This document provides an overview of calculus (dental tartar). It defines calculus, discusses its history, classification, prevalence, formation, composition, and theories of mineralization. Calculus is a hard deposit formed from mineralization of dental plaque. It consists mainly of calcium phosphate crystals like hydroxyapatite and whitlockite. Calculus forms more readily in some individuals and locations in the mouth. Various local factors in plaque are thought to increase calcium and phosphate levels and pH, leading to precipitation of crystals and calculus formation.

2. CALCULUS
PRESENTED BY
DR.PUNIT
FIRST YEAR PG

3. CONTENTS
 Definitions
 History
 Classification
 Supragingival calculus
 Subgingival calculus
 Prevalance
 Rate of formation
 Attachment of calculus
 Diagnosis
 Formation of calculus
 Theories of mineralization
 Clinical significance
 Anticalculus agents
 Indices
 Future research
 CONCLUSION
 REFERENCES

4. Calculus is derived from Greek words Calcis-lime stone,
Tartar- white encrustation inside casks.
DEFINITION:
 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

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

6. SYNONYMS
 Tartar
 Disambiguation
 Calcis
 Odontolithiasis
 Fossilized plaque

7. history

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

9. 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
(Loeet al,1965)

10.  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,
MINERALIZEDDENTALPLAQUETHAT IS PERMEATEDWITH
CRYSTALS OF VARIOUS CALCIUMPHOSPHATES.
(Perio 2000 vol.8 1995)

11. Classification
 According to location
Supragingival calculus
Subgingival calculus
 According to source of mineralization
Salivary calculus
Serumal calculus (Jenkins, Stewart 1966)
 According to surface
Exogenous
Endogenous (Melz 1950)

12.  According to initiation and rate of accumulation, calculus
formers are classified as:
-non calculus formers
- Slight calculus formers
-moderate calculus formers
-heavy calculus formers
(Muhler and Ennever 1962)

13.  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

14. SUPRAGINGIVAL CALCULUS
Location
Colour
Texture and consistency

15. DISTRIBUTION

16. INORGANIC MATRIX
70-80%
 Calcium and phosphorous constitute the major
element and Ca/P ratio ranges from 1.6 to more
than 2
(Little et al,1963;Lundberg ,1966;
Shroeder,1969)INORGANIC
CALCIUM PHOSPHATE
75.9%
CALCIUM CARBONATE
3.1%
MAGNESIUM
PHOSPHATE
TRACES
COMPOSITION

17.  The principle inorganic components are:
(Muhler and Enever,1962)

18. ORGANIC MATRIX
20-30%
Proteins 5.9-8.2%
Salivary proteins
Lipids 0.2%
Neutral fats
Free fatty acids
Cholesterol
Phospholipids
Carbohydrates 1.9-9.1%
Galactose
Glucose
Rhamnose
Galactosamine
Glucosamine
Gluconate
(Little, 1964)

19. Hydroxyapatite
58%
Magnesium
Whitolockite
21%
Octacalcium
Phosphate
1.2%
Brushite
9%
CRYSTALS
 Atleast 2/3rd of the inorganic component is in the form of
crystals. (Leug&Jenson,1958)
 The four main crystal forms are:

20.  Hydroxyapatite and Octacalcium phosphate are detected most
frequently in supragingival calculus. (97-100%)
 Brushite - mandibular anterior region; present only in the early-stage
supragingival calculus
(Rowles, 1964).
 When supragingival calculus ages- Brushite
HAP,OCP&WHT
(Shroeder,1967)
 Magnesium whitlockite - in the posterior areas

21.  The composition of calculus varies and depends upon:
1. Concentration of Ca & P
2. Relative amount of ions present locally
3. pH of saliva
4. Presence of other minerals which are calcification promoters like
urea,fluoride,silicon,etc.

22. SUPRAGINGIVALCALCULUS

at low ph &high Ca:P at high ph
SUBGINGIVALCALCULUS
OCP HAP
BRUSHITE HAP & WHT
WHT
Anaerobic
condition
Mg Zn
carbon
ates
At pH of saliva

23. LIGHT MICROSCOPY
 Calculus tooth interface is smooth
 External mineralized surface is irregular
 Covered by non mineralized plaque
 Contain many non mineralized lacunae
STRUCTURE

24. TRANSMISSIONELECTRONMICROSCOPY
 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. SCANNING ELECTRON MICROSCOPY
 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. X-ray BeamDiffraction Analysis
DISTRIBUTIONOFCALCIUMPHOSPHATECOMPOUNDS
 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.

27. SUBGINGIVAL
CALCULUS
 Location
 Colour
 Texture and consistency

28. COMPOSITION
 Similar to supragingival calculus except that it has higher
concentration of-Ca,Mg,Fl.
 Ca:P ratio is higher
 Na content increases with depth of periodontal pocket
 Salivary proteins are absent.
 Supragingival & subgingival calculus contains 37% & 58% mineral
content by volume respectively

29. CRYSTALS
 Whitlockite – mainly found
 Same HAP, more WL, less Brushite and OCP as compared to
supragingival calculus
 WL to HAP ratio is higher

30. LIGHT MICROSCOPY
 Unlike supragingival calculus, lacunae of stained organic material
were not seen within the body of subgingival calculus.
 The calculus surface previously in contact with the tooth was usually
flat and mineralized
 The external/oral surface was fairly regular and covered by a non-
mineralized plaque layer of variable thickness

31. TRANSMISSIONELECTRONMICROSCOPY
 The calcification - more homogeneous and
consisted of small randomly orientated needle- and
platelet-shaped crystals (a).
 Areas with flat "bulk-shaped" crystals seen [as
described by Sundberg & Friskopp (1985),] within
which were fewer bacterial cell structures (b).

32. SCANNING ELECTRONMICROSCOPY
 Under low magnification - clusters of small
deposits in the incisal/ occlusal part and larger
deposits that tend to fuse in apical part.
 High magnification - subgingival fracture
surface were rougher than supra gingival,
grooves and holes that gave sub gingival
fracture a ‘worm eaten’ look. Filaments did not
dominate the surface of subgingival calculus
and no pattern of orientations were seen

33. X-RAY BEAMDIFFRACTIONANALYSIS
 In subgingival calculus - OCP is scarcely found.
 The main constituent is WL and HAP.
 Brushite is totally absent

34. PREVALENCE
 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.

35. RATE OF FORMATION
 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

36.  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.

37.  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

38.  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.(Volpe
1969)

39. MICROBIOLOGY OF DENTAL CALCULUS
 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.

40. CALCULUS ATTACHMENT
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
THEFOLLOWING4 MODESOF ATTACHMENTHASBEENDESCRIBED:-

41. 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 etal 1996

42. ROLE OF MICRO-ORGANISMS IN MINERALIZATION
 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.

43. Theories of mineralization
TWOPRINCIPALCATEGORIES
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.

44. FEW PROPOSED THEORIES ARE:
1. Booster mechanism
2. Epitactic concept
3. Inhibition theory
4. Transformation theory
5. Bacterial theory
6. Enzymatic theory

45. BOOSTER MECHANISM
Calcification will occur in a particular locus when local pH +
calcium and phosphorous concentrations  precipitation of a
calcium phosphate salt.
Factors such as
1. loss of CO2 & production of ammonia could account for an
elevation in pH;
2. Acid or alkaline phosphatase activity could result in a higher
phosphate concentration;
3. Liberation of bound or complexed calcium from the salivary
proteins would produce higher calcium levels.

46. Saliva –
CO2 tension= 54- 65 mmHg
Atmosphere CO2 tension= 0.3
mmHg
CO2
CO2
CO2
Increase in salivary pH
Dissociation of phosphoric
acid
Phosphate ions
Calcium phosphate crystal
formation
BOOSTER THEORY

47. UREA
AMMONIA
INCREASEIN pH
PRECIPITATIONOF CALCIUMPHOSPHATE
pH CHANGE BY AMMONIAFORMATION
Mandel and thompson 1967- Rapid calculus producers have a higher than
average urea concentrations in saliva which increases ammonia levels in
plaque

48. EPITATIC THEORY
 Seeding agents induce small foci of calcification enlarge and coalesce to form the
calcified mass.
 Intercellular matrix or plaque plays an important role. Carbohydrate protein
complexes initiates the calcification by removing calcium from saliva by
chelation and binds with the nuclei that induce subsequent deposition of minerals.
 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.

49. NUCLEATING MOLECULES
 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)

50. INHIBITION THEORY
 Calcification at specific sites - because of inhibiting mechanism at
non-calcifying sites.
 The sites where calcification occurs , the inhibitor is apparently
altered or removed.
 Possible inhibiting substance- pyrophosphate & other
polyphosphates.
 Among controlling mechanisms is the enzyme alkaline
pyrophosphatase - hydrolyze the pyrophosphate  phosphate
(Russell and Fleisch 1970).
 Pyrophosphate inhibits calcification - prevents the initial nucleus from
growing, possibly by poisoning the growth centers of the crystals

51. TRANSFORMATION THEORY
 Hypothesis - hydroxyapatite need not arise exclusively via
epitaxis or nucleation.
 Amorphous non-crystalline deposits and brushite can be
transformed into octacalcium phosphate and then to
hydroxyapatite (Eanes et al 1970).
 It has been suggested that controlling mechanism in
transformation mechanism can be pyrophosphate (Fleisch et al
1968).

52. BACTERIOLOGICAL THEORY
 Oral microorganisms are the primary cause of calculus, and that
they are invovled in its attachment to the tooth surface.
 Leptotrichia and Actinomyces have been considered most often
as the causative microorganism.

53. ENZYMATICTHEORY
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.(Adamson.KT 1929)

54. DIAGNOSTIC AIDS
Visual examination
 Gentle air blast
 Transillumination
 Gingival tissue color change
Tactile examination
 Probe
 Explorer
Radiographs

55. Gingival tissue colour change

56. 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.
Radiograph

57. Advance diagnostic aids…
 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

58. Concept of nanobacteria
 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.

59. Role of calculus in periodontal disease summarized as:
• Brings plaque bacteria close to supporting tissues.
• Provides fixed nidus for plaque accumulation.
• Interferes with local self cleansing mechanisms.
• Reservoir for substances like endotoxins, antigenic materials and
bone resorbing factors because of its permeability and porous
nature.

60. ORAL HYGIENE AND THE CONTROL OF
CALCULUS
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.

61. SCALING AND ROOT PLANING
 It is the most commonly practiced therapeutic intervention for
calculus formation.
 Scaling and root planing is done to remove plaque and
calculus from crowns and root surface of teeth.
 Sickles, curettes and ultrasonic and sonic instruments are most
commonly used for the removal of calculus.

62. Laser
 Laser most commonly used in periodontal therapy include
1. Semiconductor diode laser(gallium,arsenide,alluminium)
2. Solid state laser such as Nd:YAG(neodenium doped-yttrium
aluminium garnet),Er:YAG &
Er,Cr:YSGG(yttrium,scandilium,garnet,galium)
3. Carbon dioxide laser
 Among all lasers - Er:YAG laser is most suitable for the non
surgical periodontal debridement.

63. ANTICALCULUS AGENT

64. CLASSIFICATION
First GENERATION:
1)DISSOLUTION
• Chelating Agents
Ethylene diamine tetra acetate
Sodium Hexa Metaphosphate
• Acids –Aromatic sulphuric acid
Nitro-muriatic Acid
20% Trichloroacetic Acid
• Spring Salts
• Sodium Ricinolate
• Alkalies
2)ALTERING PLAQUE ATTACHMENTS
 Silicones
 Ion exchange resins.

65. 3)PLAQUE INHIBITION
 Antibiotics Example : Niddamycin
 Antiseptics Example : Chloramines
4)MATRIX DISRUPTION
 Enzymes Example : Mucinase
 Dehydrated Pancreas
 Trypsin, chymotrypsin
 Carboxypeptidase, lipase, amylase
 30% UREA( solvent action on protein)

66.  2nd GENERATION
 Inhibition of crystal growth
 VitaminC (By crystal poisoning mechanism )
 Pyrophosphatase
 Pyrophosphatase + Sodium fluoride
 Zinc salts
 Biphosphonates
 Polymers & Co Polymers

67.  Earliest techniques - wooden stick + aromatic sulphuric acid &
introduced into a periodontal pocket to dissolve calculus(Barker
1872).
 Niles (1881) - the nitro muriatic acid.
 Other acids included - 20% trichloroacetic acid, bifluoride of
mercury and 10% sulphuric acid.
 Disadvantages:
i. Caustic to soft tissues
ii. Decalcify tooth structure. (Stones (1939) and grossman (1954)
so their use was discontinued
ACIDS

68. ALKALIS
 Badanes (1929) argued that it was the action of the mild alkalis
contained in the waters that dissolved the principal organic
constituents of salivary calculus.
 These findings agreed with those of Prinz (1921), but the idea failed
to find support.

69. CHELATING AGENTS
These chemicals remove calcium from solution.
• Sodium hexametaphosphate was found to remove
supragingival calculus from extracted teeth in 10 to 15 days
(Kerr & Field 1944).
• 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.

70. EDTA
 Jabro et al. (1992) found that application of EDTA gel
(SofscaleTM) resulted in ease of calculus removal.
 However, subsequent studies by Maynar et al. (1994), Smith et al.
(1994), Harding et al.(1996) and Nagy et al. (1998) have failed to
confirm this effect.
 Smith et al. (1994) noted that sufficient time has to be allowed for
the gel to penetrate the bulk of the calculus deposit and this may
negate the reason for using it.

71. ENZYMES
 Mode of action – 1.To break down plaque matrix OR
2. To affect the binding of the calculus to the tooth.
 The first enzyme to be tested- mucinase (Stewart 1952)Calculus
formation reduced & calculus formed was softer and more easily
removed (Stewart 1952).
 Aleece & Forscher (1954) - introduced mylase.
 Enzyme with high proteolytic and low amylase activity- most
effective inhibitor of calculus formation. Draus et al. (1963)
 Dehydrated pancreas (Viokase) - tested on the basis of a high
proteolytic enzyme activity - reduce calculus formation by 60%
(Jensen 1959).
 Enzymes of fungal origin have also been tested.

72. Urea
 The anticalculus effect - ability to dissolve the
mucoproteinaceous material within which the calcium salts are
deposited and/or by increasing the solubility of calcium salts in
saliva.
 It was found that increasing the concentration of urea resulted in
progressive inhibition of calcium deposition.
 A maximum inhibition of 70% was reached at a concentration of
30% urea.
 Urea concentrations greater than 30% led to a progressive
decrease in inhibition.

73.  But the addition of urea to the oral cavity  result in ammonia
production via urease activity increases the pH of saliva and
plaque increase in calculus deposition.
 Then came into research, the concept of inhibiting urease
activity.
 Ethanehydroxydiphosphonate (EHDP) or acetohydroxamic acid
(AHA) were tested for their anti calculus potential

74.  Results demonstrated a significant reduction in calculus
formation in both the EHDP and AHA groups.
 But such changes were not significant in humans. ( Son
&Muhlemann 1971)
 This finding together with the observation that AHA had been
shown to increase caries (Regolati & Muhlemann 1971) led to a
decline in interest in AHA as an anticalculus agent.

75. MISCELLANEOUS CHEMICALAGENTS
 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

76.  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.

77.  Watt et al. (1993) postulated - changing the electrostatic nature of
the tooth surface in calculus prevention
 The magnetic water was thought to bring Ca2 and PO4 ions closer
together, consequently reducing attachment.
 The group using a magnetic water irrigator had 44% greater
reduction in calculus volume and a 42% greater reduction in
calculus area when compared with the group using an irrigator
with no magnetic water.

78. CALCIUM LACTATE
 Schaeken et al. (1990) investigated a 5% calcium lactate solution on
calcium and phosphate levels in saliva.
 The group using the dentifrices with calcium lactate had a 44%
reduction in calculus and those using the calcium lactate with sodium
lauryl sulphate had a 47% reduction in calculus with respect to the
control group.
 The authors concluded that calcium lactate probably did not act as an
inhibitor of crystal growth but may offset secretion and activity of
salivary phosphoproteins.

79. ANTIMICROBIALS
 Penicillin- no effect
 Cetylpyridinium chloride- no effect
 Chlorhexidine
Chlorhexidine is a cationic bis-biguanide which acts by being adsorbed
onto the bacterial cell wall, leading to damage of the permeability
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 (Lo¨ e & Schiott 1970, Hamp et al. 1973, Tepe et
al.1983)

80. NIDDAMYCIN
 Strong activity toward a variety of gram positive organisms;
streptococci, enterococci, corynebacteria, bacilli and certain
protozoas.
 No known medical uses; not significantly absorbed orally or
systemically, and no in vivo bacterial resistance had been reported
(Stallard et al.1969).
 Research into the use of Niddamycin as an anticalculus agent was
discontinued - concern over the development of bacterial cross
resistance to other antimicrobials.

81. TRICLOSAN
 Triclosan ( trivial name of 2,4,4-trichloro-2-hydroxydiphenyl ether) a
non-ionic antibacterial agent with a wide spectrum of activity against
bacteria, fungi and yeasts.
 When delivered from a dentifrice- seems to bind to oral mucous
membranes and tooth surfaces, and is particularly well retained in
plaque.
 Triclosan is predominantly used in combination with other anti-
calculus

82. PVM/ MA copolymer
 PVM/MA Copolymer is a copolymer of methyl vinyl ether and
maleic anhydride and is used as a binder.
 Promotes uptake of triclosan by enamel and buccal epithelial
cells (Nabi et al., 1989).
 Composed of two groups: an attachment group and a
solubilizing group.
 The solubilizing group retains triclosan in surfactant micelles so
that the attachment group can have enough time to react with
tooth surfaces via calcium in the liquid adherent layer.

83. INHIBITORSOF MINERALISATION
Metals
 Use of heavy metals - suggested by Hanke (1940) - in solution,
these metals suffered from having a disagreeable metallic taste, or
caused an unsightly discoloration of the teeth.
 Mechanisms by which they can affect calculus formation:
i. Firstly, they inhibit plaque growth.
ii. Secondly, metal salts are potent inhibitors of mineralization
(Bachra & van Harskamp 1970, Thomas 1982).
Metal ions can bind to hydroxyapatite although this binding is
reversible.

84. ZINC IONS
ZINC ions
1. Reduce plaque acidogenicity (Opperman 1980)
2. Plaque growth (Saxton 1986)
 It inhibits crystal growth by binding to the surface of solid Ca P
(Gilbert 1988)
 Zn at a conc of 0.1mmol/L inhibits the formation of
DCPD,OCP and amorphous Ca P but at a higher conc of 0.5-2
mmol/L promotes the formation of amorphous CaP.

85. BISPHOSPHONATES
 Bisphosphonates are a group of synthetic pyrophosphate analogues
thought to prevent calculus deposition by inhibiting crystal growth.

86. VITAMINC
 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. 1965).
 Vitamin C inhibits crystal growth by a crystal poisoning
mechanism.

87.  Turesky et al.(1967) tested the efficacy of a chloromethyl analogue
of victamine C - victamine C solution reduced calculus deposition
by 46.8% compared to water controls.
 Mechanism:
 Vitamin C has a characteristic taste which might have
promoted saliva flow, thus reducing calculus levels.
(but Gilmore compared effect of quinine sulphate and vitamin C
and found quinine sulphate having similar taste did not inhibit
calculus formation)

88. Pyrophosphates
 Pyrophosphate could prevent calcification by
1. Interrupting the conversion of amorphous calcium phosphate to
hydroxyapatite (Fleisch & Bisaz 1962
2. Inhibiting crystal growth
3. Reduce acquired pellicle formation.
 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).

89.  Pyrophosphate - binds to two sites on the HAP surface, and one
of the two sites needs to be bound by phosphate ion to permit
crystal growth to occur. If this site is bound by pyrophosphate,
phosphate ion cannot adsorb onto crystal, and thus crystal
growth is inhibited.
 Pyrophosphate undergo rapid hydrolysis in the oral cavity by
bacterial and host phosphatases (Gaffar et al 1986)
 The addition of co polymer PVM/MA is believed to prevent
this hydrolysis

90. PREVENTIONOF CALCULUS FORMATIONIN
IMPLANT PATIENTS

91. CLINICAL MEASUREMENT
 Two indices – quantitating calculus deposits
calculus component of OHI
calculus component of PI
 Calculus surface index (Ennever 1961)
 Marginal line calculus index (Muhlem 1967)
 Volpe – manhold index (1965)
 Calculus surface severity index

92. EFFECT OF MEDICATION
 A quantitative recording of supragingival deposits among
systemically medicated and non-medicated patients presenting for
a routine dental examination and prophylaxis indicated the
following:
1) a tendency for more plaque and less calculus to form among the
older individuals (65 years and older) regardless of the use or non-
use of medication;
2) a statistically significant reduction of calculus among individuals
medicated with ß-blockers, diuretics, vitamin C, anticholinergics,
synthroid, or allopurinol despite the high quantity of plaque present.
3) neither the patient's sex nor the time interval between prophylaxis
are important factors in the quantity of calculus or plaque formed in
either medicated or non-medicated individuals
(Turesky etal1992)

93. CONCLUSION
 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.

94. REFERENCES:
 CARRANZA –CLINICAL PERIODONTOLOGY 10TH ED
 JAN LINDHE – CLINICAL PERIODONTOLOGY AND IMPLANTOLOGY 4TH ED
 SUPRAGINGIVALCALCULUS: FORMATIONANDCONTROL(YE JIN)
 SUPRAGINGIVAL CALCULUS AND PERIODONTAL DISEASE, PERIO2000
(ROBINM . DAVIESR, OGERP . ELLWOODA, NTHONYR . VOLPE&MARGAREET. P
ETRONE)
 CALCULUS REVISITED:A review
,Mandei ID and Gaffar 249-257Periodontol J9S6;
 ANTICALCULUS AGENTS
(Fairbrother KJ, Heasman PA: Anticalculus agents. J Clin Periodontol 2000; 27:285–
301. C Munksgaard, 2000.)

95.  SUBGINGIVAL CALCULUS: WHERE ARE WE NOW? A COMPARATIVE REVIEW
(E.A. Roberts-Harry*, V. Clerehugh)
 CALCULUS-DETECTION TECHNOLOGIES AND THEIR CLINICAL APPLICATION
(Grit Meissner & Thomas Kocher) PERIO 2000
 CALCULUS REMOVAL AND THE PREVENTION OF ITS FORMATION
(Søren Jepsen, James Deschner, Andreas Braun, Frank Schwarz & Jo¨ Rg Eberhard)
PERIO 2000.
 WHITE DJ: DENTED CALCULUS: RECENT INSIGHTS INTO OCCURRENCE,
FORMATION, PREVENTION,REMOVAL AND ORAL HEALTH EFFECTS OF
SUPRAGINGIVAL AND SUBGINGIVAL DEPOSITS
(. EurJ Oral Sci 1997: 105: 508-522. © Munksgaard, 1997)