detection of calculus and a 2940-nm
Er:YAG laser for treatment.
 A scale of 0–99 is used for detection of
calculus, with values exceeding 40 indicating
the definite presence of mineralized deposits.
The Er:YAG laser becomes activated when it
reaches a certain threshold and is switched off
as soon as the value falls below the threshold.
Studies assessing the efficacy of the
Keylaser3 have shown that it produces a tooth
surface that is comparable to those produced
by hand and ultrasonic instrumentation (Aoki
et al., 1994, 2000; Folwaczny et al., 2000).
The major concern with laser use is its high
cost. 61

62.  Birgitta Söder et al in 2014 after 26-Year
Observational Study states that dental calculus is
associated with death from heart infarction. A high
dental calculus index score indicate a long-lasting
oral infection burden which causes upregulation of
systemic inflammatory reactions. These, in turn, may
be involved in the development of atherosclerosis
and finally lead to death from heart infarction.
 A case-control study by Mattila et al. in 1989
revealed that patients with acute myocardial
infarction had worse dental health than age- and sex-
matched controls.
62

63.  Oikarinen et al. in 2009 revealed that radiographically
diagnosed periodontal infection was more prevalent among
patients with CAD than among control subjects.
 A prospective 7-year follow-up study indicated that dental
health significantly predicted coronary events among patients
with coronary heart disease (Mattila KJ et al 1995).
 Ho Lee in 2019 in an observational study found the association
between dental health and obstructive coronary artery disease
(CAD). The study revealed that, among various dental health
indices, only the number of lost teeth (which reflects the most
severe outcome of sustained oral infection) was independently
associated with obstructive CAD. Furthermore, the extent of
CAD increased proportionally with an increasing number of lost
teeth.
63

64.  Paunio et al. in 1993 reported that patients with
ischaemic heart disease had more missing teeth than
control subjects.
 A longitudinal study by DeStefano et al. in 1993
demonstrated that subjects with periodontitis had a
25% higher risk of future coronary heart disease than
subjects with minimal periodontal disease.
 A meta-analysis of 9 studies revealed that periodontal
disease was associated with a 19% increase in the risk
of future cardiovascular disease among the general
population (Janket SJ et al 2003)
64

65. 65

66. TOOTHBRUSHING
 Toothpaste abrasives may interfere with
supragingival calculus formation, either by removal
of the matrix for the deposition of salts or removal of
the calculus in the early stages of calcification.
 Using a quantitative scoring procedure, Villa in 1968
was able to demonstrate that thorough brushing
alone could reduce calculus formation by as much as
50 percent on the lingual surfaces of the lower
anterior teeth.
66

67.  Conventional non-surgical therapy is considered
to be the cornerstone of periodontal treatment. Its
effectiveness is based on reducing the bacterial
load from the periodontal pocket and removing
hard deposits (e.g., calculus) that can aggravate
the infection.
 Studies have concluded that the effectiveness of
different treatment modalities in thorough
calculus removal from root surfaces is impossible
(Egelberg, 1999; Oda et al., 2004).
67

68.  Different hand instruments are used for non-
surgical periodontal therapy. Scalers and
curettes have the most access to subgingival
calculus. Curettes can be used for root planning
and effective debridement of subgingival
calculus.
 Different aspects of hand and ultrasonic
instrumentation methods have been compared
(Claffey et al., 2004). In one study, ultrasonic
instrumentation consumed less time for calculus
removal than instrumentation by Gracey
curettes (Copulos et al., 1993). Another found
that there was no microscopic difference
between the Cavitron ultrasonic scaler and
Gracey curettes (Oosterwaal et al., 1987).
68

69.  Ultrasonic instruments are the principle
treatment modality for removing plaque
and calculus.
 These power-driven instruments oscillate
at very high speeds, causing micro
vibrations that aid in calculus and
subgingival plaque removal.
 Two different mechanisms are used to
create these oscillations of the ultrasonic
tip. Comparisons of magnetostrictive,
piezoelectric, and hand instruments have
had inconclusive results.
69

70.  Arabaci et al. (2007) found that the piezoelectric system
was more efficient in calculus removal compared to
magnetostrictive and hand instrumentation, but they left
tooth surface rougher.
 Other studies have shown contradictory results with each
other. Hence, it is not clear which treatment modality is
more efficient for removing plaque and calculus from the
root surface (Cross-Poline et al., 1995).
70

71. 71

72.  Strategies to prevent calculus formation may include
measures to solubilize calculus and the organic
matrix, or to inhibit plaque adhesion, formation, and
mineralization (Meissner and Kocher, 2011).
 Although decalcifying, complexing, or chelating
substances could dissolve or soften the mineralized
deposits, these chemicals carry the risk of damaging
the enamel, dentin, or cementum. Therefore, research
has focused on inhibiting plaque attachment and
altering its metabolic and chemical characteristics
(i.e., developing early mineralized plaque) by using
antiseptics, antibiotics, enzymes, and matrix-
disrupting agents (Aoki et al., 2000; Folwaczny et
al., 2000).
72

73.  One of the earliest techniques utilised a wooden stick
which was moistened with aromatic sulphuric acid
before being introduced into a periodontal pocket to
dissolve calculus and to act on the soft tissues as an
astringent.
 After 2 weeks, the tooth became firm and ‘cured’
(Barker 1872). This technique was subsequently
modified by Niles (1881) who suggested the use of
nitro muriatic acid because of its superior dissolving
action on dental calculus.
 Other acids included 20% trichloroacetic acid,
bifluoride of mercury and 10% sulphuric acid.
73

74.  The use of acids to remove or reduce the build up of
dental calculus created some problems as they are
caustic to soft tissues and decalcify tooth structure.
 Both Stones (1939) and Grossman (1954a,b)
reported that the ability of an acid to dissolve tooth
material was greater than its ability to dissolve
calculus.
 The use of acids as anticalculus agents was thus
discontinued.
74

75.  Badanes (1929) noted the beneficial effect of
natural mineral waters on the removal of
calculus. He argued that it was the action of the
mild alkalis contained in the waters that
dissolved the three principal organic constituents
of salivary calculus; globulin, mucin and calcium
oxalate. These findings agreed with those of
Prinz (1921), but the idea failed to find support.
75

76.  Chelating agents are used to dissolve crystallized
calcium salts and are capable of combining with
calcium to form stable compounds.
 These chemicals remove calcium from solution and
have been used to dissolve renal calculi.
 Sodium hexametaphosphate was found to remove
supragingival calculus from extracted teeth in 10 to
15 days (Kerr & Field 1944). The chelating agent
dissolved silicate restorations, but with no harm to
the tooth structure.
76

77.  Warren et al. (1964) exposed extracted teeth to a
saturated solution of sodium hexametaphosphate
for 24 h and found a large reduction in the
hardness of the cementum and the decalcification
of the calculus was less than that of cementum.
Because of this nonspecific demineralization
effect, the use of chelating agents in anticalculus
dentifrices ceased.
77

78.  The mode of action of enzyme formulations is to break down
plaque matrix or to affect the binding of the calculus to the
tooth.
 The first enzyme to be tested was mucinase (Stewart 1952), a
preparation with proteolytic and amylolytic activity. The
theoretical mechanism of action was to break down the mucins
(Hodge & Leung 1950) which were purported to bind calculus to
the tooth.
 A mucinase was delivered in an ammoniated dentifrice on six
subjects. Calculus formation was reduced and calculus which
did form was softer and more easily removed (Stewart 1952).
 This work was supported by that of Aleece & Forscher (1954)
who found that a mylase dentifrice produced a reduction in
calculus deposition.
78

79.  Draus et al. (1963) tested the anticalculus effect of a
number of enzymes in vitro. Extracted teeth were
placed into artificial calcifying solutions, each
containing one test enzyme. An enzyme with high
proteolytic and low amylase activity was the most
effective inhibitor of calculus formation.
 Dehydrated pancreas was tested on the basis of a
high proteolytic enzyme activity and was found to
reduce calculus formation by 60% (Jensen 1959).
 Packman et al. (1963) investigated the effect of
enzyme chewing gums on oral hygiene. They
compared dehydrated pancreas to combined enzymes
of fungal origin and found the latter to be superior in
retarding calculus formation (40.5% v 14.5%).
79

80.  The idea of using urea as a potential anticalculus agent
stems from its attributed solvent action on protein
(Holder & Mackay 1937, Muldavin & Holtzman 1938,
Holder & Mackay 1939).
 The anticalculus effect of urea was attributed to its
ability to dissolve the mucoproteinaceous material within
which the calcium salts are deposited and/or by
increasing the solubility of calcium salts in saliva
(Belting & Gordon 1966a).
 Urea was investigated as an anticalculus agent even
though its concentration is higher in submandibular
saliva of high calculus formers than in saliva of low
calculus formers (Mandel & Thompson 1967).
80

81.  The addition of urea to the oral cavity is likely to result
in ammonia production via urease activity.
 This ammonia increases the pH of saliva and plaque,
altering the solubility product of calcium and phosphate
and causing precipitation of calcium phosphate salts with
a consequent increase in calculus deposition.
81

82.  Attempts have been made to prevent calculus
deposition by coating the teeth with adhesive to
alter the binding of the calculus to the tooth.
 Dimethylpolysiloxane and cyanoacrylate
monomer adhesive - no effect
 Silicones- no effect
 Lactone- effective but caused de-mineralisation
of teeth.
 Sulphonated polystyrene membrane – effective
but temporary
82

83.  Sodium ricinoleate - interferes with the
attachment of microorganisms to teeth.
(Dossenbach & Muhlemann (1961)
 The results showed almost total absence of
microorganisms, and calculus formation was
almost totally inhibited.
 Unfortunately, sodium ricinoleate had a
particularly unacceptable taste and needed to be
applied at high concentrations.
83

84. PENICILLIN
 Dossenbach & Muhlemann (1961) investigated the
effect of penicillin lozenges on the accumulation of
calculus over 5 days in 20 dental students. The
lozenges were administered 10 times daily but there
was no decrease in the levels of calculus present.
84

85.  Cetylpyridinium chloride (CPC), a cationic
antimicrobial, was tested for anticalculus activity
as a mouthrinse on students over a 7 day period
(Muller et al. 1963).
 The students rinsed with 20 ml of the assigned
solution 3 times daily for 2 min but there were no
differences in calculus levels between CPC and
control rinses.
85

86.  Chlorhexidine is a cationic bis-biguanide which acts by
being adsorbed onto the bacterial cell wall, leading to
damage of the peameability barriers.
 At higher concentrations, precipitation and coagulation
of the cytoplasmic contents occurs (Hennessey 1977).
 Many studies have confirmed that chlorhexidine is an
excellent antiplaque agent (Loe & Schiott 1970, Hamp et
al. 1973, Tepe et al. 1983) a property which led to
chlorhexidine being evaluated as an anticalculus agent.
 Schroeder (1969) achieved a 73% reduction in calculus
formation using a 0.1% solution of chlorhexidine acetate.
86

87.  Loe et al. (1971) demonstrated that both a 0.2% chlorhexidine
gluconate rinse and a 0.2% topical application inhibited
supragingival calculus. Chlorhexidine was also more effective in
reducing calculus in rapid (52% reduction) than in slow calculus
formers (21% reduction)
 In a controlled 2-year study, Loe et al. (1976) showed that a
0.2% chlorhexidine gluconate mouthrinse actually increased
calculus although this was not ‘clinically significant’.
 Lang et al. (1982) reported a statistically significant increase in
calculus levels in children rinsing with a 0.2% chlorhexidine
gluconate solution.
 Calculus can form in the absence of bacteria (Fitzgerald &
McDaniel 1990). Dead and non-viable bacteria release
pyrophosphatase (Pellat & Grand 1986) which leads to a local
decrease in salivary natural pyrophosphate levels and
(potentially) mineralization of the bacterial cell wall. This may
explain the phenomenon that although chlorhexidine is a potent
anti-plaque agent it actually causes an increase in the formation
of supragingival calculus.
87

88.  Niddamycin is a macrolide antibiotic obtained from the
fermentation broth of a novel strain of streptomyces
caelestic. It is bacteriostatic and bacteriocidal and
selectively prevents the proliferation of certain
organisms.
 It shows a strong activity toward a variety of gram
positive organisms; streptococci, enterococci,
corynebacteria, bacilli and certain protozoas.
 Gram negative bacteria, yeasts and moulds appear to be
relatively resistant.
 It was tested as a potential anti-calculus agent because it
possessed many desirable characteristics for use in
mouthrinses and dentifrices.
88

89.  It had no known medical uses, was not significantly
absorbed orally or systemically, and no in vivo bacterial
resistance had been reported (Stallard et al.1969).
 Volpe et al. (1970) conducted a 9- month clinical trial
with 72 subjects. After a three month pretest period to
evaluate calculus accumulation, subjects used either a
0.01% Niddamycin or a control mouthrinse. The
niddamycin rinse produced a 38% reduction in calculus
formation after 3 months, a 50% reduction after 6
months, and a 33% reduction after 9 months.
 Research into the use of Niddamycin as an anticalculus
agent was discontinued, because of concern over the
development of bacterial cross resistance to other
antimicrobials.
89

90.  Triclosan is a non-ionic antibacterial agent with a
wide spectrum of activity against bacteria, fungi and
yeasts.
 Triclosan, when delivered from a dentifrice, seems to
bind to oral mucous membranes and tooth surfaces,
and is particularly well retained in plaque (Gilbert et
al. 1987, Gilbert & Williams 1987).
 Because of its proven antiplaque effects, a dentifrice
containing 0.2% triclosan and 0.5% zinc citrate was
tested as an anti calculus agent. Saxton et al. (1989)
described a significantly lower level of calculus in
the subjects using the test dentifrice over 6 months.
90

91.  Svatun & Saxton (1990) tested the efficacy of a
dentifrice containing 0.2% triclosan and 0.5% zinc
citrate on calculus and plaque growth, also over 6
months. They concluded that triclosan assisted the
control of plaque, promoted gingival health, and
inhibited calculus formation although to what extent
was unclear.
91

92.  The use of heavy metals to inhibit plaque formation was initially
suggested by Hanke (1940) who also recognised that, in
solution, these metals suffered from having a disagreeable
metallic taste, or caused an unsightly discolouration of the teeth.
 Metal salts, potentially have two mechanisms by which they can
affect calculus formation.
 Firstly, they inhibit plaque growth. Both stannous and stannic
salts inhibit growth (Svatun 1978, Ellingsen et al. 1980) as do
zinc salts (Fischmann et al. 1973, Skjorland et al. 1978, Saxton
et al. 1986).
 The mechanism by which inhibition occurs is probably via the
uptake of the metal salt by bacteria, with a consequent
disruption of intracellular metabolic processes (Aickien & Dean
1976).
92

93.  Secondly, metal salts are potent inhibitors of
mineralization (Bachra & van Harskamp 1970, Thomas
1982). The metal ion adsorbs to the surface of the
growing crystal, and prevents the attachment of lattice
ions. Consequently, crystal growth is slowed or inhibited.
 Kohut & Grossman (1986) tested a zinc chloride and
sodium fluoride dentifrice for calculus inhibitory activity
and compared it to a dentifrice containing only fluoride.
67 subjects used the test dentifrice for 3 months and
there was a significant 41.1% reduction in calculus
accumulation. The dentifrice containing the zinc chloride
significantly retarded the formation of supragingival
calculus.
 Putt & Kleber (1988) investigated the effects of chewing
gum containing aluminium citrate. 381 adult subjects
each chewed a piece of chewing gum three times daily
for 5 minutes and this led to a reduction in calculus
levels.
93

94.  Bisphosphonates are a group of synthetic pyrophosphate
analogues which interact strongly with minerals (Fleish
& Russell 1972), and are thought to prevent calculus
deposition by inhibiting crystal growth.
 Seichter et al. (1980) reported a significant reduction in
calculus formation using a dentifrice containing 0.5%
sodium etidronate but Kremers et al. (1980) using a 1.0%
sodium etidronate dentifrice, observed no effects.
 Bubani (1980) investigated a dentifrice containing 1.15%
azacycloheptane-2.2-diphosphonic acid (AHP). After 12
months usage, the dentifrice reduced calculus levels by
22.9%.
94

95.  Nilsson & Holm (1986) studied a dentifrice
containing 1.0% AHP. This study reported a 30%
reduction in calculus levels versus a placebo
mouthrinse in the 11 subjects who completed the 4-
month study.
95

96.  Vitamin C is a surface active organophosphorus
compound that has been shown to be effective in
inhibiting the in vitro crystallization of calcium
phosphate on to smears of supragingival calculus
(Turesky et al. 1965a,b). Vitamin C inhibits crystal
growth by a crystal poisoning mechanism.
 Turesky et al. (1967) tested the efficacy of a
chloromethyl analogue of vitamin C using the mylar foil
method and a silicone rubber tray to isolate the
mandibular teeth, allowing maximum contact of the
vitamin C solution with the teeth. A 1% solution was
applied topically to the teeth in 11 subjects, three times a
day for eight days. The dry weights of the foils were
determined and the vitamin C solution reduced calculus
deposition by 46.8% compared to water controls.
96

97.  Lower concentrations of pyrophosphate were noted
in the parotid saliva of calculus formers than in
saliva of non-formers (Vogel & Amdur 1967). The
concentration of pyrophosphate in the plaque of low
calculus formers was also significantly greater than
that in heavy calculus formers (Edgar & Jenkins
1972). Pyrophosphate has the ability to reduce
calculus accumulation in the laboratory (Mukherjee
1968, Briner & Francis 1973), and in animals
(Briner & Francis 1973).
97

98.  An oligomer of sulfoacrylic acid has been tested for
anticalculus activity (Gaffar et al. 1981a). The agent
was directed at preventing the increase in calcified
deposits which occurred when a cationic
antimicrobial agent such as chlorhexidine CPC is
used. Gaffar et al. (1981b) showed that the oligomer
of sulfoacrylic Acid (ND-2) in a 1% mouthrinse
significantly reduced calculus formation after 6
weeks in beagle dogs.
98

99.  The incorporation of a copolymer in a
pyrophosphate/NaF dentifrice increases the
anticalculus efficacy of that dentifrice (Schiff 1987,
Rosling & Lindhe 1987).
 This improvement has been ascribed to the presence
of the co-polymer of methoxyethylene and maleic
acid in the dentifrice (Schiff 1987).
 Later studies have also indicated that for
pyrophosphate dentifrices to be effective, they have
to contain the copolymer (Schiff et al. 1990, Singh et
al. 1990).
99

100.  While the bacterial plaque that coats the teeth is
the main etiologic factor in the development of
periodontal disease, the removal of subgingival
plaque and calculus constitute the cornerstone of
periodontal therapy.
 Calculus plays an important role in maintaining
and accentuating periodontal disease by keeping
plaque in close contact with the gingival tissue
and creating areas where plaque removal is
impossible. Therefore the clinician must possess
the clinical skill to remove the calculus and other
irritants as a basis for adequate periodontal and
prophylactic therapy.
100

101. › Meghana DP, Quaid JS, Arvind S. Interrelationship between chronic periodontitis and
anemia: A 6-month follow-up study. J Periodontol 2014 Mar 6;18(1):19-25.
› Masud M, Zahari HIM, Sameon ASN, Mohamed NAH. Manual and electronic detection of
subgingival calculus: Reliability and accuracy. Int J Adv Med Res (JAMR) 2014
May;1(1):52-56.
› Carranza’s clinical periodontology. 11th ed. Chapter 22. p. 291.
› Tannenbaum PJ, Posner AS, Mandel ID. Formation of calcium phosphates in saliva and
dental plaque. J Dent Res 1976 Nov-Dec;55(6):997-1000.
› Sahithya, RS. Essentials of periodontology. 1st ed. Chapter 20: Dental calculus. p. 213-216.
› Carranza’s clinical periodontology. 10th ed. Chapter 10. p. 172-173.
› White DJ. Dented 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):508-522.
› Anerud A, Loe H, Boysen H. The natural history and clinical course of calculus formation
in man. J Clin Periodontol 1991 Mar;18(3):160-170.
› Carranza’s clinical periodontology. 9th ed. Chapter 11. p. 183.
› Matarasso S, Quaremb G, Corraggio F, Vaia E, Cafiero C, Lang NP. Maintenance of
implants: An in vitro study of titanium implant surface modifications subsequent to the
application of different prophylaxis procedures. Clin Oral Implants Res 1996 Mar;7(1):64-
72
101

102. › Jepsen S, Deschner J, Braun A, Schwarz F, Eberhard J. Calculus removal and the
prevention of its formation. Periodontol 2000 2011 Feb;55(1):167-188.
› Allen DL, Kerr DA. Tissue response in the guinea pig to sterile and non-sterile calculus. J
Periodontol 1965 Mar-Apr;36: 121-126.
› Mandei ID, Gaffar A. Calculus revisited: A review. J Clin Periodontal 1986 Apr;13(4):249-
257.
› Ainamo J. Concomitant periodontal disease and dental caries in young adult males. Suom
Hammaslaak Toim 1970;66(6):301-364.
› Alexander AG. A study of the distribution of supra and subgingival calculus, bacterial
plaque and gingival inflam- mation in the mouths of 400 individuals. J Periodontol 1971
Jan;42(1):21-28.
› Buckley LA. The relationships between irregular teeth, plaque, calculus and gingival
disease. Br Dent J 1980 Feb; 148(3):67-69.
› Lennnon, MA.; Clerehugh, V. The identification of teenage children at high risk of
periodontal disease. Periodontal disease in Western Europe. Chicago: Quintessence; 1984.
p. 211-216.
› Nyman S, Rosling B, Lindhe J. Effect of professional tooth cleaning on healing after
periodontal surgery. J Clin Periodontol 1975 Apr;2(2):80-86. Nyman S, Lindhe J.
Considerations in the treatment of patients with multiple teeth with furcation involvements. J
Clin Periodontol 1976 Feb;3(1):4-13.
› Rosling B, Nyman S, Lindhe J. The effect of systematic plaque control on bone regeneration
in infrabony pockets. J Clin Periodontol 1976 Feb;3(1):38-53.
› Axelsson P, Lindhe J. Effect of controlled oral hygiene procedures on caries and periodontal
disease in adults. Results after 6 years. J Clin Periodontol 1981 Jun;8(3):239-248.
› Axelsson P, Lindhe J. Effect of controlled oral hygiene procedures on caries and periodontal
disease in adults. J Clin Periodontol 1978 May;5(2):133-151. 102

103. › Tagge DL, O’Leary TJ, El-Kafrawy AH. The clinical and histological response of periodontal
pockets to root planning and oral hygiene. J Periodontol 1975 Sep;46(9):527-533.
› Hellden LB, Listgarten MA, Lindhe J. The effect of tetracy- cline and/or scaling on human
periodontal disease. J Clin Periodontol 1979 Aug;6(4):222-230.
› Morrison EC, Ramfjord SP, Hill RW. Short-term effects of initial, nonsurgical periodontal
treatment (hygienic phase). J Clin Periodontol 1980 Jun;7(3):199-211.
› Chawla TN, Nanda RS, Kapoor KK. Dental prophylaxis pro- cedures in control of periodontal
disease in Lucknow (rural) India. J Periodontol 1975 Aug;46(8):498-503.
› Jones SJ. Calculus on human teeth. Apex 1972;6:55-59.
› Baumhammers A, Conway JC, Saltzberg D, Matta RK. Scanning electron microscopy of
supragingival calculus. J Periodontol 1973 Feb;44(2):92-95.
› Friskopp J, Hammarstrom L. A comparative, scanning electron microscopic study of
supragingival and subgingival calculus. J Periodontol 1980 Oct;51(10):553-562.
› Friskopp J. Ultrastructure of nondecalcified supragingival and subgingival calculus. J
Periodontol 1983 Sep;54(9): 542-550.
› Shirato M, Kamishikiryo K, Itoh A, Kado H, Maeda Y, Sekiguchi T, Fukui K, Takezawa T.
Observations of the surface of dental calculus using scanning electron microscopy. J Nihon
Univ School Dent 1981;23:179-187.
› Patters MR, Landesberg RL, Johansson LA, Trummcl CL, Robertson PB. Bacteroides
gingivalis antigens and bone resorbing activity in root surface fractions of periodontally
involved teeth. J Periodontal Res1982 Mar;17(2):122-130.
› Soben Peter. Text book of public health dentistry. 5th ed. Chapter 4. p. 126.
› Kamath DG, Nayak SU. Detection, removal and prevention of calculus: Literature review.
Saudi Dent J 2014 Jan;26(1): 7-13.
› Archana V. Calculus detection technologies: Where do we stand now? J Med Life
2014;7(Spec Issue 2):18-23. 103

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