Dental calculus, or tartar, is a hardened deposit that forms on teeth. It begins as dental plaque, which mineralizes on the tooth surface. Calculus forms in two locations: supragingival calculus forms above the gumline and is whitish in color, while subgingival calculus forms below the gumline and is dark in color. Several factors influence calculus formation, including saliva composition and bacterial activity. Calculus promotes the retention of dental plaque and can contribute to periodontal disease if not removed.

1. LECTURE NOTES ON ORAL BIOLOGY 2
CALCULUS
BY: DR. CHLOE MARIANELLI M. HERNANDO
DENTAL CALCULUS
▪ Is an adherent, calcified deposit that forms on the surfaces of teeth and dental
appliances, PROSTHSESIS
▪ A hard deposit that is formed by mineralization of dental plaque on the surface of
natural teeth and dental prosthesis, generally covered by unmineralized plaque.
▪ Dental plaque is the precursor of calculus (which is mineralized plaque).
▪ Calculus is covered with plaque on its surface.
▪ Both plaque and calculus are formed on non-shedding surfaces.
▪ We don’t see calculus formation on the gingiva and buccal mucosa because these are
the shedding surfaces and the epithelium undergoes constant shedding unlike areas of
restoration and prosthesis which facilitate plaque and calcular formation.
▪ Calcis- lime stone
▪ Also known as “Odontolithiasis/ Fossilized Plaque”
▪ Commonly known as “tartar”
▪ For 5000 years, Calculus was termed as the primary ecological factor for the initiation
and progression of periodontal disease but later on studies which was done by low at all
through the experimental model of gingivitis it showed that it was not the calculus but
the plaque which was responsible for the occurrence of gingivitis.
▪ Hippocrates- he has written about the association of dental calculus with oral diseases
▪ Albucacis- who basically used certain instruments to remove the dental calculus and he
saw that once the dental calculus was removed by these instruments the oral diseases
subsided
CLASSIFICATION
1. According to Location
a. Supragingival Calculus
▪ Is the tightly adherent calcified deposit that forms on the clinical crown of
the teeth above the free gingival margins.
▪ It is clinically visible.
▪ It is also called “salivary calculus” because it forms from the saliva
▪ Usually whitish yellow in colour and can stained by tobacco or food
pigments.
▪ Its consistency is hard and clay like.
b. Subgingival Calculus
▪ Is a calcified deposit that is formed on the root surface below the free
marginal gingiva.
▪ It is believed to be formed from the gingival exudate and hence called
“serumal calculus” .

2. ▪ Is dark brown or greenish black in color and the deposit are firmly attach to
the teeth surface.
▪ These are firm and hard and cannot be removed easily.
▪ There are found on any root surface with a periodontal pocket.
JOURNAL:
● The distribution of different morphologic types of subgingival calculus on each division
of the mesial and distal proximal root surfaces was evaluated with a magnifier.
● Results: Regardless of the morphologic type, calculus deposits were observed at around
30% of proximal root surfaces. The coronal thirds of the root surfaces were found to
have significantly more calculus deposits than the middle thirds (P < .05). In general, it
was observed that most of the deposits were of the thin, smooth veneer type on all root
surfaces.
● Conclusion: Within the limits of this study, the distribution of various calculus types was
similar on different parts of the root surface; however, calculus was found more
frequently on the coronal thirds than on the more apical regions.
1 = crusty, spiny, or nodular
2 = ledge or ring
3 = thin, smooth veneers
4 = finger- or fernlike
5 = individual calculus islands/spots
6 = supramarginal upon submarginal deposits

3. ASSESSMENT AND EVALUATION
1. VISUAL EXAMINATION
Supragingival calculus is usually recognized by direct vision
▪ Small amount of supragingival calculus that have not been stained are frequently
invisible when they are wet with saliva.
Subgingival calculus deposits can sometimes be detected visually by blowing air
down the gingival crevice.
▪ Dark edge of calculus may be seen at or just beneath the gingival margin due to
its dark color that shine from through the thin gingival margin.
2. PROBING
▪ A periodontal probe is needed that can be adapted close to the root surface all
the way to the bottom of a pocket.
▪ While probing, a rough subgingival tooth surface can be felt when calculus is
present.
3. RADIOGRAPHS- The deposits may also be visible on radiographs although this is not
always reliable.
4. CLINICAL RECORDS- The various indices for recording and scoring calculus.
THE HARMFUL EFFECT
The primary effect of calculus is not due to mechanical irritation (as was originally thought)
but is related to its always being covered by bacteria and play a major role in P.D. disease by
keeping the plaque in close contact with the gingival tissue and creating areas where plaque
removal is impossible.
COMPOSITION

4. ▪ 70-90% inorganic salts.
▪ 75.9% of it is in crystalline form.
▪ Calcium & phosphorus constitute the major elements.
▪ The organic portion of calculus consists mainly of:
a. Protein-polysaccharide complexes.
b. Desquamated epithelial cells.
c. Leukocytes.
d. Various types of microorganisms.
e. while lipids account for only a minor fraction.
▪ NB: Bacterial content: At periphery – Gram-negative rods and cocci predominate.
Filamentous organisms, Diphtheroids, Bacterionema and Veillonella species are also
present.
▪ Generally two or more crystal forms occur in a calculus sample, with hydroxyapatite
and Octacalcium phosphate being the most common.
▪ Brushite is more common in the mandibular anterior region and magnesium whitlockite
in the posterior areas.
2. According to Mineralization
a. Salivary Calculus- supragingival calculus because it is exposed to the saliva is
mineralized through saliva.
b. Seruminal Calculus- is not exposed to saliva and it is exposed to the subgingival
exudates like gcf and other components of subgingival exudates so this is termed as
the seruminal calculus
3. Based on accumulation and formation of calculus
a. Non- Calculus Formers
b. Slight Calculus Formers- have higher levels of parotid pyrophosphate.
c. Moderate Calculus Formers
d. Heavy Calculus Formers- have higher salivary levels of calcium and phosphorus than
do light calculus formers.

5. CALCULUS FORMATION
• Calculus formation continues until it reaches maximum levels in about 10 weeks and 6
months, after which there is decline in its formation due to mechanical wear from food
and from lips, cheeks and tongue.
• This decline is referred to as “reversal phenomenon”.
• Calculus formation occurs in what three basic steps:
a. Pellicle formation.
b. Biofilm formation (maturation)
c. Mineralization.
THEORIES OF CALCULUS FORMATION
Calculus formation is the result of petrification of dental plaque biofilm, with mineral ions
provided by bathing saliva or crevicular fluids. Supragingival calculus formation can be
controlled by chemical mineralization inhibitors, applied in toothpastes or mouthrinses.
1. BOOSTER MECHANISM
▪ Used to increase the signal so in similar lines there are certain agents which
boost the signal strength which further causes calcification mechanism
▪ Can be further divided into 3 mechanisms:
a. First one is associated with carbon dioxide
 inside the oral cavity there are certain salivary ducts which releases the
saliva inside the oral cavity and the saliva which is produced by the
salivary ducts will have high carbon dioxide tension so the pressure of
carbon dioxide released from these ducts are somewhere between 54 to
65 MMHG whereas in the atmosphere this pressure of carbon dioxide is
0.3 MmhG so in the atmosphere the pressure is far less as compared to
the one which is present in the saliva so automatically what happens is
that the carbon dioxide from the oral cavity is dissipated into the
atmosphere. now once this happens the pH of the saliva is automatically
increased that means the saliva inside the mouth becomes alkaline in
nature and this further causes the dissociation of the acids which are
present so the acid such as the phosphoric acid dissociation occurs and it
releases or it causes the formation of the secondary and the tertiary
phosphate ions. Now these phosphate ions act as a booster mechanism
and causes the precipitation of the calcium and phosphate crystals so
these crystals precipitate and directly they get deposited onto the tooth
office or onto the plug and further causes plaque calcification/ calculus
formation.
b. Second is associated with the colloidal proteins from the saliva
 involves the colloidal proteins in the saliva so again the saliva inside the
mouth will contain certain colloidal proteins now these colloidal proteins
have a tendency to bind with the calcium and the phosphate ions and
once these binding occurs it forms a super saturated solution now what

6. do we understand when we say super saturated solution so let's take a
quick example if we have a glass of water and we add salt to it and we
mix it then obviously the salt will get dissolved inside the water now if we
keep adding salt to the water there will be a stage when the water will
get super saturated and there will be precipitation of the salt crystals at
the bottom of the glass so similarly even the saliva will become super
saturated which results in the precipitation of calcium and phosphate
crystals and where exactly are these crystals settling down? right onto
the tooth surface and again the plaque is getting calcified forming the
dental calculus
c. Third is associated with the proteins produced by the bacteria
 This is through the precipitation of proteins from the plaque sample now
according to this theory these proteins will now breakdown into amino
acids and the leftover amino acids will then produce ammonia now when
ammonia formation occurs then automatically the pH of the saliva is
increased so again the saliva is becoming more alkaline in nature and this
further again causes the precipitation of the calcium and the phosphate
crystals thus increasing calcification of plaque formation.
2. BACTERIOLOGICAL THEORY
▪ Certain bacteria such as prevotella intermedia and fusobacterium nucleatum
have seen to produce ammonia itself
▪ This ammonia will again cause increase in the pH of the saliva causing the saliva
to become more alkaline and further causing the precipitation of the salts
leading to mental calculus formation
▪ This theory is not really accepted because of the fact that calculus formation is
seen even in germ free organisms so this theory is not really accepted.
3. EPITACTIC CONCEPT
▪ According to this concept, seeding agents induce small foci of calcification. These
foci enlarge and coalesce to form calculus.
▪ The seeding agents in calculus are not clearly known, but suspected agents could
be intercellular matrix of plaque, carbohydrate-protein complex and plaque
bacteria.
▪ Epic tactic refers to the crystal growth or the mineral deposition that takes place
▪ In this we need to understand that the saliva consists of the calcium and
phosphate crystals whereas on the tooth surface there is formation of dental
plaque which further contain the proteins and the carbohydrate complexes
▪ Now according to the epic tactic theory the calcium and phosphate crystals are
not enough to precipitate over the dental plaque so instead what happens is
they promote the growth of the hydroxy appetite crystals on to the proteins and
the carbohydrate complexes on the dental plaque so these proteins and
carbohydrates act as a seeding agent to promote the hydroxy appetite crystal

7. formation so these hydroxy apatite crystals first form small foci of calcification
and these slowly get enlarged and they collapse with each other to form a big
calculus mask and this process is termed as the heterogeneous nucleation
process
▪ In the epic tactic theory there is precipitation of the hydroxy apatite crystals to
form a calcified mass and what is the seeding agent it is the proteins and the
carbohydrates of the dental plaque which act as a seeding agent and promote
this nucleation process
4. INHIBITION THEORY
▪ This theory consider the possibility of calcification occurring only at special site
because there exist an inhibiting mechanism at non-calcifying sites.
▪ Wherever calcification occur the inhibitor is either altered or removed.
▪ One such inhibiting agent could be polysulphate, which prevent the initial
nucleus from growing by possibility ‘poisoning’ the growth center of crystal
▪ If we see dental calculus in the oral cavity obviously it is not uniform so there are
certain areas where the calculus formation is more and there are certain areas
where the calculus formation is very less. Why is there this discrepancy?
▪ Now this is because of the inhibition theory
▪ According to this theory, the areas where the calculus formation is seen in those
areas the inhibitory agents are either removed or they are altered by these
inhibitory agents like the pyrophosphates, POLYSULPHATES, which are present
in the saliva.
▪ So these pyrophosphates basically chelates the calcium that means they remove
the calcium and further prevent the crystal growth so when calcium does not get
deposited on the dental plaque obviously plaque is not going to get calcified so it
prevents the crystal growth so basically what are they doing they're poisoning
the growth centers, thus the term inhibition.
5. TRANSFORMATION THEORY- it states that there are presence of certain non crystal
deposits inside the saliva further gets transformed to form the Octa calcium phosphate
and the hydroxyapatite crystals so this is the transformation theory wherein non crystal
deposits are forming the important hydroxy appetite and the octane calcium phosphate
crystals.

8. 6. ENZYMATIC THEORY- Certain enzymes like esterases are either produced by the
bacteria or they can be produced by the host as well and this esterases is further
capable of hydrolyzing the fatty esters to form the free fatty acids
ATTACHMENT OF DENTAL CALCULUS TO THE TOOTH AND IMPLANT SURFACE
▪ Although some irregularities may also be encountered on oral implant surfaces.
▪ the attachment to commercially pure titanium generally is less intimate than to
root surface structures.
▪ This in turn, would mean that calculus may be chipped off from oral implants
without detriment to the implant surface.
LOCAL CONTRIBUTING FACTORS
1. ANATOMIC FACTORS
a. 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.

9. SEQUELAE OF FOOD IMPACTION
✓ Feeling of pressure and the urge to dig the material from between the teeth.
✓ Vague pain which radiates deep in the jaws.
✓ Gingival inflammation with bleeding and a foul taste in the involved area.
✓ Varying degree of inflammatory involvement of the periodontal ligament with an
associated elevation of the tooth in its socket, prematurity in functional contact and
sensitivity to percussion.
b. Cervical enamel projection (CEP) and enamel pearls:
▪ They appear as narrow wedge-shaped extensions of enamel pointing from the
cementoenamel junction (CEJ) toward the furcation area.
▪ The clinical significance of CEPs is that they are plaque retentive and can
predispose to furcation involvement.
c. Intermediate bifurcation ridge:
▪ The intermediate bifurcation ridge is a convex outgrowth of cementum that runs
longitudinally between the mesial and distal roots of a mandibular molar.
▪ These ridges are found more frequently on first molars.
▪ These irregular contours make plaque and calculus removal more difficult and
inadequate plaque and calculus removal can lead to failure of periodontal
treatment.

10. d. The palatogingival groove:
▪ Often begins at the cingulum and extends apically for a variable distance.
▪ If the palatogingival groove is associated with bone loss and attachment
loss, the clinician may attempt to remove the groove through
odontoplasty or to reduce its depth to minimize plaque retention .
2. IATROGENIC FACTORS
a. 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.
b. Overcontoured crowns and restorations - end to accumulate plaque and possibly
prevent the self- cleaning mechanisms of the adjacent cheek, lips, and tongue.
Restorations that fail to reestablish adequate interproximal embrasure spaces are
associated with papillary inflammation.
c. 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 facultative species) and inhibiting the patient's
access to remove accumulated plaque.
d. Prosthesis
▪ Gross iatrogenic irritants such as poorly designed clasps, prosthesis saddles
and pontics exert a direct traumatic influence upon periodontal tissues.
e. 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.
3. MALOCCLUSION
▪ 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.
4. HABITS
▪ The tooth surface, usually the root surface, can be abraded away by improper
toothbrushing technique, especially with a hard toothbrush.

11. ▪ 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.
a. 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.
b. 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.
c. Smoking- is one of the most significant risk factors currently available to
predict the development and progression of periodontitis.
d. 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.
REFERENCES
✓ CARRANZA’S CLINICAL PERIODONTOLOGY (11TH EDITION)
✓ ESSENTIALS OF CLINICAL PERIODONTOLOGY AND PERIODONTICS (SHANTIPRIYA REDDY)
(4TH EDITION)
✓ https://pubmed.ncbi.nlm.nih.gov/9395117/