4. Although , dental plaque is considered as the primary etiologic agent in development
of periodontal diseases , presence of calculus is also of great concern to the clinicians
because it facilitates plaque formation by providing the surface for its formation
and keeps it in close contact with the gingival tissue.
5. Mineralized biofilms, penetrated by crystals of various calcium phosphates,
develop above or below the free gingival margin as moderately hard deposits
that are white/yellowish in color.
They are superficially covered with vital, non-mineralized biofilms.
non-mineralized biofilm calcifies dental calculus(mineralized biofilm).
DYNAMIC PROCESS
6. Once a tooth erupts, various materials gather on its surfaces which are frequently
called TOOTH ACCUMULATED MATERIALS/DEPOSITS;
SOFT DEPOSTIS:
Acquired pellicle
Microbial plaque
Material alba
Food debris
HARD DEPOSITS:
Calculus
Stains
8. 1. CARRANZA 11th Ed.= Consists of mineralized bacterial plaque that forms on the
surfaces of natural teeth and dental prosthesis.
2. GPT 4TH Ed. = Hard concretion that forms on the teeth or dental prosthesis
through the calcification of bacterial plaque.
9. 3. GREENE 1967 = A deposit of inorganic salts composed primarily of
calcium carbonate and phosphate mixed with food debris , bacteria and
desquamated epithelial cells.
4. SCHROEDER 1969 = Mineralized dental plaque that is permeated with
crystals of various CaP.
12. The word calculus is Latin for "small pebble" related to Greek chalix "small stone, pebble,
rubble“.
Calculus was a term used for various kinds of stones. This spun off many modern words,
including "calculate" (use stones for mathematical purposes), and "calculus", which came to
be used, in the 18th century, for accidental or incidental mineral buildups in human and
animal bodies, like kidney stones and minerals on teeth.
13. Tartar originates from Greek word (tartaron), as the term for the white
encrustation inside wine casks,aka potassium bitartrate commonly known
as cream of tartar.
This came to be a term used for calcium phosphate on teeth in the early 19th
century.
15. For nearly 5,000 years, from the time of the Sumerians, calculus was
considered to be the prime etiologic agent in periodontal disease.
HIPPOCRATES
(460-377 BC)
ALBUCASIS
(936-1013 BC)
PARACELSUS
(1535)
PIERRE
FAUCHARD
(1728)
First formal
association
between
dental
deposits
and oral
diseases
First to
address
relationship
between
calculus
and
periodontal
diseases
Coined the
term tartar
Slime layer
Stony crust
16. In the past 25 years, however, calculus has been deposed by plaque, and the
hardened criminal has come to be viewed as a fossilized remnant of minor
significance (Mandel 1974). This shift in perception, which became most
apparent in the 1960's, was largely a response to following lines of
investigation:
17. (1) ELECTRON MICROSCOPIC studies of developing plaque and calculus
demonstrated that supra and subgingival calculus was mineralized plaque
covered by an unmineralized bacterial layer (Mandel 1960, Zander et al 1960)
(Courtesy Dr. John Sottosanti, La Jolla, CA.)
Bacterial layer
Calculus
Cemental surface
18. (2) EXPERIMENTAL DEMONSTRATION in humans that allowed plaque 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).
(3) The pre-eminence of plaque was given further support by EXPERIMENTS IN
ANIMALS in which periodontal disease could be induced in uninfected hamsters by
innoculation of bacteria from plaques in which the disease had occured spontaneously
(lordan & Keyes 1964)
19. The only ambiguity during this transition period between the era of calculus
and the era of plaque was generated by some epidemiologic studies that
displayed a stronger correlation between calculus and disease than plaque and
disease (Ramfjord 1961, Lilienthal et al, 1965). These studies were reviewed
thoroughly and critically by Schroeder (1969) in his classic text on calculus.
21. • The author concluded that the epidemiologic studies could not
provide significant information on causality because they
employed indices attempting to correlate
MEAN VALUES for
deposits and disease
specific relationship
between deposits and
disease in the same sites
22. • In one of the few studies in which SPECIFIC SITE RELATIONSHIPS
WERE CONSIDERED, Enzer (1960)
Whether the calculus produced a higher level of gingivitis was not
established.
only 11 % of the
examined tooth
surfaces had
supra and or
subgingival
calculus
concurrent with
gingivitis
plaque
associated with
gingivitis was
found at 75% of
the tooth
surfaces
23. • "Initial damage to the gingival margin is presumably due to
immunological (antigen) and/or enzymatic effects caused by the
microorganisms of the plaque. This process is enhanced by the
formation of supragingival dental calculus, which provides further
retention and thus promotes new plaque accurnulations.
• Plaque induced chronic inflammation eventually results in the
formation of periodontal pockets in which subgingival calculus is
deposited. The latter is a secondary phenomenon; it is not a cause of
pocket formation but a concomitant manifestation.
24. Schroeder (1969) pointed out that with subgingival calculus ,we may be
dealing with a dependent rather than an independent variable:
CALCULUS COULD BE THE RESULT RATHER THAN THE CAUSE OF
THE DISEASE.
26. •Examined 153 army recruits.
•High correlation between calculus and gingivitis.
•calculus could be the result rather than the cause since the inflammatory
exudate could contribute to the mineralization of the plaque.
AINAMO 1970
•Distribution pattern of supra,subgingival calculus,plaque and gingival
inflammation.
•Highest prevalence of gingival inflammation irt interdental papilla and
lowest with buccal margins.
•Coincided with highest prevalence of subgingival calculus on interprox
surface
•Distribution pattern of gingival index was much closer to plaque than to
calculus.
•PLAQUE had much closer relation with inflammation than calculus
ALEXANDER 1971
• Examined 300 subjects aged between 15-17 years.
• Supported findings of study by ALEXANDER 1971.
BUCKLEY 1980
27. • Effects of SRP and personal oral hygiene vs personal oral
hygiene alone on periodontal ST.
• SRP+PERSONAL ORAL HYGIENE showed significantly greater
improvement in periodontal health.
TAGGE ET AL 1975
• Effects of initial non surgical periodontal treatment on clinical
severity of periodontitis in pockets varying from 1-7mm.
• Significant reduction in gingival inflammation following calculus
removal.
MORRISON ET AL
1980
29. • Supragingival calculus starts forming with 6 years of age.
0-15yrs=37-70%
16-21yrs=44-88%
>40yrs=86-100%
• Subgingival calculus is least before 20 yrs of age.
>40yrs=47-100%
30. • The prevalence of both types of calculus was approximately 3% higher in boys
than girls.
• Approximately 8% of teeth had supragingival calculus only and 4% had
subgingival deposits.
• Maxillary incisors and bicuspids - least involved.
33. SUPRAGINGIVAL CALCULUS SUBGINGIVAL CALCULUS
Location Coronal to gingival margin Below the crest of marginal
gingiva.
Visibility Visible in the oral cavity Not visible. found by tactile
exploration with a explorer.
Color White or whitish yellow Dark brown or greenish black
Consistency Hard clay like Hard and flint like
Shape Amorphous bulky Thin, flattened
Attachment Easily detached from tooth Firmly attached
Source Main mineral source - saliva
(Salivary calculus)
Main mineral source – crevicular
fluid
(Serumal calculus)
34. SUPRAGINGIVAL CALCULUS SUBGINGIVAL CALCULUS
Composition •Mainly Brushite & OCP
•Salivary proteins : Present
•Mg whitlockite : Lesser
•Sodium content : Lesser
•Mainly Mg whitlockite
•Sodium content : Increases with
depth of pocket
•Brushite & OCP : Lesser
•Salivary proteins : Absent
Distribution •Most frequent sites
1)Lingual surfaces of the mand.
anteriors opposite Wharton’s duct
2)Buccal surfaces of the max.
molars opposite Stenson’s duct.
•Surfaces of dentures and dental
prosthesis.
•May be generalized or localized
on single teeth or a group of teeth.
•Related to pocket depth
•Proximal surfaces have heaviest
deposits, lightest deposits on facial
surfaces. (Lovdal et al.1958)
40. PRINCIPLE INORGANIC COMPONENTS
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)
40
Calcium
39 %
Phosphorous
19 %
Carbon dioxide
1.9 %
Magnesium
0.8 %
Na, Zn, Sr, Br, Cu,
Ag, Al, Fe, F
Traces
41. FLOURIDES IN CALCULUS
1. Concentration of flourides in calculus varies and is influenced by the
amount of flourides,received from fluoride in drinking water ,topical
application,dentrifices or any form that is received by contact with
external surface of calculus.
2. Flouride concentrations were highest in or near the outermost region
of calculus.
42. CRYSTALS
1. Atleast 2/3rd of the inorganic component is in the form of crystals.
(Leug&Jenson,1958)
2. Electron microscopy and x-ray diffraction studies showed 4 distinct phosphate
crystal forms:
Hydroxyapati
te
58%
Magnesium
Whitlockite
21%
Octacalciu
m
Phosphate
12%
Brushite
9%
97-100% bulk of
supragingival calculus.
Exterior layers – OCP
Inner layers of old calculus – HA
Posteriors and sublingually
Mandibular anterior region.
identified in recent calculus.
43. The long-thin-type and bone-like-type
(B) crystals can be observed in this
calcifying region.
45. SUBGINGIVAL CALCULUS
Composition similar to supragingival calculus with some differences:
1. More homogenous with equally high density of minerals.
2. Same HA content ,more Mg.
3. Less brushite and OCP.
4. Ratio of Ca:P is higher subgingivally.
5. Sodium content increases with depth of pocket.
6. Salivary protein found in supragingival calculus is not found in subgingival
calculus.
45
46. BACTERIAL CONTENT
1. The percentage of gram +ve and –ve filamentous organisms is greater within
calculus than in remainder of oral cavity.
2. The microorganisms at the periphery are predominantly gram –ve rods and cocci.
3. Most of the organisms within the calculus is nonviable.
Supragingival
calculus
Gram +ve
filaments
predominate
Gram –ve
filaments &
cocci
Subgingival
calculus
Superficial
layers- gram –
ve filaments
Deep &middle-
gram +ve
filaments
48. • Dental calculus develops when
nonmineralized biofilms, extremely rich in
oral bacteria, become mineralized with
calcium phosphate mineral salts.
• These mineralized biofilms form both
supragingivally and subgingivally.
Nonmineralized dental biofilm entraps
particles from the oral cavity, including large
amounts of oral bacteria, human proteins,
viruses and food remnants, and preserves
their DNA.
49. 1. Calculus is dental plaque which has undergone mineralization. basic steps:
1. Pellicle formation
2. Initial adhesion and attachment of bacteria
3. Colonization and Plaque Maturation
50. 1. PELLICLE FORMATION
Following tooth eruption or a dental prophylaxis, a thin saliva- derived layer, called the
acquired pellicle, covers the tooth surface.
ACQUIRED PELLICLE: It may be defined as a homogenous, membranous, acellular film
that covers the tooth surface and frequently form interface between the tooth ,the dental
plaque and calculus (SCHLUGER)
51. 2. INITIAL ADHESION AND ATTACHMENT
PHASE I - TRANSPORT TO TOOTH
SURFACE
PHASE II INITIAL ADHESION
PHASE III ATTACHMENT
52. 3. COLONIZATION AND PLAQUE MATURATION
When the firmly attached microorganisms start growing and the newly formed bacterial
clusters remain attached, microcolonies or a biofilm can develop.
Gram +ve coccoidal organisms are the first settlers to adhere to the pellicle and
subsequently filamentous bacteria gradually dominate the maturing plaque biofilm.
53. Soft plaque is hardened by precipitation of mineral
salts which usually starts between the first and the
fourteenth day of plaque formation. Calcification has
been reported to occur as soon as 4 to 8 hours.
Calcifying plaque may become 50% mineralized
within 2 days and 60% to 90% mineralized in 12
days
Early plaque contains a small amount of inorganic
materials which increases as a plaque develops into
calculus
54. 54
7th DAY : Coccoid bacteria is still present but
the surface and central portions contains
mass of filamentous organism
12th DAY : Plaque compose of entirely of
gram variable filamentous bacteria in a fairly
granular or amorphous ground substance
14th DAY : The starting time of calcification
area in different individuals and in different
teeth in same individual
55. 1. Calculus formation continues until it reaches a maximum from which it
maybe reduced in amount.
2. The time required to reach the maximum level has been reported as
10weeks,18 weeks and 6 months.
3. Sources Of Minerals
a. Supragingival calculus – saliva.
b. Subgingival calculus – the gingival sulcus fluid and inflammatory
exudates.
55
58. 1. Studies focusing on the various factors influencing calcification in heavy and
light calculus formers identified two major factors:
(i) a different biochemical composition of saliva between heavy and light
calculus formers during early plaque development; and
(ii) higher levels of calcium, three times higher levels of phosphorus and
lower levels of potassium in the saliva of heavy calculus formers than in the
saliva of light calculus formers.
58
59. On average, calculus formers deposit daily calculus in the range of 0.10–
0.15% dry weight.
The mineralization process of the biofilm appears to be complete in 12
days, but half of the mineralization occurs in the first 2 days . Following
mineralization, the roughened surface of the calculus provides an ideal
ground for the deposition of new biofilm.
61. 1. Attachment by means of the secondary
cuticle .
The dental cuticle is believed to be formed by
the epithelial attachment as it contacts the
cementum. It remains attached to the
cementum when this epithelium separates
from the root surface. It is then exposed to the
saliva and the microorganisms which make up
the calculus matrix. Apparently these
microorganisms can attach themselves to the
cuticle.Calculus can be easily removed
because of smooth attachment.
A—Cementum B—Cuticle C—Calculus
62. 2. Mechanical interlockng to the surface
irregularities.
The dental cuticle is often destroyed by
microorganisms in the mouth or by the
dentist in giving an oral prophylaxis. The
calculus matrix is then attached to the
minute spaces of the cementum which
correspond to the previous location of
Sharpey's fibers.
A—Cementum B—Calculus
63. 3. Attachment by penetration of
microorganisms making up the
calculus matrix into the
cementum.
These microorganisms may be found
in the outer part of the cementum and
may also have penetrated to various
depths.Calculus penetrates
completely into the cementum and is
called as the calculo cementum.
A—Cementum B — Calculus C—Dentin. Micro-
organisms of calculus matrix have penetrated through
cementum and along dentino-cemental junction.
64. 4. Attachment into areas of cementum
resorption.
Resorption of the cementum often
occurs with or without various degrees of
repair. In periodontal disease these
areas become exposed to the saliva by
pocket formation. They often present
undercuts, and when calculus forms
here a mechanical locking occurs.
A—Cementum B—Micro-organisms extending from
calculus matrix into cementum. C—Calculus D—Dentin
67. PRECIPITATION THEORY/
BOOSTER THEORY
1. In 1878, MAGITOT was of opinion that tartar consisted mainly of mineral
matter formed by the precipitation of earthy carbonates and phosphates from
saliva.
2. These mineral salts were united with organic matter, epithelial cells,fatty
globules and leukocytes.
68. BOOSTER CONCEPT =according to this concept mineral precipitation results from Local
rise in the degree of saturation of calcium and phosphate ions which maybe brought
about in several ways:
↑PH of
saliva
Supersaturation
of colloidal
proteins in
saliva
Enzymatic
mechanisms
of bacteria
CO2 theory and
Ammonia theory
69. ↑pH of saliva
Ammonia is a breakdown product of urea.
The abundant supply of urea from major salivary glands secretions tends to
increase pH in plaque.
The increase in pH of plaque is primarily due to proteolytic activity in plaque which
may result in formation of amines,urea and ammonia.
70. Supersaturation of colloidal proteins in saliva
Colloidal proteins in saliva have tendency to bind
with calcium and phosphate ions.
With stagnation of saliva, colloids settle out and
the supersaturated state is no longer maintained,
leading to precipitation of calcium phosphate
salts. (Prinz 1950)
70
71. 71
Phosphatase-liberated from dental plaque,
desquamated epithelial cells or bacteria
An important factor in the hydrolysis of organic
phosphates present in the saliva
To produce free phosphates that could be
precipitated as calcium salts in calculus.
Enzymatic mechanisms of bacteria
73. EPITACTIC CONCEPT/
HETEROGENOUS NUCLEATION
1. The term epitaxy 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.
2. Seeding agents provoke small foci of calcification enlarge and coalesce to
form the calcified mass.
73
74. Saliva
concentration of
Ca & P is not high
enough to
precipitate
promote the
growth of
hydroxyapatite
crystals
Tooth surface
has plaque
Contains
protein-carb
complex
Act as seeding
agents to
promote HA
crystals
formation
75. 75
HA crystals
bind to
protein-carb
complex on
plaque
Small foci of
calcification
Enlarge and
coalese
Form
calcified
mass
Calcification will be initiated by a carbohydrate-protein complex which removes calcium
from saliva by chelation process and binds with it to form nuclei that stimulates subsequent
deposition of minerals.
Possible Seeding agents include protein-carb complex of plaque and plaque bacteria.
76. 76
INHIBITION THEORY
• The sites where calcification occurs , the inhibitor is apparently altered or removed.
• Possible inhibiting substance- pyrophosphate in saliva & other polyphosphates.
• Among controlling mechanisms is the enzyme alkaline pyrophosphatase –
hydrolyze the pyrophosphate → phosphate (Russell and Fleisch 1970).
78. 78
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).
79. LOCAL RISE
in pH,Ca and
P
concentration
BRUSHITE
develop
spontaneously
During
maturation
It is modified
to crystals of
higher Ca:P
ratio
79
80. BACTERIOLOGICAL THEORY
• Oral microorganisms are the primary cause of calculus, and that they
are involved in its attachment to the tooth surface.
• Leptotrichia and Actinomyces have been considered most often as the
causative microorganism.
81. 81
ENZYMATIC THEORY
• 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.
82. 82
Esterase is an enzyme that is present in the cocci and filamentous organisms
leukocytes, macrophages, and desquamated epithelial cells of dental plaque.
hydrolysing
fatty esters
free fatty acids.
form soaps with
calcium and
magnesiun,
converted into
the less-
soluble
calcium
phosphate
salts.
Ppt on plaque
85. 1. Pyrophosphate
occurs naturally in saliva and plays a role in inhibiting calculus formation. These
molecules chelate calcium , slowing the rate of nucleation (crystal formation) and
calcification of plaque. The pyrophosphate binds to calcium in a growing crystal,
essentially slowing further crystal growth at that site and effectively decreasing
calculus build-up
86. 2. Salivary proteins
Statherin, the acidic PRPs, cystatins, and histatins, are primarily responsible for the
maintenance of the homeostasis of the supersaturated state of saliva with respect to
calcium phosphate salts.
Statherin is a very potent inhibitor of crystal growth in comparison with other salivary
proteins as it has been shown to exhibit unusually high affinities for hydroxyapatite.
Statherin inhibits both nucleation and growth of hydroxyapatite crystal and its
concentration.
88. 88
Urea source – saliva, bacteria in plaque and extraoral factors.
Sites with high velocity - increased urea dependent response.
This explains site specificity of calculus
89. 89
FLUORIDE AND CALCULUS FORMATION
The caries-inhibiting ability of fluoride is well-known.
Fluorides also have been shown to have anti-bacterial action
and to inhibit the acid production by the bacteria.
Thus, fluorides may have the potential to increase the plaque
pH, which may contribute to increased calculus formation.
90. 90
SILICON
Silicon is found in drinking water and food, commonly in the form of silicic acid and
silica.
Silica and silicic acids have the calcium-binding capacity and they stimulate
calcium phosphate precipitation.
Garre et al.1989 - rate of calculus formation was found to be more in Indonesian
population – accounted for consumption of larger amount of rice, which is enriched
in silicon.
94. 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.
– Using transillumination, a dark, opaque, shadow like
area seen on a proximal tooth surface may be
subgingival calculus. Without calculus, stain, or thick
soft deposit, the enamel is translucent.
95. Gingival Tissue Color Change
• Dark calculus may reflect through a thin margin and suggest the presence of
subgingival calculus.
96. Tactile Examination
– 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.
rough
subgingival
tooth surface
97. APPEARANCE ON RADIOGRAPHS
• Highly calcified interproximal calculus deposits –
detectable as radioopaque projections into the
interdental space. The apical location of plaque is
not sufficiently calcified to be visible on
radiograph, so the calculus location does not
indicate bottom of periodontal pocket. Hence,
conventional oral radiography was a poor
diagnostic method for the detection of calculus
(Buchanan et al,1987)
98. 98
ADVANCE DIAGNOSTIC AIDS
Calculus Detection Systems Only
PERIOSCOPE–Fiberoptic endoscopy-based technology
DETECTAR–Spectro-optical technology
DIAGNODENT–Auto fluorescence-based technology
Calculus Detection + Removal Systems
PERIOSCAN–Ultrasound technology
KEYLASER–Laser-based technology
99. PERIOSCOPE
• Dental endoscope in deep pockets and furcations
can show calculus otherwise undetectable,
especially burnished calculus.
• Minimally invasive approach that was introduced in
the year 2000.
• When inserted into periodontal pocket - images
subgingival root surface, tooth surface and calculus.
• Fiberoptic system permits visualization of the
subgingival root surface, toothstructure and calculus
in real time on a display monitor.
101. DetecTar™/ OPTICAL SPECTROMETRY
• DetecTar™( Dentsply professional,USA) -
light emitting diode and fiber-optic
technologies.
• The device contains a diode which emits a
light that travels up to the tip of the probe.
When calculus is detected, the optical fiber
reflects light.
• A microprocessor analyses the reading and
instantly emits an audible signal (beep) to
notify the clinician the presence of calculus.
102. • Kasaj et al 2008 - optical fiber in the device recognizes the characteristic spectral
signals of calculus caused by absorption, reflection and diffraction of red light.
• Advantages:
• Portability
• Audible and luminous signals
103. Diagnodent™
• Diagnodent™ involves use of an InGaAsP based
red laser diode which emits a wavelength of
655nm through an optical fibre causing
fluorescence of tooth surface and calculus.
• Calculus contains various non-metals and metals,
such as porphyrins and chromatophores which
make it able to emit fluorescent light when
irradiated with a light of certain wavelength.
• Diagnodent is a commercially available calculus
detection device (Meissner and Kocher, 2011).
104. PERIOSCAN
• 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.
105. WORKING PRINCIPLE OF PERIOSCAN
– Perioscan™ is an ultrasonic device that works on
acoustic principles.
– Tip of the ultrasonic insert is oscillating
continuously.
– 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.
106. KEYLASER 3
• Keylaser3™ combines a 655nm InGaAsP diode for detection
of calculus and a 2940nm Er: YAG laser for treatment.
• A scale of 0-99 is used for detection of calculus.Values
exceeding 40 indicate definite presence of mineralized
deposits.
• 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.
• Cost factor can be a limiting aspect for using lasers for
detection and treatment
108. • Simplified calculus index (Green & Vermillion ’64 ).
• Calculus component of periodontal disease index (Ramfjord 1959 ).
• Calculus surface severity index (Ennever J et al ’61).
• Marginal line calculus index (Muhleman & Villa ’67).
• Volpe- Manhold index (Volpe A R & Manhold J H ’62)
109. SIMPLIFIED ORAL HYGIENE INDEX (OHI-S)
– 1964 John C Greene & Jack R vermillion.
– INSTRUMENTS: Mouth mirror,no:23 explorer
– CI-S = Total score / No : of surfaces examined
110.
111. • CALCULUS COMPONENT OF PERIODONTAL DISEASE INDEX (PDI)
– Developed by RAMFJORD IN 1959.
– Calculus component – assess the presence and extent of calculus on the facial and
lingual surfaces of the six index teeth.
– Instruments – MOUTH MIRROR, DENTAL EXPLORER
– Calculation – No of teeth examined/ total teeth.
SCORE CRITERIA
0 No calculus
1 Supragingival calculus extending only slightly below the free
gingival margin (not more than 1mm)
2 Moderate amount of supragingival and subgingival calculus or
subgingical calculus alone
3 An abundance of supragingival and subgingival calculus
112. CALCULUS SURFACE SEVERITY INDEX (CSSI)
• Assesses the presence or absence of calculus on the four surfaces of the four
mandibular incisors.
• Each surface is given a score of 1 for the presence of calculus or 0 for the absence of
calculus.
• Maximum score for each subject is 16.
• In applying the scoring method, calculus was considered to be present in any amount,
supragingival or subgingival, and it could be detected either visually or by touch. If the
examiner was uncertain about the presence of calculus on a given surface, the surface
was called calculus free.
113. MARGINAL LINE CALCULUS INDEX (MLCI)
• Muhlemann H.R. and Villa P in 1967.
• Frequently used in short-term clinical trials (i.e less than 6 weeks) of anticalculus
agents.
• This index was developed to assess the accumulation of supra gingival calculus on the
gingival third of the tooth or along the margin of the gingiva .
114. • Method :
– The examination is done on the four mandibular incisors using a mouth mirror,
after drying the tooth surfaces with air.
– MLCI score per person is determined by totaling the scores per tooth and dividing
by the number of teeth examined.
Code
0
1
2
3
Criteria
No calculus present
Calculus observable, but less than 0.5 mm in width and / or thickness
Calculus not exceeding 1.0mm in width and / or thickness.
Calculus exceeding 1.0 mm in width and / or thickness.
115. VOLPE-MANHOLD INDEX
• Developed by Volpe A.R. and Manhold J.H. in 1962.
• Calculus formation in vivo is performed using a colored periodontal probe placed
against the lingual surface of the anterior tooth that will be scored with the probe and
placed at the most inferior border of any calculus present. The different colors at the
probe end represent units, and the amount of calculus present can be measured:
• The calculus is measured in increments of 0.5mm,from 0 to 5.0 mm from the inferior
border of the visible calculus.
117. • 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.
• Pockets harboring undetectable subgingival calculus deposits appeared to have a
significantly greater percentage of coccoid forms and fewer motile rods and total
motile morphotypes (Brown et al., 1991).
118. • Periopathogens, such as Aggregatibacter actinomycetemcomitans,
Porphyromonas gingivalis, and Treponema denticola have been
found within the lacunae of both supra- and subgingival calculus.
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.
118
119. 119
Gram staining of bacteria
showing Gram positive cocci and
bacilli
Dark field microscopic imaging
showing presence of rods and
cocci
Acridine orange staining showing
apple green colored appearance
of bacteria
121. • Before 1960 the belief was that calculus was the principal etiologic factor in periodontal
disease.
• Current view is that the initial damage to the gingival margin in the periodontal disease is
due to the pathogenic effect of microorganisms in plaque.
• Effect could get more pronounced by calculus accumulation because it further provides
retention of more plaque microorganisms.
• Although strong associations between calculus deposits and periodontitis have been
demonstrated in experimental (Waerhaug 1952, 1955) and epidemiologic studies (Lovdal
et al 1958), it has to be realized that calculus is always covered by an unmineralized layer
of viable bacterial plaque.
• Others produced findings suggesting bone loss and attachment loss were not directly
associated with subgingival calculus.
122. ROLE OF CALCULUS IN PERIODONTAL DISEASE SUMMARIZED AS
Rough surface
act as a niche
which harbor
bacterial plaque
Provides fixed
nidus for plaque
accumulation.
Brings plaque
bacteria close to
supporting
tissues
Act as irritant to
periodontal
tissues
Distends
periodontal
pocket wall
Inhibit ingress of
PMNLs
Interferes with
local self
cleansing
mechanisms.
Reservoir for
substances like
endotoxins,
antigenic
materials
Makes plaque
removal more
difficult to the
patient
124. A number of studies have been reported on the inhibition of calculus at some
stage in its formation. A review of these studies now will follow a classification that
consists of four types of agents:
1. agents that alter the character of the surface of enamel;
2. agents that attempt to reduce the formation of plaque or inhibit its
mineralization such as antimicrobial compounds and agents with detergent
qualities;
3. enzymes that interfere with the deposition of plaque by depolymerization of its
matrix;
4. agents that dissolve the mineral of calculus, or chelate its metallic elements.
125. • The approach of choice in most of the current anti-tartar products include
inhibiting crystal growth and thus preventing development of mineralized
plaque.
125
128. • CHELATING AGENTS
– Chelating agents are used to dissolve crystallized calcium salts and are capable of combining with
calcium to form stable compounds.
– 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.
129. • EDTA
– Jabro et al. (1992) found that application of EDTA gel 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.
130. • ACIDS
– Earliest techniques - wooden stick + aromatic sulphuric acid & introduced into a
periodontal pocket to dissolve calculus (Barker 1872).
– Niles (1881) - the nitro muriatic acidsuperior dissolving action on calculus.
– Other acids included - 20% trichloroacetic acid, bifluoride of mercury and 10%
sulphuric acid.
– Disadvantages:
- Caustic to soft tissues
- Decalcify tooth structure. (Stones (1939) and grossman (1954) so their use
was discontinued
131. • ENZYMES
– Mode of action
– To break down plaque matrix OR
– To affect the binding of the calculus to the tooth.
– The first enzyme to be tested- mucinase.
– The theoretical mechanism of action was to break down the mucins (Hodge & Leung
1950) which were to bind calculus to the tooth. 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).
132. • UREA
– The anticalculus effect - ability to dissolve the muco-proteinaceous material within which
the calcium salts are deposited and/or by increasing the solubility of calcium salts in
saliva.
– 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.
– 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.
– In research, the concept of inhibiting urease activity, Ethane hydroxy diphosphonate
(EHDP) or aceto hydroxamic acid (AHA) were tested for their anti calculus potential
133. • NIDDAMYCIN
Niddamycin is a macrolide antibiotic with 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.
135. 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.
4.Pyrophosphate inhibits calculus formation by inhibiting calcium phosphate
deposition in plaque.
Lower concentrations of pyrophosphate were noted in the parotid saliva of
calculus formers than in saliva of non-formers (Vogel & Amdur 1967).
136. – 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 - 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.
137. • ZINC IONS
– Reduce plaque acidogenicity (Opperman 1980) & inhibit its formation.
– It inhibits crystal growth by binding to the surface of solid Ca P (Gilbert 1988).
– Zinc competes with calcium for bacterial binding sites.
– Inhibit both the adsorption of bacteria to the tooth surface and growth of existing
plaque. (Saxton 1986)
138. • TRICLOSAN
– Triclosan a non-ionic antibacterial agent with a wide spectrum of activity against
bacteria(gram positive and gram negative) fungi and yeasts.
– When delivered from a dentifrice- seems to bind to oral mucous membranes and tooth
surfaces, significantly reduce the rate of formation of supragingival calculus.
– Anti-bacterial activity is time dependent and it should stay in the oral cavity for a sufficient
time to exert its anti-bacterial action.
– Delivery system – PVM/MA copolymer – retention in plaque and saliva
139. • 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.
140. • ANTI-CALCULUS (TARTAR CONTROL) DENTIFRICES
– Dentifrices containing anti-calculus agents reduce the formation of calculus but do not
reduce the levels of preexisting calculus.
– Anti-calculus agents, marketed as anti-tartar ingredients, include tetra-potassium and
tetrasodium pyrophosphates, sodium hexametaphosphate, and zinc.
– Zinc compounds used as anti-tartar agents include zinc citrate trihydrate and work by
inhibiting crystal growth and controlling bacterial growth.
142. • While the bacterial plaque that coats the teeth is the chief causative factor in the
initiation and progression of periodontal disease, the removal of subgingival plaque
and calculus constitutes the foundation stone of periodontal therapy.
• Calculus plays a key role in maintaining and accentuating periodontal disease by
withholding the plaque in close contact with the tooth surface and gingival tissue,
leading to various pathological changes thereby creating areas where plaque
removal is impossible.
Therefore, adequate skill of the clinician is essential to remove the calculus and other
irritants, which forms the basis for adequate periodontal and prophylactic therapy
odontiasis. : cutting of the teeth
Odontolithiassis- odonto means tooth and lithiasis means stony concretions(calculus)
Calcis, in Greek, was a term used for various kinds of stones, coming from the term for limestone. This spun off many modern words, including "calculate" (use stones for mathematical purposes), and "calculus", which came to be used, in the 18th century, for accidental or incidental mineral buildups in human and animal bodies, like kidney stones and minerals on teeth.
Tartar, on the other hand, originates in Greek as well, but as the term for the white encrustation inside casks, aka potassium bitartrate commonly known ascream of tartar. This came to be a term used for calcium phosphate on teeth in the early 19th century."
HIPPO-noted deleterious effects of calculus n gum..called calculus as pituita
ALBUCASIS-ARABIAN PHYSICIIAN.HE emphasized on need for removal of these deposits around the teth.designed setoff scaling instrumnts for rem calculs.
PARACELSUS -stony concretions that forms in humans,noting their physical comparability to the deposits that develop at bottom of wine casks.
He also observed that these could be found not just around the teeth, but also in urinary bladder,gall bladder etc.
Termed tartaric diseases.
PIERRE FAUCHARD=refered slime layer as substance which accumulates on teth surf which when left untreated
growing literature on the impact of antibiotics on plaque and periodontal disease (Mitchell & Holmes 1965),
critically analyzed over 600 works on the epidemiology, physiology and clinical significance of calculus ; its dis - tribution, chemistry, histochemistry, electron micro - scopic appearance, crystal formation and X-ra y diffraction analysis. Schroeder synthesizes a concept of calculus from these works , pointing out facts and theories a nd setting forth questions which remain to be a n - swered.
the manifest subgingival dental calculus in turn favors and promotes the chronicity of the inflammation and thus contributes towards making it progressively worse," Although calculus is no l
Various epidemiologic studies have been done to find out supra n subgin distributionof it calculus nd its correlation with associated perio status. calculus could be
the result rather than the cause since the
inflammatory exudate could contribute
to the mineralization of the plaque.
Alexander noted, however that the number of individual papillae and margins that were infiammed was substantially higher than the number of surfaces with subgingival calculus. In general there was a much closer match in distribution patterns for gingival index and plaque than for gingival index and subgingival calculus.
TO EVALUATE EFFECTS OF CALCULUS REMOVAL ON PERIOD HEALTH
Early plaque of heavy calculus former - more calcium, three times more phosphorous and less potassium than that of noncalculus former
Total protein and total lipid levels - elevated in Heavy calculus formers.
Light calculus formers - higher levels of parotid pyrophosphate.
ACCORDING TO SOURCE OF MINERALIZATION (Jenkins, Stewart 1966)
ACCORDING TO INITIATION AND RATE OF ACCUMULATION (Muhler and Ennever 1962)
ACCORDING TO SURFACE (Melz, 1950)
Inorganic salts;
Dental enamel contains 96%
Dentin contains 65%, and
Cementum and bone contain 45% to 67%.
Mature calculus has approximately 75% to 85%
MIXTURE OF PROTEIN POLYSACHARIDE COMPONENTS ,DESQUAMTD EPI CELLS,LEUKOCYTES AND VARIOUS TYPES OF MICROORGNSM
In plaq==5-10 mg/kg of wet wt
Appearance of crystals (Kodaka et al 1988)
OCP – platelet like crystals
HA - Sandgrain or rod like crystals
W – hexagonal (cuboidal, rhomboidal) crystals
Calculus is dental plaque which has undergone mineralization.
All surfaces of the oral cavity are coated with a pellicle. Following tooth eruption or a dental prophylaxis, a thin saliva- derived layer, called the acquired pellicle, covers the tooth surface.
Transport to the surface – involves the initial transport of the bacterium to the tooth surface.
Initial adhesion – reversible adhesion of the bacterium, initiated by the interaction between the bacterium and the surface , through long-range and short-range forces
Attachment – a firm anchorage between bacterium and surface will be established by specific interactions.
Gram- positive coccoidal organisms are the first settlers to adhere to the formed enamel pellicle, and subsequently, filamentous bacteria gradually dominate the maturing plaque biofilm (Scheie,1994)
Transport to the surface – involves the initial transport of the bacterium to the tooth surface.
Initial adhesion – reversible adhesion of the bacterium, initiated by the interaction between the bacterium and the surface , through long-range and short-range forces
Attachment – a firm anchorage between bacterium and surface will be established by specific interactions.
Gram- positive coccoidal organisms are the first settlers to adhere to the formed enamel pellicle, and subsequently, filamentous bacteria gradually dominate the maturing plaque biofilm (Scheie,1994)
All plaque does not necessarily undergo calcification.
As calcification progressess Number of filamentous bacteria increases.
Reversal phenomenon
The rate of calculus formation and the amount of calculus formed depends on multiple factors, including diet, especially alkaline foods (15, 17) and sugars (39), genetic variations in the salivary content (29) and other factors, such as age, race, gender, presence of disease and the bacterial load of the subject (29, 58)
Diet and nutrition –depends more upon its consistency than upon its content.
*Increased calculus formation - increase in dietary calcium, phosphorus, bicarbonate, protein and carbohydrate.
Age – there is an increase in calculus deposition with an increasing age.(Schroeder et al,1969).
Habits – In populations that practice regular oral hygiene and with access to regular professional care have low tendency for calculus formation.
Anerud et al 1983 study comparing the prevalence of calculus in adult males, aged 19-30 years, was undertaken in the United States, Norway and Sri Lanka. Lowest Norwegians.
Four modes of attachment of the organic calculus matrix to the root surface were observed.
It is readily understandable that if the calculus is locked i n an undercut resorption area of the cementum (Figure 5), its removal would be extremely difficult or even impossible without removal of some of the cementum. Dislodgment with a scaler would probably result in breaking off the calculus from the outside of the cementum leaving the anchored part. This would make reattachment of the soft tissue impossible and calculus will again develop and continue to be an irritant to the adjacent gingival tissues. Therefore curettage, as it is understood by the periodontist, wit h its implication of cementum removal is' a "must" in this case. O n the other hand, if th
Calculo cementum - Calculus embedded deeply in cementum may appear morphologically similar to cementum
Cal gets attch to the microdpressions without actually aletering the cm surf
Some mchanismsin the ora; cavity that will boost the process of pptn of mineralas n cal formtn
SALIVARY PH THEORY=HODGE AND LEUNG 1950
A rise in pH of saliva causes precipitation of CaP salts by lowering the precipitation constant.
Major sg produce saliva with coz tension of 54-65mmh and atm coz tension is only 0.3.as a result of this disparity coz from saliva is relaeased into the atm.by this saliva in mouth bcm alkaline due to increased ph.and there is dissolution of phosphoric acids into phosphate ions which will act as a booster by further increasing the alkalinity and cause pptn of ca and p ions on teeth.
This explains formtn of copious amntnof cal near salivary dland.
But this cdnt explain why subgingv formtn where gcf is the mmajor source.
Phosphatase liberated from dental plaque, desquamated epithelial cells, or bacteria precipitate calcium phosphate by hydrolysing organic phosphates in saliva, thus increasing the concentration of free phosphate ions.
By breakdown of amino acids
Leftover aa prodce ammonia
Icres ph
This is heterogenous nucleation process bcz tr is inv of different compunds like HA,Ca p,proteuns n carbs comple
Pla bacter
Explains why there in non uniformity of calc in different sites of oral cavity.
Areas of calc form inb agents are either reomv or altered.
P.intermedia and fusobact produce ammonia..which increase ph nd alkalinity ‘’
Not accepted cz cal form is seen evne in germ free organisms
Mg and disphosphtns will block apatute crystalliztn and stabilize CAP as amorphous mat.not used clinically
POISON GROWTH CENTRES
It is a multifunctional peptide that possesses a high affinity for calcium phosphate minerals, maintains the appropriate mineral solution dynamics of enamel, promotes selective initial bacterial colonization of enamel, and functions as a boundary lubricant on the enamel surface.
It is the only salivary protein that inhibits the spontaneous precipitation of calcium phosphate salts from the supersaturated saliva. It inhibits primary as well as secondary precipitation of calcium phosphate salts [2]. In addition, statherin may function in the transport of calcium and phosphate during secretion of salivary glands. Statherin concentration is not subject to circadian rhythms unlike other salivary peptides [3]. Besides that, statherin promotes bacterial adhesion to enamel surfaces, although weakly compared with other salivary macromolecules [4], and acts as a boundary lubricant at the enamel interface [5].
UREA
Product from the metabolism of nitrogen-containing substances.
Secreted in normal saliva 5 and 10 mmol/L, but can be as high as 30 mmol/L in patients with renal disease.
Gingival crevicular fluid contains up to 60mmol/L urea.(Golub et al 1971).
At a neutral pH, urea is hydrolyzed by urease to NH4+ and bicarbonate
BACTERIA RESPONSIBLE FOR THE UREOLYSIS IN DENTAL PLAQUE
Sissons et al (1988) - the ureolytic fraction of the flora detected on urea-agar plates.
The plaque bacteria giving strong ureolytic reactions were all Gram-positive cocci streptococci only.
Bacteria suspected to have a role in ureolysis - Salivarius, Actinomyces, Haemophillus, Enterobacteriaceae.
Sissons et al 1989- S. salivarius major contributor to ureolysis, though it’s a minor component.
Visual-gentle air blast,transillumntn
Tactile examination- Clerehugh 1996 used WHO # 621
probe and a fine subgingival explorer is also used.
While probing for sulcus/pocket, a can be felt if calculus is present
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.
indium gallium arsenide phosphate (InGaAsP)
Due to their differences in composition, calculus and teeth fluoresce at different wavelength ranges.
Tooth 477 -497 nm
Calculus 628-685 nm
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 bluelight when calculus is present.
Erbium dopped Yttrium Aluminium Garnet
Keylaser 1 and 2 can be used for removal of calculus only.
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.
GOOD 0.0 – 0.6
FAIR 0.7 – 1.8
POOR 1.9 – 3.0
16,21,24,36,41,44
Uses :
In clinical trials
In assessing patient progress
For patient motivation
To obtain the VMI scores, the three tooth planes,the mesial ,distal and gingival on the lingual surface of the lower 6 anterior teeth are examined.
The calculus is measured in increments of 0.5mm,from 0 to 5.0 mm from the inferior border of the visible calculus.
Study by moolya et al to study viablitiy of mo.
Found out that Bacteria reside within channels and lacunae in contrast to earlier studies, which stated that micro-organisms are killed once plaque calcifies to form calculus. Viable bacteria were found within calculus.
Even thg calculus by itself does not induce inflammation due to these reasons it can be considered as a significatr factor in progression of perio disease.
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. 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
Results demonstrated a significant reduction in calculus formation in both the EHDP and AHA groups.
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.
To inhibit crystal growth effectively, the concentration of pyrophosphate has to reach a critical level.
Zinc is added to toothpaste & mouthrinses – as an antibacterial agent to control plaque, reduce malodor and reduce calculus formation
Good oral substantivity.
5-chloro 2(2,4 dichlorophenoxy) phenol / 2,4,4-trichloro-2-hydroxydiphenyl ether
Bacteriostatic activity – prevention of amino acid uptake by the bacteria
Bactericidal activity – disruption of the integrity of cytoplasmic membrane – leakage of cellular contents
