DENTAL CALCULUS

SUBMITTED BY – BATCH F
DEPARTMENT OF PERIODONTICS AND IMPLANTOLOGY
GUIDED BY – DR. SWETA SONI
DR. JITENDRA SHARMA
INTRODUCTION

Calculus

Calculus consists of mineralized bacterial plaque that forms on

the surfaces of natural teeth and dental prostheses. ( Source –
Newman and Carranza )

Dental calculus is an adherent, calcified or calcifying mass that

forms on the surfaces of teeth and dental appliances. It is
covered on its external surface by vital, tightly adherent,
nonmineralized plaque.
Dental Calculus
TYPES OF DENTAL CALCULUS

Depending upon the position of calculus in relation to the

marginal gingiva it is classified as:
1. Supragingival calculus
2. Subgingival calculus
 SUPRAGINGIVAL CALCULUS
 Supragingival calculus is located coronal to the gingival margin and therefore is
visible in the oral cavity.
 It is usually white or whitish yellow in color; hard, with a claylike
consistency; and easily detached from the tooth surface.
 After removal, it may rapidly recur, especially in the lingual area of
the mandibular incisors.
 The color is influenced by contact with such substances as tobacco
and food pigments.
 It may localize on a single tooth or group of teeth, or it may be
generalized throughout the mouth.
 The two most common locations for the development of
supragingival calculus are the buccal surfaces of the maxillary
molars and the lingual surfaces of the mandibular anterior teeth.
 Saliva from the parotid gland flows over the facial surfaces of the
upper molars via the parotid duct, whereas the submandibular duct
and the lingual duct empty onto the lingual surfaces of the lower
incisors from the submaxillary and sublingual glands, respectively.
 SUBGINGIVAL CALCULUS

 Subgingival calculus is located below the crest of the

marginal gingiva and therefore is not visible on routine
clinical examination.
 The location and extent of subgingival calculus may be
evaluated by careful tactile perception with a delicate dental
instrument such as an explorer.
 Subgingival calculus is typically hard and dense; it
frequently appears to be dark brown or greenish black in
 Microscopic studies demonstrate that deposits of subgingival
calculus usually extend nearly to the base of periodontal
pockets in individuals with chronic periodontitis but do not
reach the junctional epithelium.
 When the gingival tissues recede, subgingival calculus
becomes exposed and is therefore reclassified as
supragingival. Thus, supragingival calculus can be composed
of both supragingival calculus and previous subgingival
calculus.
DIFFERENCE BETWEEN SUPRAGINGIVAL
AND SUBGINGIVAL CALCULUS
DIFFERENCE BETWEEN PLAQUE AND
CALCULUS
 PREVALENCE
1) The formation of supragingival calculus was observed early in life
in individuals, probably shortly after the teeth erupted.
2) The first areas to exhibit calculus deposits were the facial aspects of
maxil lary molars and the lingual surfaces of mandibular incisors.
3)The deposition of supragingival calculus continued as individuals
aged, and it reached a maximal calculus score when the affected
individuals were 25-30 years old.
4) At this time, most of the teeth were covered by calculus, although
the facial surfaces had less calculus than the lingual or palatal surtiaces.
5) Calculus accumulation appeared to be
symmetric, and by the age of 45 years, these
individuals had only a few teeth (typically the
premolars) without calculus deposits.
6) By the age of 30 years, all surfaces of all teeth
had subgingival calculus without any pattern of
predilection
7)Both supragingival calculus and subgingival
calculus may be
 COMPOSITION
Inorganic Content
Dental Calculus is primarily composed of inorganic component
(70-90%).
 Calcium phosphate (Ca3[PO4]²) – 76%
Magnesium phosphate (Mg3[PO4]²) – 4%
Calcium carbonate [CaCO³] – 3%
Carbon dioxide (C0²) – 2%
And traces of other elements such as sodium, zinc, strontium,
bromine, copper, manganese, tungsten, gold, aluminium, silicon, iron
and fluorine.
 The percentage of inorganic constituents in calculus is similar to that
of other calcified tissues of the body.
 At least two-third of the inorganic component is crystalline in
structure.
 The four main crystal forms and their approximate percentages are as
follows:
 hydroxyapatite, 58%
 magnesium whitlockite 21% ( whitlockite is a mineral that is an
unusual form of calcium phosphate, found in rock deposit )
 octacalcium phosphate, 12% ( is a precursor to tooth ename, dentin,
and bones)
 Hydroxyapatite and octacalcium phosphate are
detected most frequently (ie, in 97-100% of all
supragingival calculus) and constitute the bulk of
the specimen.
 Brushite is more common in the mandibular
anterior region, and magnesium whitlockite is
found in the posterior areas.
 The incidence of the four crystal forms varies with
the age of the deposit.
Organic Content
 The organic component of calculus consists
of a mixture of the followings:
-Protein-polysaccharide complexes.
-Desquamated epithelial cells.
-Leukocytes
- Various types of microorganisms.
 2%-9% of organic component is
carbohydrate, which is derived mainly from
saliva.
Salivary proteins account for about 6% -
8% of the organic components of calculus.
Lipids account for 0.2% of the organic
 The composition of subgingival calculus is similar to
that of
supragingival calculus, with some differences-
 1. Subgingival calculus has the same hydroxyapatite
content but more magnesium whitlockite and less
brushite and octacalcium phosphate.
2. The ratio of calcium to phosphate is higher in
subgingival calculus, and the sodium content
increases with the depth of periodontal pockets.
 These altered compositions may be attributed to
fact that the origin of subgingival calculus is
plasma, whereas supragingival calculus is partially
composed of salivary constituents. Salivary
proteins present in supragingival calculus are not
found in subgingival calculus.
Dental calculus, salivary duct calculus, and
calcified dental tissues are similar in inorganic
Supragingivalcalculus Subgingival Calculus
ATTACHMENT OF CALCULUS TO TOOTH
SURFACE
 Zander HA reported four types of attachment.
Later on Shroff mentioned that the type of attachment
probably depends on time duration since the calculas
formed on the tooth.
Four modes of calculus attachment to the tooth
structure are :
1) attachment of calculus with organic pellicle
 2) attachment with the mechanical interlocking system into
surface irregularities , such as resorption lacunae and caries.
This type of attachment makes the removal of calculus
difficult as calculus embedded beneath the cementum
surface penetrate into the dentin.
3) penetration of calculus bacteria into cementum .
4) close adaptation of calculus undersurface depressions to
the gently. Sloping mounds of the unaltered cementum.
 FORMATION OF DENTAL CALCULUS
 Calculus is mineralized dental plaque.
It is formed by the precipitation of mineral salts, which
usually starts between the 1st and 14th day of plaque
formation.
Calcification has been reported to occur within as little as
4-8 hours.
Calcifying plaques may become :-
▪︎50% mineralized in 2 days and
▪︎60-90% mineralized in 12 days.
 -Each plaque contains a small amount of
inorganic material, which increases as the plaque
develops into calculus.
-All plaque does not necessarily undergo
calcification.
-Plaque that does not develops into calculus
reaches a plateau of maximum mineral content
within 2 days.
 》 Source of mineralization:-

 1. Supragingival calculus – saliva (prime source)

2. Subgingival calculus – GCF (serum transudate), which
furnishes the minerals for subgingival calculus
 -Calcium conc. In plaque is 2-20 times higher than in
saliva.
 -Early plaque of heavy calculus formers contains more Ca,
3 times more P & less K than that of non-formers,
suggesting that P may be more critical than Ca for plaque
mineralization.
Calcification entails the binding of Ca ions to the
carbohydrate-protein complexes of the organic matrix and
the precipitation of crystalline Calcium phosphate salts.
 Calcification of the supragingival plaque &
attached component of subgingival plaque
begins along the inner surface adjacent to
the tooth structure.
-Calcification starts in the separate foci
which increase in size and coalesce to form
solid masses of calculus.
 For the initial mineralization to occur:-
1. Calcium phosphate supersaturaion
2. Certain membrane associated components.
3. Regulation of nuclear inhibitors
Calcification may accompanied by the :-
a. Alterations in the bacterial content
b. Staining qualities of plaque. (Foci of calcification change
from basophilic to eosinophilic)
 Calculus is formed in layers, often separated by
a thin cuticle that gets embedded in the calculus
itself as the calcification progresses.
-Initiation and rate of calculus accumulation is
dynamic....it vary among individuals, among
tooth variety in the same dentition & at
different times in the same person.
 》 On the basis of these differences persons may be
classified as:-
a. Calculus formers
-Heavy
-Moderate
-Slight
. Non-calculus formers
Avg. Daily increment in calculus formers is from =
0.10 – 0.15% of dry weight calculus.
 The time required to reach max. Level of calcification
has been reported to be = between 10 weeks and 6
months.
》 Reversal phenomenon:- Calculus formation
continues until it reaches a max. After which it may
be reduced in amount.
So, the decline in calculus from the point of max.
Calculus formation is referred to as the reversal
phenomenon.
It may be explained by:-
The vulnerability of bulky calculus to
mechanical wear from food & from the
cheeks, lips & tongue movement.
Theories Regarding the mineralization of
calculus.
The theoretical mechanism by which plaque
becomes mineralised is stratified into 6 types

1. PRECIPITATION MECHANISM
2. BACTERIOLOGICAL THEORY
3. EPITACTIC THEORY
4. TRANSFORMATION THEORY
5. ENZYMATIC THEORY
6.INHIBITION THEORY
PRECIPITATION MECHANISM

AKA. Booster mechanism

Precipitation theory was given by MAGITOT in 1878. In his

opinion tartar mainly consisted of mineral matter formed by
earthy carbonates and phosphates from the saliva.

It is further dissociated into 3 types:

1. Salivary pH theory
2. Colloidal precipitation
3. bacterial protein mechanism
Salivary pH theory
● Given by Hodge and Leung in 1950
● It is associated with carbon dioxide.
● A rise in the pH of saliva causes precipitation of calcium
phosphate salts by lowering the precipitation constant.
● The pH is elevated by the loss of carbon dioxide, it is due to
the pressure gradient of carbon dioxide in the atmosphere and
oral cavity.
● Due to the alkaline nature of saliva, secondary and tertiary
phosphate ions are formed which act as booster ions and
deposition of phosphate and calcium crystals takes place on
the surface of the tooth.
 Colloidal protein theory
As given by Prinz, 1921

This theory states that the colloidal protein in saliva can

bind with calcium and phosphate ions, which further
form a supersaturated solution.

● In this supersaturated solution calcium and phosphate

precipitate and settle down onto the surface of the
tooth.

● This is how dental calculus is formed.

 Bacterial protein mechanism
 This theory states that the already present dental
plaque contains various numbers of bacteria.
 These bacteria form some proteins(Amino
acids) which are further converted into ammonia
 Ammonia increases the pH of saliva and results
in the precipitation of calcium and phosphate
and formation of dental calculus.
 2. Bacteriological theory
 According to this theory, the primary cause of calculus
formation is oral microorganisms and their involvement
in attachment to the tooth surface.
Leptotrichia, prevotella intermediate(gram -ve), and fusobacterium
nucleatum has been considered most often as the causative
microorganisms.
This theory is not accepted because it was seen that calculus formation is
seen even in germ free organisms.
 3. Epitatic theory
 Given by Mandel in 1957.
 In his opinion, in saliva, the concentration of certain ions like calcium
and phosphate is not high enough to precipitate but is ample enough to
promote the growth of hydroxyapatite crystals once an initial seed or
nucleus is formed.
 The term epitactic refers to crystal formation through seeding by
another compound which is similar to hydroxyapatite crystals, leading
to precipitation of calcium salts from the metastable solution of saliva.
 Seeding agents provoke small foci of calcification enlarge and coalesce
to form the calcified mass.
● Intercellular matrix or plaque plays
an important role. Calcification will be initiated by a
carbohydrate/protein complex which removes calcium
from saliva by chelation process and binds with the
nuclei
that stimulates subsequent deposition of minerals
 4. Transformation theory

 Given by Fleischet Al in 1968.

 The most noticeable hypothesis states that
hydroxyapatite need not arise exclusively via epitaxis
or nucleation.
 Octa calcium phosphate is formed by the
transformation of amorphous non-crystalline deposits
and brushite and then they are transformed into
hydroxyapatite (Eanes et al 1970).
 It has been suggested that the controlling mechanism
in transformation mechanism can be pyrophosphate.
5. 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.
6.Inhibition theory
Inhibition theory:
Calculus is not uniform, in some places it is more or its is less.
This discrevency is because in some areas inhibitory agents are
altered or are removed.
These inhibitory agents are nothing but pyrophosphates present in
saliva. It chelates calcium i.e, removes calcium and further prevent
crystal growth i.e calcium does not get deposited in plaque and
therefore it won't get mineralized and prevents crystal growth.
1)Inhibitory agents are removed or altered in
places where calculus is formed
2) forms pyrophosphate (saliva)
3)which chelates calcium (antagonizes
ability of inorg. P to crystallise with
calcium). And therefore prevent crystal
growth.
 Role of microorganisms In mineralisation of calculus

Mineralization of plaque generally starts extracellularly around gram positive

and gram negative organisms but start intracellularly also.
As the extracellular matrix consists of proteins,polysaccharides and nucleic
acids.
 Filamentous organism like actinomycetes, diptheroids like Cornybacterium
diptheriae and bacterionema and veillonella have ability to form intracellular
apatite crystals.
Mineralization spreads until matrix and bacteria are calcified.
Bacterial plaque may actively participate in mineralization of calculus by
forming phosphates which change the ph of plaque and induce mineralization.
pH of plaque is changed by first the normal booster mechanism
in which
1) CO2 present in the saliva.
II) The bacteria release ammonia from proteins present in
plaque which inrease pH of saliva ,makes it alkaline and hence
induce mineralization.
III)bacteria release phophatase which will break down
phosphoric acid into phosphates and these phosphates will
react with calcium and form calcium phophates and will get
deposited on tooth surface.
IV) esterase formed by bacteria break down fatty esters into
fatty acis which will form soap with calcium and magnesium
But bacteria are only passively involved are simply
calcified with other plaque components.
The occurence of calculus like deposits are also also
seen in germ free animals support this opinion. E.g
germ free mice
Germ free animals are those that have no
microorganisms living in them,They are raised in and
isolated and protected environment.
However other experiments suggest transmissible
factors are involved in calcification formation and that
penicillin in diets of some of these animals reduce
calculus formation.
ETIOLOGICAL SIGNIFICANCE

 Distinguishing between the effects of calculus and

plaque on the gingiva is difficult, because calculus is
always covered with a non mineralized layer of plaque.
A positive correlation between the presence of calculus
and the prevalence of gingivitis exists, but this
correlation is not as great as that between plaque and
gingivitis.
 The initiation of periodontal disease in young people is
closely related to plaque accumulation, whereas
calculus accumulation is more prevalent in chronic
periodontitis found in older adults.
The incidence of calculus, gingivitis, and periodontal
disease in creases with age. It is extremely rare to find
periodontal pockets in adults without at least some
subgingival calculus being present, al though the
subgingival calculus may be of microscopic
proportions.
 Calculus does not contribute directly to gingival
inflammation, but it provides a fixed nidus for the
continued accumulation of bac terial plaque and its
retention in close proximity to the gingiva.
Subgingival calculus is likely to be the product rather
than the cause of periodontal pockets. Plaque initiates
gingival inflammation, which leads to pocket
formation, and the pocket in turn provides a sheltered
area for plaque and bacterial accumulation.
 The increased flow of gingival crevicular fluid
associated with gingival inflamma tion provides the
minerals that mineralize the continually accumulat ing
plaque, resulting in the formation of subgingival
calculus. Aggressive periodontitis areas with
detectable subgingival calculus were much more
likely to experience a loss of periodontal attachment
than sites that did not initially exhibit subgingival
calculus.
 Although the bacterial plaque that coats the teeth is the
main etiologic factor in the development of periodontal
disease, the re moval of subgingival plaque and calculus
constitutes the corner stone of periodontal therapy.
Calculus plays an important role in maintaining and
accentuating periodontal disease by keeping plaque in
close contact with the gingival tissue and by creating
areas where plaque removal is impossible. Therefore,
the clinician must not only possess the clinical skill to
remove the plaque and calculus, but he or she must also
be very conscientious about performing this task.
Inhibition of Calculus Formation
Use of anti-calculus agents in
toothpastes,mouthrinses and chewing gums can
reduce thequantity and quality of calculus.
 However, as the effects of mouthrinses,
toothpaste and chewing gum are mostly less
limited to the supragingival area, such anti-tartar
agents have only been proven effective for the
control of supragingival calculus.
In order to have an inhibitory effect on the
formation of subgingival calculus, the anti-
calculus agents must be applied topically in
gingival pockets.
The efficacy of these agents for the control of
subgingival calculus is largely unknown.
Anti-calculus agents currently used include
triclosan, in combination with polyvinyl methyl
ether (PVM) and maleic acid (MA) co-polymer,
and crystal growth inhibitors such as
pyrophosphate with PVM ⁄ MA copolymer, zinc
As a broad-spectrum antimicrobial agent, triclosan
can prevent bacterial uptake of essential amino acids,
and, at higher concentrations, destroy the integrity of
the cytoplasmic membrane.
Triclosan also exerts both direct and indirect anti-
inflammatory effects. A number of clinical studies
have confirmed the anti-calculus efficacy of triclosan.
Pyrophosphate has been shown to reduce
crystal growth by binding to the crystal surface.
Moreover, pyrophosphate can impede the
conversion to hydroxyapatite and reduce pellicle
formation.
Pyrophosphate is susceptible to rapid
breakdown by phosphatases and
pyrophosphatases in the mouth, but this
The co-polymer also appears to have a weak effect on
the crystal growth . Pyrophosphate at various
concentrations in dentifrices, mouthrinses, chewing
gums and whitening strips has been shown to work as
an anti-calculus agent.
Significant reductions in calculus formation were also
achieved by use of polypyrophosphates, such as
hexametaphosphate, as advanced mineralization
inhibitors.
Phytate, which has structural similarities to
pyrophosphate, is capable of inhibiting the formation of
brushite and hydroxyapatite crystals in vitro and in
vivo.
CLINICAL ASSESSMENT OF CALCULUS

 The clinical assessment can be done by:

1. . Visual examination by use of compressed air:
- Small amount of unstained supragingival calculus are
frequently invisible when they are wet with saliva.
-Blowing air down the gingival crevice helps to detect
subgingival calculus deposits.
- Dark edge of calculus may be seen at or just beneath the
gingival margin.
2.Exploring:
-An explorer may be used when visual
examination is not definite.
-A fine subgingival explorer “TU-17” can detect
the subgingival calculus.
3. Probing:
-A fine calculus probe with light touch is used to
detect the subgingival calculus. While probing
for sulcus or pocket a rough subgingival tooth
surface can be felt when calculus is present.
Although there are other causes of roughness,
subgingival calculus is the most common.
 4 Radiographs:
-Although the calculus deposit is visible
on radiographs but is not always reliable
for diagnosis.
-Radiographs may be useful in diagnosis
of subgingival calculus.
-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
ADVANCE DIAGNOSTIC AIDS (Calculus Detection
Systems Only)
PERIOSCOPE–Fiberopticendoscopy-
basedtechnology34,35
DETECTAR – Spectro-optical technology
DIAGNODENT – Autofluorescence-based technology
Calculus Detection + Removal Systems
PERIOSCAN – Ultrasound technology
KEYLASER – Laser-based technology