Detailed information about the dental calculus regarding its composition, classification, clinical appearance, stages of formation, theory of mineralization and many descriptive clinical images and illustrations.

1. Dental calculus
Dr. Basma F. Alanbari
B.D.S , MS.c.(Periodontics)
Assistant lecturer
Al Rafidain Dental College

2. Dental calculus
• Dental Calculus is an adherent, calcified
deposit that forms on the surfaces of teeth and
dental appliances.
• dental plaque is the precursor of calculus
(which is mineralized plaque).
• Calculus iscovered with plaque on its surface.

3. Clinical appearance & distribution

4. Supragingival calculus
• recognized as , or even
mass of moderate hardness.
• the color may change as a result of the contact
with substances such as tobacco & food
pigments.

5. distribution
• predominantly found adjacent to the opening
of the excretion ducts of the major salivary
glands.
• Mostly on the facial surfaces of maxillary
molars & lingual surfaces of mandibular
molars.

6. The subgingival calculus
• to or even in color, hard in
consistency.
• Firmly attached to the tooth surface.
• More prelevant on the proximal surfaces and
lingual surfaces than on the buccal tooth
surfaces and it is found in most periodontal
pockets.

7. Enamel & dental calculus

8. Dentin & dental calculus

9. Cementum & dental calculus

12. Visual examination by use of
compressed air
• 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.

13. • 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.

14. 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 for a rough subgingival tooth
surface can be felt when calculus is present.

15. • Radiographs: The
deposits may also be
visible on radiographs
although this is not
always reliable.
• Clinical records: The
various indices for
recording and scoring
calculus.

16. 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.

17. Composition
• 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:
• Protein-polysaccharide complexes.
• Desquamated epithelial cells.
• Leukocytes.
• Various types of microorganisms.
• 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.

18. Calculus formation
• Calculus is mineralized dental plaque.
• The soft plaque is hardened by the precipitation of
mineral salts, which usually starts between the first and
fourteenth days of plaque formation.
• Saliva is the source of mineralization for supragingival
calculus, whereas the serum
transudate called
gingival crevicular fluid
furnishes the minerals for
subgingival calculus .
• Mineralization consists of crystal formation.

19. Four main crystal
1) Hydroxyapatite, approximately 58%.
2) Magnesium whitlockite, approximately 21%.
3) Octacalcium phosphate, approximately 21%.
4) Brushite, approximately 9%.
• 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.

20. Calculus formation
• Calculus formation continues until it reaches as a maximum, after
which it may be reduced in amount.
• The time required to reach the maximal level has been reported as
10 weeks, 18 weeks and 6 months.
• The decline from the maximal accumulation may be explained by
the susceptibility of bulky calculus to mechanical wear from food
and from cheeks, lips and tongue.

21. Mineralization theories
• Saliva is supersaturated solution with respect
to calcium & phosphate salts and thus it is able
to support crystal growth
• but spontaneous precipitation does not occur
unless the solution is seeded
• which mean by the presence of the crystal on
which a new crystal can form.

23. Bacterial theory
• microbial metabolic product local changes that
deposition of Ca. salts.
• Mineralization of plaque starts extracellularly around both g+ve
and g-ve 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.

24. 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.

25. Epitaxis theory
• Seeding agents theory: The carbohydrate –protein
complexes may initiate calcification by removing
calcium from the saliva and binding with it to form
nuclei that induce deposition of minerals.
• Seeding agents induce small foci of calcification that
enlarges and unites together to form calcified mass.

26. Why calcification occurring only at
specific site and does not occur at
others?

27. The Inhibition theory
• According to this theory this is because of the existence of an
inhibiting mechanism at non calcifying sites.
• Where calcification occurs, the inhibitor is apparently altered or
removed.
• Inhibiting substance is thought to be pyrophosphate .by chelating
CA its able to unhibit calcium phosphate deposition in plaque.
pyrophosphate inhibits calcification by preventing the initial nucleus
from growing, possibly by “poisoning” the growth centers of the
crystal.

28. heavy, light calculus formers &
noncalculus formers
• Heavy calculus formers have higher salivary
levels of calcium and phosphorus than do light
calculus formers.
• Light calculus formers have higher levels of
parotid pyrophosphate.

29. Attachment of dental calculus to the
tooth and implant surface
• Dental calculus generally adheres firmly to
tooth surfaces.
• thus, the removal of subgingival calculus may
be expected to be rather difficult.

30. The reason for this firm attachment to
the tooth surface is the fact that:
1) The pellicle beneath the bacterial plaque also
calcifies: This results in an intimate contact with
enamel , cementum or dentin crystals.
2) The surface irregularities are also penetrated by
calculus crystals and, hence, calculus is locked to the
tooth.
This is particularly the case
on exposed root cementum,
where small pits and irregularities
occur at the sites of the previous insertion
of Sharpey's fibers.

31. • 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.

32. Other local contributing factors

33. 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.

34. 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.
• Destruction of alveolar bone.
• Gingival recession.
• Periodontal abscess formation.
• Caries of the tooth.

35. 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.

36. 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.

37. d. Palatogingival groove
• The palatogingival groove often begins at the cingulum
and extends apically for a variable distance.
• Deep pocketing of maxillary incisors, especially isolated,
should prompt an examination for this plaque – retentive
root anomaly.
• 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 .

38. 2. Iatrogenic factors
• Inadequate dental procedures that contribute to
the deterioration of the periodontal tissues are
referred to as iatrogenic factors.

39. 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.
• 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.

40. • Overcontoured crowns and restorations tend 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.
• Overhanging margins:
(1) 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
(2) inhibiting the patient's access to remove
accumulated plaque.

41. b. Prosthesis
• Gross iatrogenic irritants such as poorly
designed clasps, prosthesis saddles and pontics
exert a direct traumatic influence upon
periodontal tissues.

42. c. 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.

43. d. 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.

44. 3. 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.

45. 4. Habits as contributing factors

46. • 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.

47. • 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.

48. b. 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.

49. 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.

50. c. Tobacco use
• Smoking is one
of the most
significant risk
factors currently
available to
predict the
development
and progression
of periodontitis.

51. 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.

52. Thanks