3. CALCULUS
Mineralized bacterial plaque that forms on the surfaces of natural teeth and dental
prostheses.
Most important contributing factor
- Provides fixed nidus .
- Keeps plaque in close contact with the gingival tissues
Albandar et al 1998 – aggressive periodontitis – areas with detectable sub gingival
calculus – greater loss of periodontal attachment loss.
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4. Definitions
Calculus is a hard deposit that forms by mineralization of dental
plaque and is generally covered by a layer of unmineralized plaque
When a dental plaque calcifies the resulting deposit is called calculus
(GRANT)
Dental calculus is defined as the calcified or calcifying deposits that
are found attached to the surfaces of teeth and other solid structures in
the oral cavity. (LINDHE)
5. According to location
1. Supragingival calculus
2. Subgingival calculus
According to source of mineralization
1. Salivary calculus
2. Serumal calculus
Depending on the rate of formation (Muhlar and Ennever 1962)
1. Heavy calculus former
2. Moderate calculus former
3. Slight calculus former or Non calculus former.
Classification
5
7. Difference between supragingival and subgingival calculus
SUPRA GINGIVAL CALCULUS
• coronal - gingival margin
• White or whitish yellow
• Hard , Clay like
• Easily detached from
tooth surface
• Saliva- mineralization
• Composition
SUB GINGIVAL CALCULUS
• Below - crest of the
marginal gingiva .
• Dark brown or greenish
black in color
• Hard and dense,flint like
• Firmly attached to the tooth
• Serum trasudate – GCF
furnishes the minerals
• Composition
8. Third National Health and Nutrition Examination
Survey (NHANES III) evaluated 9689 adults in the U.S. between 1988 & 1994
91.8% of the
subjects had
detectable
calculus and
55.1% had
subgingival
calculus. Prevalence
of sub-
gingival
calculus
increased
with age
Males-
significantly
more
subgingival
calculus,
more teeth
with calculus
than females
More often
on mesial
than buccal
surfaces
8
9. Distribution of dental calculus on
dentition
Lingual
surfaces of the
lower anterior
teeth.
Buccal
surfaces of
the upper
molars
11. Prinz -1928.
BOOSTER CONCEPT
11
PHYSIOCHEMICAL THEORY:
1 • THE SALIVARY pH THEORY
2
• COLLOIDAL PRECIPITATION
THEORY
3 • PRECIPITATION OF PROTEINS
12. The Salivary pH Theory
12
Calculus formation
Precipitation of calcium phosphate salts
Lowered precipitation constant
Increased pH of the saliva
Loss of carbon di-oxide
Formation of ammonia
Dental plaque bacteria / protein denaturation Burchard (1895-1898)
Postulated the rise in
pH caused due to loss
of CO2 from the saliva
Rapp , 1946
Carbonic anhydrase in
the saliva leads to
increased uptake of
CO2 .
As CO2 is lost, there is
precipitation of calcium
and phosphates.
15. Mineralization of plaque stars extracellularly around both gram
positive and negative organisms or intracellularly.
Filamentous organisms form intracellular apatite crystals,
Calculus formation spreads , until the matrix and bacteria are
calcified
Some believe that , bacteria actively participate in the
mineralization of calculus by forming phosphatases, changing
the plaque pH
Not accepted… formation of calculus in germ free animals
The prevalent opinion is that these bacteria are only passively
involved and are simply calcified with other plaque components
15
BACTERIAL THEORY (Naeslund
1926 )
17. Amorphous non-crystalline deposits and
brushite can be transformed to octocalcium
phosphate and then to hydroxyapatite (Eanes
et al, 1970).
Controlling mechanism may be
pyrophosphate
(Fleisch et al, 1968).
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TRANSFORMATION THEORY
18. Calcification - only at specific
sites.
calcification occurs- inhibition is
altered or removed.
PYROPHOSPHATE - inhibits
calcification
preventing the initial nucleus from
growing, possibly by “poisoning”
the growth centres of the crystal.
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INHIBITION THEORY:
19. ESTERASE
Dental plaque bacteria / WBC macrophages /
desquamated epithelial cells
Release of enzyme esterase
Hydrolysis of free fatty esters
Fatty acids + calcium – magnesium
Formation of soaps
Formation of less soluble calcium phosphate
salts
Precipitation of calcium phosphate salts
Calcium formation 15-5-2017
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20. Attachment of calculus
Attachme
nt to tooth
surface
(Zander,
1953)
organic pellicle
to enamel*
Mechanical
locking into
surface
irregularities*
Close
adaptation to
gentle sloping of
unaltered
cementum
surface
Penetration
of calculus
into
cementum*
Moskow (1969)
suggested a fifth
method.
Attachment to
cemental tears
and separations
Shroff (1955 the
type of calculus
attachment
probably depends
on the length of
time the calculus
has been on the
tooth
Calculocementum
( Selvig G 1970)
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22. Anatomic factors
Favours retention of bacterial deposits
Difficult - periodontal debridement and oral hygiene
procedures.
Furcal invasions vary in horizontal and vertical depth as a
result of such features as cervical enamel pearls, root
trunk length, furcation entrance dimensions, root
anatomy and variations in the anatomy of the roof of the
furcation.
Anatomic factors
22
23. 1) Cervical enamel projections and enamel pearls
Ectopic deposits of enamel apical
cemento enamel junction
Hou and Tsai –
Prevalence of cervical enamel projections in
molars with and without furcation
involvement.
- Molar with Cervical enamel projection–
82.5% - furcation involvement.
- 17.5% - absence of cervical enamel
projection
23
24. Cervical Enamel Projections
Masters and Hoskins - 1964
Grade 1: short but distant change in
the contour of the CEJ extending
towards the furcation
Grade 2: approaches the furcation,
without making contact with it.
Grade 3: extends into the furcation.
Roussa –
• Grade 1 and 2 – more prevalent.
• Mandibular second molars
24
25. 2) Enamel Pearls
Less prevalent than cervical
enamel projections
Contribute to etiology of
furcation involvement
Moskow and Canut –
prevalence - 1.1 – 9.7%.
maxillary third molars.
mandibular third molars and
maxillary second molar second
most common sites.
25
26. 3) Root Trunk Length
The severity of furcation involvement -
between the amount of attachment loss and
the distance from the cemento enamel
junction to the furcation entrance – the root
trunk length.
The shorter the root trunk length
the earlier the exposure
more difficult the plaque control.
Hou et al :
Type A – third or less of the cervical area of the
root.
Type B- include up to half of the length of the
root
26
27. 3)Root Trunk Length
Hue et al : Prevalence
Maxillary first molars – type B ( 47.1%) or type A (41.0%)
than type C (11.9%)
Mandibular first molars - type A (83.5%)
Maxillary and mandibular second molars – Type B (60.%,
52.6%)
Others - maxillary molars (3.6 – 4.8mm from CEJ) > mandibular
molars (2.4 – 3.3mm )
the shortest distance - found in the mandibular first molars-
exposure of the furcation at an early stage of periodontitis.
27
28. 4 ) Size Of Furcation Entrance
. Bower, 1979 reported that 81% of all
furcation entrance diameters
measure < 1 mm, with 58% < 0.75
mm, which is less then width of curettes.
Chui et al - 49% - <0-75mm.
Additional challenge in management of
molar furcation approach
Difficult to debride.
28
29. 5)Bifurcation Ridges
Described by Everett et al, 1958
Sveirdstrom & Wennstrom, 1988 - morphology of bifurcation
ridges
- Pits and ridges – roof of furcation – complicate therapy
- Intermediate ridges – connect mesial and distal roots – cementum
- buccal and lingual ridges – dentin with overlying layers of
cementum.
- Central bifurcation ridge – mandibular molars.
Hou & Tsai, 1997 - ridges are strongly associated with
attachment loss in furcations
29
30. Bifurcation Ridges
Fluting of roots / root concavities - molars.
Roof of furcation's, coronal and apical to
furcation's and on interproximal root
surfaces.
Vermino, 1980 - 78% - palatal aspect of
the buccal root of maxillary first
premolars .
Progression of attachment loss -
harbouring bacterial plaque.
30
31. 6)Bicuspid teeth
maxillary first bicuspids - two roots – buccal and palatal
Joseph et al :
- furcal concavity - palatal aspect of the buccal root - 62 % of
bifurcated teeth.
78% reported by Gher and Vernino.
The mean furcation width was 0.71mm
Concavities was found on the proximal surfaces of all teeth
studied, with a deeper concavity on the mesial than the distal
aspect.
31
32. 7)Palatal Groove
The radicular lingual / palatal groove - infolding of the inner
enamel epithelium and Hertwing’s epithelial root sheath
create a groove that passes from the cingulum of maxillary
incisors apically onto the root.
Cruz Filho - 3% lingual surface of the maxillary lateral incisor
-
< 1% of maxillary central incisors - buccal and
or lingual surfaces
Other report the prevalence of 0.79
21% in both maxillary incisors and 1.9 – 14% in lateral incisors
32
33. • Incisors - shallow U shaped groove
• Kogon –
half of the grooves extend more than 5mm apical to
the CEJ
Act as funnels – accumulation of plaque
- Withers et al 1981
33
34. Iatrogenic Factors
Deficiencies in the quality of dental restorations or prosthesis
are contributing factors to gingival inflammation and
periodontal destruction.
Location of gingival margin for restoration
Space between the margin of restoration and unprepared
tooth
Contour of restoration
Occlusion
Materials used
Procedure and design
Iatrogenic Factors
34
35. Margins of restorations
Over Contoured Crown
Design Of Removable Partial Dentures
Restorative And Endodontic Procedures
Iatrogenic Factors
35
36. 1)Margins Of Restorations
Over hanging margins
1) increases plaque formation
retentive areas
1) Changed the ecologic balance
2) Compromises hygiene practice.
Subgingival margins
Waerhaug - restorations placed in a sub gingival location -
detrimental to periodontal health.
Increased plaque, severe gingivitis and deeper pockets.
36
37. 2)Over Contoured Crown
Leads to accumulation of plaque and prevent the self-
cleaning mechanisms of oral tissues .
proximal contacts , contour of the marginal ridges ,
developmental grooves - prevent interproximal food impaction
– prevent periodontal disease.
Hancock et al 1980 – food impaction – periodontal pathosis.
Jernber G et al 1983 - probing depth , clinical attachment loss
– increased in open contact and food impaction.
37
38. 3)Dental Materials
Restorative materials are not in themselves injurious to the
periodontal tissues
Self curing acrylics
Silicate
Kourkouta et al – highly glazed porcelain – less plaque than
enamel
Composites – more likely to harbor bacterial plaque.
Wang et al 1998 – metal pontics – higher amount of periodontal
pathogens than porcelain.
Plaque accumulation maintained – finished and polished surfaces.
38
39. 4)Design Of Removable Partial Dentures
Favor the accumulation of plaque.
Quantitative and qualitative
changes
Increase in spirochetal
microorganisms
Mobility of abutment teeth, gingival
inflammation, pocket formation
increase
Studies by Zlataric et al
Zlataric et al
39
40. 5)Restorative And Endodontic Procedures
Rubber dam clamps, matrix bands, burs – lacerate
the gingiva – inflammation
Gingival retraction cord – impacted debris – foreign
body reaction.
40
41. Miscellaneous Factors – Malocclusion
• Poorly aligned teeth themselves are not associated with a greater degree of gingivitis
• complicate oral hygiene procedures - increased plaque accumulation - subsequent gingival
inflammation.
• Behfelt et al - direct relationship between tooth displacement and gingival inflammation
• Reduced interproximal spaces – less effective removal of plaque
• Extreme anterior overbite - palatal recession in maxillary incisors.
41
42. Miscellaneous Factors – Vertical Root Fracture
Longitudinal , confined to the root of the
tooth.
Mesiodistal, buccolingual plane – occur at
any point along the root.
Narrow, isolated periodontal pocket. Recurrent
42
43. Mucogingival deformities – Aberrant frenal attachment
Aberrant frenal attachments may be a problem, especially in
shallow vestibules or areas of minimal attached gingiva.
frenum is stretched - the muscle attachments may pull the
marginal tissue away from the tooth - accumulation and apical
migration of bacterial plaque – gingival recession
43
44. Miscellaneous Factors – Orthodontic Therapy
Orthodontic therapy affects the periodontium
by
Favouring plaque retention
Directly injuring the gingiva as a
result of overextended bands
Creating excessive forces,
unfavourable forces, or both on
the tooth and supporting
structures.
Modify the gingival ecosystem
- Orthodontic band
- Excessive orthodontic forces – necrosis
of PDL and adjacent alveolar bone ,
apical root resorption.
44
45. Habits and self – inflicted Injuries
important factors in initiation and progression of
periodontal diseases
Mechanical form of trauma can arise from
1) Improper use of toothbrush and oral jewellery.
- Whittle and lamden - tongue piercing - lingual
recession with pocket formation and bone loss
were seen.
- Tooth brush trauma – acute and chronic.
2) Wedging of tooth picks between the teeth
3)Application of finger nail pressure against the
gingiva
45
46. Habits and self – inflicted Injuries
Acute gingival inflammation - sensitivity or non specific tissue
injury.
Simple erythema - painful vesicle formation - ulceration.
Strong mouth washes, topical application of corrosive drugs such
as aspirin or cocaine, and accidental contact with drugs such as
phenol or silver nitrate.
46
47. Smokeless tobacco
Snuff and chewing tobacco – two forms
Localized gingival recession, clinical attachment loss,
leucoplakia, and possibly enhanced susceptibility to
severe periodontitis.
The incidence of gingival recession among adolescents who use
smokeless tobacco has been reported as 42% compared to 17%
among non users.
The NHANES III - effect of smokeless tobacco on the periodontium -
double the incidence of severe periodontitis.
47
49. Radiation therapy
Cytotoxic effects on both normal cells and malignant cells.
>60 Sv – salivary production impaired – xerostomia –
greater plaque accumulation and reduced buffering
capacity by saliva.
Periodontal attachment loss and tooth loss has been
reported to be greater in cancer patients who were treated with
high-dose unilateral radiation as compared with the non radiated
control side of the dentition
49
50. Tobacco smoking
Smoking is strongly related to severity of diseases and to
recurrent and refractory diseases.
Numerous studies have shown the association of smoking
with periodontitis.
50
51. Conclusion
The primary goal of periodontal therapy is to produce an environment that is conducive
to oral health.
It is absolutely necessary that a clinician looks beyond oral cavity for factors which
may complicate the disease process.
This will enable us to help our patients reach the common goal of Prevention and
management of periodontal disease which in turn improves the general health as well.
51