Dental

calculus
It is an adherent calcified mass that forms
on the surface of natural teeth and dental
prostheses by mineralization of dental
plaque.
it is also considered as plaque retentive
factor.
 calculus

Supragingival Subgingival
 Supragingival c. Subgingival c.
Location Coronal to the gm. Below the crest of the gm.

Visibility Visible in the oral cavity. Not visible.

Color White or whitish yellow Dense, dark brown or greenish

Its color is affected by contact black.
with tobacco or food pigments.
Consistency Hard, clay like. Hard, flint like.

Attachment It is easily detached from the Firmly attached to the tooth

tooth surface. Recurs rapidly surface
after removal especially in
lingual area of mandibular
incisors.
Site Occurs most frequently on
buccal surfaces of maxillary Either appears indepently or on
molars opposite (Stensen’s duct) areas where supragingival
and on lingual surface of calculus already presents.
mandibular anterior teeth
opposite to (Wharton’s duct).
Source of minerals From saliva, so it is called From the blood serum or GCF,
Supragingival calculus on buccal surfaces of maxillary
molars opposite stensen duct
Extensive supragingival calculus on the lingual surfaces of lower
anterior teeth.(wharton’s duct)
A 31-year-old Caucasian male with extensive supragingival and
subgingival calculus deposits throughout his dentition.
Morphology of subgingival
caculus
Subgingival calculus may appear as:
• [1] Crusty,spiny or nodular
deposits

• [2] Ring like or ledge

like formation encircling
the tooth

• [3] Veneer type consisting

of a thin, glassy smooth
layer
• [4] Finger like and fern like
Formation which are
less frequently
seen

• [5] Island or spots of

calculus
Different types of crystals can be seen
between and within the bacterial remnants;

*Hydroxyapatite appears as small needle-

shaped crystals.
*Octacalcium phosphate appears as long
ribbon like crystals oriented in bundles.
*Brushite can be seen in young deposits as
large crystalline aggregates.
Matrix of subgingival calculus appears to be
more homogeneous than that of
supragingival calculus.
Both types of calculus are covered by a layer of
unmineralized plaque.
Plaque covered subgingival calculus is formed
of cocci rods and filaments.
Plaque covered supragingival calculus is
composed of filamentous organisms which are
oriented perpendicularly to underlying calcified
portions.
Presence of empty spaces or tubular holes is
representing the sites of degenerating
organisms or noncalcified bacteria.
Residues of food, epithelial cells and blood
–derived cells are present as minor
contributors to the structure of mature
calculus.
*Microscopic studies demonstrate that the
calculus is usually extended near but it
doesn’t reach the base of pockets in
chronic periodontal lesions
• Calculus appears during early teenage
years and increases with age.
• Both types of calculus are found but
supragingival calculus is more common in
young age.
• In individuals with poor oral hygeine.
• No sex prevelence.
• Geographic variation has been noted.
• Supragingival calculus and subgingival calculus
may be seen on radiograph but detection of
them is low.
• Well calcified supragingival calculus is
detectable forming irregular contours on the
radiographic crown.
• Both supragingival and subgingival calculus are
easily detectable interproximally .They form
irregular shaped projections into the interdental
space.
Radiographic picture of
calculus
 Supragingival calculus

Inorganic content organic

content
70-90%
inorganic components(70-
90%)
Calcium 39%
Phosphorus 19%
Carbon dioxide 1.9%
Magnesium 0.8%
Traces of sodium, zinc, bromine, copper ,iron
fluorine, strontium,tungesten, gold,
aluminum, and silicon .
2/3 of the inorganic content are crystalline in
structure
Crystal forms:
Hydroxyapatite 58%
Magnesium whitlockite 21% ( in the
posterior area)
Octacalcium phosphate 12%
Brushite 9% (in the mandibular anterior
region)
The organic content
Mixture of protein-polysaccharide complexes,
desquamated epithelial cells, leukocytes and
various types of microorganisms.

Salivary proteins account for 5.9%-8.2%.

Lipids account for 0.2%

• Same hydroxyapatite content
• More magnesium whitlockite
• Less brushite and octacalcium phosphate.
• Higher ratio of calcium to phosphate.
• More sodium.
• No salivary proteins.
Four modes of attachment of
calculus to the tooth surface:

(1)Organic acquired pellicle:

This binds strongly to the
tooth surface and acts as
adherent layer for developing
plaque and calculus. Pellicle
attaches supragingival
calculus to enamel surface
and subgingival calculus to
cementum surface. Calulus attached to pellicle
(2)Mechanical locking:
Into surface irregularities such as
{caries and resorped lacunae}.

(3) Close adaptation:

Of calculus under surface
depressions to sloping mounds of
cementum surface {cemental
defects}.
Calculus attached to
carious surface

Under surface of
calculus
cementum
mounds in
calculus
(4)Penetration:
Of calculus bacteria into cementum
and dentin.

Calculus
embedded
within the
cementum
Calculus embedded
beneath cementum
and penetrating to
the dentin
N.B:
Calculocementum :
Is calculus embedded deeply in
cementum and appears
morphologically similar to cementum.
It differs:

*From Person to person.

* In different teeth.
* At different times in the same person.

Persons are classified as:

Calculus formers. Non calculus formers.

Heavy Moderate Slight

The plaque of heavy formers exhibits higher
levels of calcium and phosphorus than
those of light formers within a few days
after a prophylaxis.

Causes of marked differences in propensity

to calculus formation are:
(1)Salivary environment.
(2)Dietary factors.
(3) Differences in bacterial flora.
Heavy salivary calculus formation could be related
to:
•High PH.
• high Concentration of homogeneous nucleators
(calcium).
• high Heterogeneous nucleators (salivary or bacterial
proteins or lipids).
•Low levels of inhibitors (pyrophosphate) which is
present at higher level in light calculus formers.
•Heavy formers usually have higher values of
submandibular urea, total protein, calcium and lipids.
 Average daily increment in calculus formers is
from 0.1% to15% of dry weight.
Calculus formation continues until reaches a
maximum from 10 to18 weeks and 6 months.
After maximum accumulation there is a
(Reversal phenomenon)
This is reduction of calculus level after
maximum formation due to mechanical wear
from food, cheek, lips and tongue.
N.B :
Anticalculus dentifrices reduce quality and
quantity of formed calculus and make it easier
to remove by dentist
• Calculus is formed by mineralization of
dental plaque.
• Plaque undergoes mineralization in 4-8
hours.
• 50% of plaque is mineralized in 2 days
• 60-90% of plaque is mineralized in12 days
Mineralization starts by binding of calcium ions
to the carbohydrate-protein complexes of
organic matrix and the precipitation of
crystalline calcium phosphate salts.
Crystals are formed first in the intercellular
matrix then on the bacterial surfaces and
finally within the bacteria.
 According to (Carranza and Newman, 1996) there
are two important theories concerning calculus
mineralization:

{1} Local rise in degree of saturation of calcium and

phosphorus ions.
{2} Epitactic concept or heterogeneous nucleation.
.
I )Local rise in degree of saturation of
calcium and phosphorus ions theory :

Calcification of plaque is due to precipitation of

calcium phosphate salts which is due to:

(1)Increase of PH due to:

Decrease carbon dioxide.

Formation of ammonia by plaque bacteria or by
protein degradation during salivary stagnation.
(2) Loss of super saturation state during
salivary stagnation:
Colloidal protein binds calcium and
phosphorus ions, so it maintains super
saturation state.
During salivary stagnation, colloidal protein is
degraded and leads to loss of maintenance of
super saturation state which leads to calcium
and phosphorus precipitation.
3)Two important enzymes help in calcium and
phosphorus precipitation:

Phosphatase Esterase
Source Dental plaque, Bacteria, leukocytes and
desquamated epithelial macrophage.
cells and bacteria
Action .It causes hydrolysis of It causes hydrolysis of fatty
organic phosphate in ester into free fatty acid
saliva which causes which is forms soaps with
increase in concentration Ca, this soap later on is
of free phosphate ions. converted into soluble
calcium phosphate salt.
II )Epitactic concept or heterogeneous
nucleation theory:

Seeding agents induce small foci of calcification

that enlarge and coalesce forming calcified mass.
These seeding agents may be;
*Plaque bacteria.
*Intercellular organic matrix.
Carbohydrate protein complexes initiate
calcification by removing Ca from saliva by
chelation and bind with it to form nuclei. These
nuclei cause more deposition of minerals.
• Mineralization of plaque starts
extracellulrly around both gram negative
and gram positive organisms.
• It may also start intracellularly .
• Calculus formation spreads until the matrix
and bacteria are calcified.
•The more prevalent opinion is that; bacteria
are passively involved and be calcified with
other plaque components this opinion was
approved by formation of calculus in germ-
free animals.
• The other opinion is effective role of bacteria
either by;
{1} forming seeding agents.
{2} producing enzymes (phosphatase and
esterase).
{3} changing plaque PH.
• Calculus itself doesn’t contact gingival surface,
but it is always covered by a layer of plaque
• *Calculus itself doesn’t irritate the gingival
tissue directly but :
-It provides an area of plaque accumulation
-It keeps the plaque in close contact with the
gingival tissue
-It acts as a physical barrier between gingiva
and tooth surface so prevents gingival repair
or healing
-It creates an area of difficulty for removal of
plaque