2. CONTENTS
o Introduction
o Definition
o History
o Classification
o Prevalence
o Composition
o Structure
o Mode of attachment
o Formation
o Theories of mineralization
o Etiological significance
o Anticalculus agents
o Conclusion
o References
2
3. INTRODUCTION
The primary cause of gingival inflammation is
bacterial plaque, along with other predisposing
factors. These predisposing factors include calculus,
faulty restorations, complications associated with
orthodontic therapy, self-inflicted injuries, use of
tobacco, and others.
3
4. For the periodontal diseases:
The primary etiologic factor is dental plaque.
The associated factor: is the dental calculus,
it helps in new formation of the plaque.
The modifying factor: a systemic disease,
it aggravates the disease when the plaque is presents.
4
5. CALCULUS
“Calculus consists of mineralized bacterial plaque that
forms on the surfaces of natural teeth and dental
prostheses.”…. Carranza
“A hard deposit attached to the teeth usually consisting of
mineralized bacterial plaque [AAP 1992]”
“Mineralized dental plaque that is permeated with crystals
of various calcium phosphates [Schroeder,1969]”
5
6. Calculus formation has been reported to occur in germ-free
animals as a result of calcification of salivary proteins
Is a mineralized dental plaque that occurs in the tooth
surfaces & dental prosthesis, it has many forms:
1.Bridging over the gingival margin.
2.Follow the festooning shape of the dentition.
3.Lobular form.
4.In case of malalignment :protected area for the plaque
calculus
6
7. HISTORY
Hippocrates (460 – 337 BC)
association of oral deposits and disease
pituita (calculus)
Albucasis (936 – 1013 AD)
Arabian physician and surgeon
Explained relationship between calculus and
disease
a need for thorough removal of deposits
7
8. Paracelsus (1535)
Swiss German physician and alchemist
Introduced term tartar as a designation for a
variety of stony concretions that form in humans
Tartaric disease
8
9. CLASSIFICATION
According to location
supragingival calculus
subgingival calculus
According to source of mineralization
salivary calculus
seruminal calculus (Jenkins, Stewart 1966)
According to surface
exogeneous
endogeneous (Melz 1950)
9
11. Supragingival calculus
11
Location -The tightly adherent calcified deposits that form on
the clinical crowns of the teeth above the free gingival
margin.(visible in oral cavity)
Color -usually white-yellow in colour but can darken with age and
exposure to tobacco
Texture and consistency –hard clay like consistency.
Easily detachable from tooth surface
Salivary secretions are the main source of mineral salts.
12. Prevalence
Schroeder et al in 1969 in a review of world data
noted that
Supragingival calculus is more prevalent than
subgingival calculus.
Both types have been found from early childhood.
The percentage of people with both types rises
from 8th to 40th years
40% - 95% in the 20 – 30 year age group
80% - 100% in the over 30 years.
No reports of sex difference in prevalence /
intensity has been reported; but some geographic
variation has been noted.
12
13. A Longitudinal study was done by Anerud and coworkers
(1991) among Srilankan tea laborers and Norwegian
academicians for 15 years and all periodontal parameters
recorded.
Undisturbed by active professional intervention or home
care between 1970 and 1985 in sri lanka,
Or when removed at regular intervals between 1969 and
1988 in norway.
1. Srilankan tea laborers
Had no oral hygiene / dental care
Supragingival calculus formation started early in life soon
after tooth eruption
First areas to show calculus deposits were facial aspects of
maxillary molars and lingual aspects of mandibular incisors
Calculus continued to accumulate with age, reaching a
maximum at 25 – 30 years.
Anerud A, Löe H, Boysen H: The natural history and clinical course of calculus formation in man, J Clin Periodontol 18:160, 1991.
13
14. By age 45, few teeth were without calculus.
By age 30 all surfaces of all teeth had
subgingival calculus without any pattern of
predilection.
2. Norwegian academicians
Had good oral hygiene and frequent visits
for dental care throughout their lives.
So there was less accumulation of calculus
However supragingival calculus still formed
on facial surfaces of upper molars and
lingual surface of lower incisors in 80% of
teenagers.
It did not extend to other teeth and did not
increase with age.
14
15. COMPOSITION OF CALCULUS…..
INORGANIC COMPOUND
(70% TO 90%)
ORGANIC COMPOUND
75.9% -Ca3(PO4) 2
3.1% - CaC03
Traces of Mg3(PO4)2
Ca-39%, Ph- 19% , CO2- 1.9%
Other metals-
Na,Zn,Br,Cu,Ag,Mn,Al,Si,Fe,
strontium,tungsten,fluorine.
•Protein-polysaccharide complexes
• desquamated epithelial cells
• leukocytes, and
•various types of microorganisms
•1.9% - 9.1% carbohydrate---galactose, glucose,
rhamnose, mannose, glucuronic acid,
galactosamine, and sometimes arabinose,
galacturonic acid, and glucosamine.
•5.9% to 8.2% Salivary proteins
•0.2% Lipids neutral fats, free fatty acids,
cholesterol, cholesterol esters,
and phospholipids
15
16. 2/3rd of the inorganic component is crystalline in
structure…..four main crystal forms are
97% to 100% of all
supragingival
calculus
Hydroxy
apatite
58%
Octa-
calcium
12%
Common in
mand-ant
region
Brushite
9%
Magnesium
whitlockite
21%
Common
in
posterior
areas
16
17. The percentage of inorganic constituents in calculus is
similar to that in other calcified tissues of the body.
New and old calculus consists of four different crystals of
calcium phosphate (Schroeder 1969):
17
Hydroxyapatite (HA) Ca5(PO4)3 × OH 58%
Magnesium whitlockite (W) β-Ca3(PO4)2 21%
Octacalcium phosphate (OCP) Ca4H (PO4)3 × 2H2O 12%
Brushite (B) CaH (PO4) × 2H2O 9%
18. The predominant mineral in exterior layers is
Octacalciumphosphate, while Hydroxyapatitie is dominant
in inner layers of old calculus.
Whitelockite is only found in small proportions.
Brushite in recent calculus, not older than 2 weeks, form
the basis for supragingival calculus formation.
The appearance of the crystals is characteristic
18
Octacalciumphosphate Platelet-like crystals
Hydroxyapatite Sand grain or rod-like crystals
Whitelockite Hexagonal (cuboidal, rhomboidal)
crystals
19. Between 1.9% and 9.1% of the organic component is
carbohydrate which consists of
Galactose
Glucose
Rhamnose
Mannose
Glucuronic acid
Galactosamine,
sometimes arabinose, galacturonic acid, and glucosamine.
All these organic components are present in salivary
glycoprotein,
exception of arabinose and rhamnose.
19
20. Salivary proteins account for 5.9% to 8.2% of the organic
component of calculus and include most amino acids.
Lipids account for 0.2% of the organic content in the
form of
Neutral fats
Free fatty acids
Cholesterol
Cholesterol esters
Phospholipids
20
21. Light microscopy
The interface with the tooth surface was fairly smooth
and slightly curved following the shape of the tooth
whereas the external mineralized surface was
generally irregular and covered by a non-mineralized
plaque layer of variable thickness.
It contains many non-mineralized lacunae and, in
some sections, the lacunae formed a continuous
connection with the external bacterial plaque, and
extended to the calculus/tooth interface
21
22. Transmission Electron Microscopy
The ultra structure of young and mature supragingival calculus was
similar. The mineralized intermicrobial areas of the body of the
calculus contained predominantly small, randomly orientated needle-
shaped/platelet-shaped crystals. Areas containing crystals of larger
columnar and roof-tile shapes were also observed
22
23. scanning electron microscopy
Supragingival calculus always appeared in one piece with a
relatively smooth surface.
Under low magnification the Supragingival calculus was thin at
the incisal/occlusal part and thickened apically.
Under high magnification the Supragingival calculus is covered
with dense layer of filament .These filaments were 1micron thick
with an estimated length of 25 to 100 microns.
Fracture surface of Supragingival calculus generally had a
smooth, crystalline appearance.
23
25. Subgingival calculus
25
Location-below the crest of marginal gingival (not visible on
routine examination)
Color-dark brown or greenish black
Texture and consistency-hard and dense crusty, spiny or
nodular deposites
Firmly attached to tooth surface.
Crevicular fluid and inflammatory exudates are the main source
of mineral salts.
Found on any root surfaces with a periodontal pocket.
26. Subgingival calculus –
Same hydroxyapatite content,
More magnesium whitlockite
Less brushite and octacalcium phosphate.
The ratio of calcium to phosphate is higher
Sodium content increases with the depth of periodontal
pockets.
Salivary proteins present are not found subgingivally.
On average the density is 58% and ranges from 32% to
78%. Maximal values of 60–80% have been found.
26
27. Light microscopy
The calculus surface previously in contact with the
tooth was usually flat and mineralized while the
external/oral surface was fairly regular and covered
by a non-mineralized plaque layer of variable
thickness.
27
28. Transmission Electron Microscopy
The calcification within the body of subgingival calculus was
more homogeneous than supragingival calculus and consisted of
small randomly orientated needle- and platelet-shaped crystals.
There were also areas with flat "bulk-shaped" crystals,
Sundberg & Friskopp (1985)
28
29. Scanning electron microscopy
Subgingival calculus usually appeared in band like clusters of
deposits with varying sizes and rough surfaces.
under low magnification it has complex appearance. There are
clusters of small deposits in the incisal/ occlusal part and larger
deposits that tend to fuse in apical part.
High magnification revealed that 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
29
30. ATTACHMENT TO THE TOOTH SURFACE
Four modes of attachment have been described
(Zander,1953)
1. Attachment by means of an organic pellicle
30
32. 3. Close adaptation of calculus undersurface
depressions to the gently sloping mounds of
the unaltered cementum surface
32
33. 4. Penetration of calculus bacteria into cementum
Calculus embedded deeply in cementum may appear
morphologically similar to cementum and thus has
been termed calculocementum.
33
34. FORMATION OF CALCULUS
Precipitation of mineral salts starts between 1st and 14th days of
plaque formation.
Calcification starts --4 to 8 hours
…….Tibbetts L, Kashiwa H. J Dent Res 1970
50 % mineralized in 2 days
60% to 90% mineralized in 12 days
……Sharawy a, Sabharwal K. et al J Periodontol 1966
All plaque does not necessarily undergo calcification.
Microorganisms are not always essential in calculus formation
because calculus occurs readily in germ-free rodents……Gustafsson B,
Krasse B . Acta Odontol Scand 1962
34
35. Saliva is the source of mineralization for supragingival calculus.
GCF furnishes the minerals for subgingival calculus.
Plaque has the ability to concentrate calcium at 2 to 20 times its
level in saliva .
Early plaque of heavy calculus formers contains more calcium, 3-
times more phosphorus, and less potassium than that of non-
calculus formers. phosphorus may be more critical than calcium
in plaque mineralization
35
36. Calcification entails the binding of
Calcium ions + Carbohydrate protein complexes
Calcium phosphate salts.
Calcification begins along the inner surface of the
supragingival plaque and in the attached component of
subgingival plaque adjacent to the tooth.
Crystals form initially in the intercellular matrix and on
the bacterial surfaces and finally within the bacteria
36
37. Separate foci of calcification increase in size and
coalesce to form solid masses of calculus
37
38. The initiation of calcification and the rate of calculus
accumulation vary from person to person, for different
teeth, and at different times in the same person.
On the basis of these differences, persons may be
classified as heavy, moderate, or slight calculus formers
or as noncalculus formers. The average daily increment
in calculus formers is from 0.10% to 0.15% of dry
weight.
Turesky S, Renstrup G, Glickman I. J
Periodontol 1962.
38
39. Calculus formation continues until it reaches a maximum,
after which it may be reduced in amount.
The time required to reach the maximal level has been
reported as 10 weeks and 6 months .
The decline from maximal calculus accumulation, referred
to as reversal phenomenon,
39
40. THEORIES REGARDING THE
MINERALIZATION OF CALCULUS
By two theoretic mechanisms
1. Mineral precipitation
results from a local rise in the
degree of saturation of
calcium and phosphate
ions……
A. Rise in the pH o f
the saliva.
B.Colloidal proteins in saliva.
C.Phosphatase liberated from dental plaque, desquamated
epithelial cells, or bacteria.
2. Seeding agents induce small
foci of calcification that
enlarge and coalesce to form a
calcified mass …….Neuman
W,Neuman M
40
41. 1. Mineral precipitation results …………….
A. Rise in the pH o f the saliva.
Causes precipitation of calcium phosphate salts by lowering the
precipitation constant.
The pH may be elevated by the
1. Loss of carbon dioxide
2. Formation of ammonia by dental plaque bacteria.
3. By protein degradation during stagnation
………………Blanton P, Hurt W, Largent M. J Periodontol 1977
41
42. CO2 THEORY
From the major salivary gland,co2 is secreted at a high
CO2 tension , about 54 to 65 mm Hg , whereas the CO2
pressure in atmospheric air is only about 0.3 mm Hg.
Saliva emerging from the salivary ducts is believed to lose
CO2 to the atmosphere as a result of this large difference
in CO2 tension , the pH in saliva will increase when CO2
escapes , the concentration of less soluble secondary and
tertiary phosphate ions increases. therefore ,the solubility
of calcium phosphate is exceeded and crystals form.
42
43. B.Colloidal proteins in saliva.
Colloidal proteins in saliva bind calcium and phosphate ions
and maintain a supersaturated solution with respect to calcium
phosphate salts.
With stagnation of saliva, colloids settle out and the
supersaturated state is no longer maintained, leading to
precipitation of calcium phosphate salts.
43
44. C. Phosphatase liberation
Phosphatase liberated from dental plaque,
desquamated epithelial cells, or bacteria precipitate
calcium phosphate by hydrolyzing organic phosphates
in saliva, thus increasing the concentration of free
phosphate ions.
44
45. Esterase is another enzyme that is present in the cocci and
filamentous organisms, leukocytes, macrophages, and
desquamated epithelial cells of dental plaque.
Fatty esters free fatty acids soaps
with calcium and magnesium
Converted into the less-soluble calcium phosphate salts.
45
46. 2.Seeding agents induce small foci of
calcification
This referred to as the epitactic concept or more
appropriately, heterogeneous nucleation.
The seeding agents are not known
But it is suspected that the intercellular matrix of plaque
plays an active role.
The carbohydrate-protein complexes may binds with
calcium from the saliva (chelation) to form nuclei that
induce subsequent deposition of minerals.
46
47. INHIBITION THEORY
Calcification occurring only at specific sites because of the
existence of an inhibiting mechanism at non-calcifying sites.
One of the inhibiting substance is thought to the pyrophosphate
and the controlling mechanisms is thought to be an enzyme
alkaline pyrophosphate which can hydrolyse pyrophosphate to
phosphate (Russell and Fleisch, 1970).
47
49. Mineralization of plaque starts extracellularly around both
gram-positive organisms and gram negative organisms.
Filamentous organisms, diphtheroids, and Bacterionema and
Veillonella species have the ability to form intracellular apatite
crystals.
Calculus formation spreads until the matrix and bacteria are
calcified.
49
50. Bacterial plaque may actively participate in the
mineralization of calculus by forming phosphatases, which
changes the pH of the plaque and induces mineralization
( Ennever 1983 )But the prevalent opinion is that these
bacteria are only passively involved and are simply
calcified with other plaque components
…….Razzo A,Martin G, Scott D . et al 1962
The occurrence of calculus-like deposits in germ-free
animals supports this opinion.
50
51. SUPRAGINGIVAL AND SUBGINGIVAL
CALCULUS
SUPRAGINGIVALCALCULUS SUBGINGIVALCALCULUS
Coronal to the gingival
margin
Located below the crest of the
marginal gingiva.
Visible in the oral cavity Not visible in the oral cavity
Clerehugh et al. used a World Health
Organization #621 probe
White or whitish yellow in color
(tobacco and food pigments)
Dark brown or greenish black in
color
Hard with clay like consistency Hard / flint-like in consistency
Lingual area of the mandibular
incisors and buccal surfaces of the
maxillary molars.
Present subgingivally
Salivary calculus Seruminal calculus
Source of minerals--Salivary
secretions
GCF
51
52. Supragingival Subgingival
Prevalence Usually common
upto age of 9 years
0-15 yrs: 37-70%
16-21 yrs: 44-88%
Above 40 yrs: 86-
100%
Slightly lower than that of
supragingival, but approaches a
range of 47- 100% after age of 40
yrs
Composition Mainly Brushite
and Octacalcium
phosphate
a) More amount of Magnesium
whitlokite, less of brushite
and octacalcium phosphate.
b) Higher concentration of Ca,
Mg and F than supragingival
calculus
52
53. A positive correlation between the presence of calculus and the
prevalence of gingivitis exists. …….. Ramfjord
S.1961
Strong associations between calculus deposits and periodontitis
have been demonstrated in experimental (Waerhaug 1952, 1955) and
epidemiologic studies (Lovdal et al. 1958)
But this correlation is not as great as that between plaque
and gingivitis.
The nonmineralized plaque on the calculus surface is the
principal irritant, but the underlying calcified portion may
be a significant contributing factor
53
54. It does not irritate the gingiva directly but provides a
for the continued accumulation of plaque and
retains it in close proximity to the gingiva. ……..
(Friskopp &Hammarstrom 1980, Friskopp 1983)
Although 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.
54
55. Calculus & gingivitis ‘positive correlation” < plaque & gingivitis.
In young: periodontal condition & plaque than calculus ,
but with age situation is reversed” increase incidence of calculus,
gingivitis & periodontal diseases
Non mineralized plaque on calculus surface principle irritant.
Underlying calcified proteins is a significant factor: not
irritate the gingiva.
Directly but provide fixed nidus continuous accumulation of the
plaque & holds it to the gingiva.
Subgingival calculus may be the product rather than the cause of
periodontal pocket
55
56. HOW plaque irritates gingiva.
convert continually accumulating plaque into sub gingival calculus
increase flow of gingival fluid” due to gingival inflammation
pocket provides sheltered area for plaque & bacterial accumulation
pocket formation
Inflammation
56
57. The effect of calculus is secondary
by providing an ideal surface configuration conducive to further plaque
accumulation and subsequent mineralization’ .
Calculus deposits may develop in areas with difficult access for oral
hygiene
Or may by the size of the deposits –
Jeopardize proper oral hygiene practices.
Calculus may also amplify the effects of bacterial plaque by keeping
the bacterial deposits in close contact with the tissue surface,
Thereby influencing both bacterial ecology and tissue response.
57
58. Pathologic condition in which
increase in calculus formation
In children with cystic fibrosis
(Wotman et al.1973)
Patients on dialysis for renal disease, as their salivary
urea levels are high and the urea can be converted by
plaque bacteria to ammonia, which increases plaque pH
(Peterson S,1985)
In patients who are tube fed, as their plaque is not
exposed to fermentable carbohydrates.
(Mandel 1995)
58
59. Factors affecting the rate of
calculus formation
Diet and nutrition –the significance of diet in calculus
formation depends more upon its consistency than upon
its content.
Increased calculus formation has been associated with
an increase in dietary calcium, phosphorus, bicarbonate,
protein and carbohydrate.
59
60. Age – there is an increase in calculus deposition with
an increasing age.(Schroeder et al,1969). This
increase, is not only increase in the number of
surfaces, but also the size of calculus deposits. This
may be due to change in quantity and quality of saliva
with age, favouring the mineralization properties
Smoking- is associated with an elevated risk for
supragingival calculus deposition. Smoking may exert
its influence systemically (elevated levels of salivary
calcium and phosphorus) or locally via a conditioning
of tooth surfaces.
60
61. Salivary pH- increase pH increases the calculus
formation.
Habits – In populations that practice regular oral hygiene
and with access to regular professional care have low
tendency for calculus formation.
Salivary flow rate – increased salivary flow rate
decreases the calculus formation. Salivary flow rate affects
calcium phosphate saturation.
61
62. Salivary calcium concentration- Elevated salivary calcium
concentration, increases the rate of calculus formation.
Higher total salivary lipid levels – is associated with increased
calculus formation
Emotional status- increased calculus formation has been
associated with disturbed emotional status.
Nucleation inhibitors - Mg blocks apatite crystallization and
stabilizes calcium phosphate as amorphous mineral (Ennever
and Vogel, 1981)
62
63. Periodontal healing
If calculus is associated with progressive periodontal
attachment loss and has an effect on disease
progression
healing after periodontal treatment would be reduced in the
presence of calculus.
When the influence of retained subgingival calculus on
periodontal healing following flap surgery was
investigated
inflammation was more intense when calculus was present
(Fujikawa in 1988)
63
64. Subgingival calculus
Clinical studies shows the importance of frequent
and thorough removal of root deposits by scaling
and root planning to prevent attachment loss
(Pihlstrom et al 1983).
Morphologic studies show that calcified deposits
are porous and act as a reservoir for irritating
substances.
64
65. ATTACHMENT ON
IMPLANT SURFACE
Acquired pellicle forms on an implant surface when the
metal surface initially comes into contact with tissues
(Baier, 1982).
Adsorption of proteins does not occur on the surface of
pure titanium (Ti).
5- to 6-nm oxide layer composed of TiO2 forms on the
surface of Ti when exposed to air.
65
66. At physiological pH, the TiO2 layer carries net -ve
charges, which enable the TiO2 layer to bind cations like
Ca2
+ (Abe,1982).
This makes the surface of an implant +vely charged and,
consequently, attracts the high-weight molecules carrying
-ve charges, notably proteins.
Some irregularities may also be encountered on oral
implant surfaces.
66
67. Assesment of calcified deposit
Simplified calculus index (Green & Vermillion ’64 )
Calculus component of periodontal disease index
(Ramfjord )
Calculus surface index (Ennever J,, Sturzenberger
& Radike)
Calculus surface severity index(EnneverJ et al ’61)
Marginal line calculus index (Muhleman & Villa ’67)
Volpe- Manhold index (Volpe A R & Manhold J H
’62)
67
71. is a concentration of microorganisms,
desquamated epithelial cells, leukocytes, and a mixture of
salivary proteins and lipids, with few or no food particles, and
it observed in plaque.
It is a yellow or grayish-white, soft, sticky deposit and is
somewhat less adherent than dental plaque.
The irritating effect of materia alba on the gingiva is caused
by bacteria and their products
71
72. Most is rapidly liquefied by bacterial
enzymes and cleared from the oral cavity by
salivary flow and the mechanical action of the
tongue, cheeks, and lips.
Dental plaque is not a derivative of food debris
Nor is food debris an important cause of
gingivitis.
72
73. on the tooth surface are called
dental stains.
Cause aesthetic problem and do not cause
inflammation of the gingiva.
The use of tobacco products coffee, tea, certain
mouthrinses, and pigments in foods can contribute to
stain formation.
73
75. 1.IATROGENIC FACTORS.
Inadequate dental procedures
that contribute to the
deterioration of the
periodontal tissues are referred
to as iatrogenic factors.
Margin of restoration.
Contours and open contact.
Materials.
Partial dentures.
Restorative dentistry
procedure.
Malocclusion.
Habits,eg. tongue thrusting.
Orthodontic treatment.
Extraction of impacted third
molars
75
76. Restorative dentistry
The improper use of rubber dam clamps, matrix bands and burs
can lacerate the gingiva resulting in varying degree of
mechanical trauma and inflammation.
Restorations can do more harm than good to the patient’s oral
health if performed improperly.
Overhanging margins of restorations and crowns accumulate
additional plaque by limiting the patient’s access.
76
77. Overcontoured crowns and restorations tend to accumulate plaque
and possibly prevent the self cleaningmechanisms of the adjacent
cheek, lips,and tongue.
Restorations that fail to reestablish adequate interproximal
embrasure spaces are associated with papillary inflammation.
Overhanging margins
Changing the ecologic balance of the gingival sulcus to an area
that favors the growth of disease associated organisms
(predominately gram negative anaerobic species) at the expense of
the health-associated organisms (predominately gram positive
species) and
Inhibiting the patient's access to remove accumulated plaque.
77
78. Proximal contact relation:
The integrity and location of the proximal contacts
prevent interproximal food impaction.
Food impaction is the forceful wedging of food into the
periodontium by occlusal forces.
Classification of food impaction
Plunger cusp
78
79. Cervical enamel projection (CEP) and enamel pearls
They appear as narrow wedge-shaped extensions of
enamel pointing from the cementoenameljunction (CEJ)
toward the furcation area.
CEP classified into….
Grad 1 –CEJ of tooth to furcation entrance
Grade 2 – approches entrance but doesn’t into furcation
Grade3 – extends horizontally into furcation
The clinical significance of CEPs is that they are plaque
retentive and can predispose to furcation involvement.
79
80. Prosthesis
Gross iatrogenic irritants such as poorly designed clasps,
prosthesis saddles and pontics exert a direct traumatic influence
upon periodontal tissues.
Types of pontics….
Ovate pontic is good compare to other pontics. plaque easily
removed from pontic because of convex surface of pontics
80
81. Orthodontic procedures
Orthodontic therapy may affect the periodontium by
brackets favoring plaque retention, by directly injuring the
gingiva as a result of overextended bands, chemical
irritation by exposed cement and by creating excessive,
unfavorable forces, or both.
Effect of band on periodontium
Short term effect
Long term effect
Microbiology around orthodontic band
Effect of orthodontic force on periodontium
81
82. Extraction of impacted third
molar
The extraction of impacted third molars often results in
the creation of vertical bone defects distal to the second
molars.
Careless use of elevators or forceps during extraction
results in crushing of alveolar bone.
82
83. Malocclusion as contributing
factors
Crowded or malaligned teeth can be more difficult to
clean than properly aligned teeth.
In deepbite, maxillary incisors impinge on the mandibular
labial gingiva or mandibular incisors on the palatal
gingiva, causing gingival and periodontal inflammation.
83
84. Habits as contributing factors
The tooth surface, usually the root surface, can be abraded
away by improper toothbrushing technique, especially with a
hard toothbrush.
The abrasives in toothpaste may contribute significantly to this
process.
The defect usually manifests as V-shaped notches at the level
of the CEJ.
Flossing & tooth picks can also cause damage to dental hard
and soft tissues.
Flossing clefts may be produced when floss is forcefully
snapped through the contact point so that it cuts into the
gingiva. Also, an aggressive up and down cleaning motion can
produce a similar injury.
84
85. Mouth breathing
Mouth breathing can dehydrate the gingival tissues and
increase susceptibility to inflammation.
These patients may or may not have increased levels of
dental plaque. In some cases, gingival enlargement may
also occur.
Excellent plaque control and professional cleaning should
be recommended, although these measures may not
completely resolve the gingival inflammation.
85
86. Tongue thrusting
Tongue thrusting is often associated with an anterior open
bite.
During swallowing the tongue is thrust forward against
the teeth instead of being placed against the palate.
When the amount of pressure against the teeth is great, it
can lead to tooth mobility and cause increased spacing of
the anterior teeth.
This problem is difficult to treat but must be recognized
in the diagnostic phase as a potentially destructive
contributing factor.
86
87. Factitious injuries
Self-inflicted or factitial injuries can be difficult to
diagnose because their presentation is often unusual
These injuries are produced in a variety of ways including
pricking the gingiva with a fingernail , with knives, hair
pins and by using toothpicks or other oral hygiene
devices.
87
88. Radiation therapy has cytotoxic effects on both normal cells and
malignant cells.
Radiation treatment induces an obliterative endarteritis that
results in soft tissue ischemia and fibrosis while irradiated bone
becomes hypovascular and hypoxic.
Adverse affects of head and neck radiation therapy
Dermatitis and Mucositis
Muscle fibrosis and Trismus
Xerostomia
Use of a chlorhexidine digluconate mouthrinse may help
reduce the mucositis.
88
89. Xerostomia results in greater plaque accumulation and a
reduced buffering capacity from what saliva is left.
The use of effective oral hygiene, professional dental
prophylactic cleanings, fluoride applications, and frequent
dental examinations are essential to control caries and
periodontal disease.
Prophylactic antibiotics before receiving appropriate
nonsurgical periodontal therapy
The risk of osteoradionecrosis must be evaluated before
extracting a tooth or performing periodontal surgery in an
irradiated site
89
90. Periodontal attachment loss and tooth loss was greater
in cancer patients who were treated with high-dose
unilateral radiation as compared with the nonradiated
control side of the dentition
90
91. Pathogenic potential of dental
calculus
Until 1960,calculus is major etiologic factor in
periodontal disease. its , pathogenicity attributed to its
rough outer surface which mechanically irritated the
adjacent tissue.
Shroeder 1969 stated that initial damage to gingival
margin in periodontal disease is due to immunologic and
enzymatic effect of microorganisms in plaque.
Supragingival calculus promotes new plaque
accumulations.
91
92. 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.
92
93. PREVENTION OF CALCULUS
1. Professional removal of calculus – By scaling and root
planning.
2. Personal bacterial plaque control – tooth brushing,
flossing and supplementary methods is a major factor in the
control of dental calculus reformation.
3. Anti- calculus agents used in Commercial Dentifrices -
Chemotherapeutic agents have been used to supplement the
mechanical removal of dental plaque
(Aleece and Forscher,1954; Grossman, 1954; Zacherl et al., 1985;
Volpe et al., 1992).
93
94. The major strategies that have been
investigated are to:
(i) Dissolve or soften the mature deposit by
removing the inorganic portion
(ii) Affect the calculus matrix, i.e., to change the
‘skeleton’ around which calculus is deposited
(iii) Alter the attachment of the calculus to
the tooth surface
(iv) Prevent plaque from forming
(v) Inhibit crystal growth and thereby prevent
the development of mineralized plaque
94
96. Agents for softening of
mature dental calculus
ACIDS
Wooden stick moist with aromatic Sulphuric acid inserted in
pocket
Dissolve calculus
Act as an astringent on tooth surface
BAKER IN 1872
IN 1881 NILES use NITRO MUTRAIC ACID and find its
superior dissolving action on calculus.
Other acid used are 20%trichloroacetic acid ,bifloride of
mercury
97. But STONES in 1939 and GROSSMANN in 1954
said
Acid are caustic to soft tissues
Decalcify the tooth structure
98. 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.
98
99. Chelating agent
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.
99
100. 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.
100
101. EDTA
Jabro et al. (1992) performed a split mouth study on
fifteen adult patients with moderate to heavy calculus.
Contralateral quadrants were treated with EDTA gel
(SofscaleTM) and the subjects and operators were asked
to comment on the ease of removal of the calculus
deposits. Both subjects and operator reported easier
calculus removal using the gel.
102. 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.
102
103. ANTI TARTAR DENTRIFICES
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).
103
104. 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
104
105. Gaffar et al. (1987) showed that a 3.2% pyrophosphate, 1%
copolymer and 0.24% NaF mixture reduced calculus levels in
rats by 57%.
105
106. 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
anticalculus.
0.2% triclosan
0.2% triclosan and 0.5% zinc citrate was tested as an anti calculus
agent
106
107. 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.
Kohut & Grossman (1986) tested a zinc chloride and sodium
fluoride dentifrice for calculus inhibitory activity
Zinc chloride (2%)
Zinc citrate (0.5%)
107
108. CONCLUSION
Calculus therefore is a secondary etiologic factor for
periodontium. But its presence makes adequate plaque
removal impossible and prevents patients from performing
proper plaque control. its removal from tooth surface is a
primary requirement to achieve periodontal health. The
clinician should well trained in the adequate removal of
calculus which is 1st step in periodontal therapy.
The design and sharpness of instruments , anatomical
factors, depth of calculus deposition and operator’s
experience play role during subgingival calculus removal.
108
