 DENTAL CALCULUS IS A

MINERALIZED BACTERIAL PLAQUE

THAT FORMS ON SURFACES OF
NATURAL TEETH AND DENTAL
PROSTHESES
 SUPRAGINGIVAL CALCULUS

 SUBGINGIVAL CALCULUS
 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 claylike consistency, and easily detached
from the tooth surface
 After removal, it may rapidly recur, especially in
the lingual area of the mandibular incisors
LINGUAL TO LOWER ANTERIORS
OPPOSITE STENSON’S DUCT IN MAXILLARY FIRST
MOLAR AREA
WHITISH YELLOW COLOUR, HARD CLAY LIKE
CONSISTENCY
ABUNDANT CALCULUS CAUSING INFLAMMATION OF
GINGIVA
 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
 Clerehugh et al used a World Health
Organization #621 probe to detect and score
subgingival calculus
DARK BROWN COLOUR AND HARD CONSISTENCY
 The third National Health and Nutrition
Examination Survey (NHANES III) evaluated
9689 adults in the United States between 1988
and 1994. This survey revealed that 91.8% of the
subjects had detectable calculus and 55.1% had
subgingival calculus
 Both supragingival calculus and subgingival
calculus may be seen on radiographs.
 Highly calcified interproximal calculus deposits
are readily detectable as radioopaque projections
that protrude into the interdental space.
 The sensitivity level of calculus detection by
radiographs is low.
 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 radiographs.
 INORGANIC COMPONENTS (70% TO 90%)
 ORGANIC COMPONENTS

INORGANIC PORTION
 75.9% CALCIUM PHOSPHATE
 3.1% CALCIUM CARBONATE
 TRACES OF MAGNESIUM PHOSPHATE, AND OTHER
METALS.

THE PRINCIPAL INORGANIC COMPONENTS

 CALCIUM 39%
 PHOSPHORUS, 19%
 CARBON DIOXIDE, 1.9%
 MAGNESIUM, 0.8%
 TRACE AMOUNTS OF SODIUM, ZINC, STRONTIUM, BROMINE,
COPPER, MANGANESE, TUNGSTEN, GOLD, ALUMINUM,
SILICON, IRON, AND FLUORINE
 At least two thirds of the inorganic components are crystalline
in structure.

 Hydroxyapatite, approximately 58%

 Magnesium whitlockite, approximately 21%
 Octacalcium phosphate, approximately 12%
 Brushite, approximately 9%
Mixture of protein-polysaccharide complexes, desquamated
epithelial cells,leukocytes, and various types of microorganisms.

 Between 1.9% and 9.1% of the organic component is

carbohydrate which consists of galactose, glucose, rhamnose,
mannose, glucuronic acid, galactosamine, and sometimes
arabinose,galacturonic acid, and glucosamine.

 Salivary proteins account for 5.9% to 8.2% of the organic

component of calculus and include most amino acids.

 Lipids account for 0.2% of the organic content in the form of

neutral fats, free fatty acids, cholesterol, cholesterol esters and
phospholipids.
 SUPRAGINGIVAL SUBGINGIVAL
1. ABOVE GINGIVAL 1. BELOW GINGIVAL
MARGIN. MARGIN.
2. WHITISH YELLOW. 2. BROWN OR GREEN
3. SOURCE IS SALIVARY BLACK
SECRETIONS. 3. SOURCE IS GINGIVAL
4. MORE BRUSHITE, EXUDATE.
OCTACALCIUM 4. LESS BRUSHITE,
PHOSPHATE. OCTACALCIUM
5. LESS MAGNESIUM PHOSPHATE.
WHITLOCKITE. 5. MORE MAGNESIUM
6. SALIVARY PROTEINS WHITLOCKITE.
PRESENT. 6. SALIVARY PROTEINS
7. LESS SODIUM CONTENT. ABSENT.
7. HIGH SODIUM CONTENT.
1. By means of organic pellicle.

2. Mechanical interlocking into the surface irregularities

like resorption lacunae & caries.

3. Penetration of calculus bacteria into the cementum.

(Calculocementum)

4. Close adaptation of calculus undersurface depressions

to the unaltered cementum surface.
 The soft plaque is hardened by the precipitation of mineral salts,
which usually starts between the l st and 14th days of plaque formation.
However, calcification has been reported to occur in as little as 4 to 8
hours.
 Calcifying plaques may become 50 % mineralized in 2 days and 60%
to 90% mineralized in 12 days.
 All plaque does not necessarily undergo calcification.
 Early plaque contains a small amount of inorganic material, which
increases as the plaque develops into calculus. Plaque that does not
develop into calculus reaches a plateau of maximal mineral content
within 2 days.
 Microorganisms are not always essential in calculus formation
because calculus occurs readily in germ-free rodents.
 Saliva is the source of mineralization for supragingival calculus,
whereas the serum transudate called gingival crevicular fluid
furnishes the minerals for subgingival calculus.
 Plaque has the ability to concentrate calcium at 2 to 20 times its level
in saliva
 Calcification entails the binding of calcium ions to the carbohydrate
protein complexes of the organic matrix and the precipitation of
crystalline calcium phosphate salts.
 Crystals form initially in the intercellular matrix and on the bacterial
surfaces and finally within the bacteria.
 Calcification begins along the inner surface of the supragingival
plaque and in the attached component of subgingival plaque adjacent
to the tooth.
 Separate foci of calcification increase in size and coalesce to form
solid masses of calculus.
1. Mineral precipitation results from a local
rise in the degree of saturation of calcium
and phosphate ions by -
 BOOSTER MECHANISM: Local rise in pH causes precipitation of
calcium Po4. Release of ammonia, loss of carbon dioxide causes the former.

 COLLOIDAL PROTIENS In saliva settle due to stagnation. Calcium and

phosphate ions bind to the colloidal proteins, which settle down during
stagnation and precipitate calcium and phosphorous salts.

 PHOSPHATASES Hydrolyze organic phosphates. This increases the

concentration of Po4 ions. This causes precipitation of calcium phosphate
2. Seeding agents induce small foci of
calcification that enlarge and coalesce to
form a calcified mass
(EPITACTIC CONCEPT or HETEROGENEOUS
NUCLEATION)
 Mineralization of plaque starts extracellularly around both gram-positive
organisms and Gram negative organisms.

 It may also start intracellularly.

 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.

 Bacterial plaque may actively participate in the mineralization of calculus by

forming phosphatases, which changes the pH of the plaque and induces
mineralization
Periodontal disease is basically caused by bacterial plaque. The process is enhanced by
calculus in following manner

 BRINGS PLAQUE CLOSER TO SUPPORTING

STRUCTURES.

 INTERFERENCE WITH SELF CLEANSING

MECHANISM.

 INTERFERENCE WITH ORAL HYGIENE.

 While the bacterial plaque that coats the teeth is
the main etiologic factor in the development of
periodontal disease, the removal of subgingival
plaque and calculus constitute the cornerstone
of periodontal therapy.
 Materia alba is a concentration of microorganisms,desquamated
epithelial cells, leukocytes, and a mixtureof salivary proteins and
lipids, with few or no food particles, and it lacks the regular internal
pattern observed in plaque

Pigmented deposits on the tooth surface are called dental stains. Stains
are primarily an aesthetic problem and do not cause inflammation of
the gingiva.
- IATROGENIC FACTORS
- MARGINS OF RESTORATIONS
- CONTOURS AND OPEN CONTACTS
- MATERIALS
- DESIGN OF RPD’S
- RESTORATIVE PROCEDURES
- MALOCCLUSION
- PERIODONTAL COMPLICATIONS ASSOCIATED WITH
- ORTHODONTIC THERAPY
- PLAQUE RETENSION AND COMPOSITION
- GINGIVAL TRAUMA AND BONE HEIGHT
- TISSUE RESPONSE TO ORTHODONTIC FORCES
- EXTRACTION OF IMPACTED THIRD MOLARS
- HABITS AND SELF-INFLICTED INJURIES
- TOOTH BRUSH TRAUMA
- CHEMICAL IRRITATION
- TOBACCO USE
- RADIATION THERAPY
Inadequate dental procedures that contribute to the deterioration of the
periodontal tissues are referred to as iatrogenic factors.

 Margins of Restorations (location,overhangs,roughness)

 Contours/Open Contacts (overcontoured,undercontoured)
 Materials
 Design of Removable Partial Dentures
 Restorative Dentistry Procedures
 Overhanging margins of dental restorations contribute to the
development of periodontal disease by

 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)

 2) inhibiting the patient's access to remove accumulated plaque

 Roughness in the sub-gingival area is
considered to be a major contributing factor to
plaque build-up and subsequent gingival
inflammation.
 The subgingival zone is composed of the
margin of the restoration, the luting material,
and the prepared as well as the unprepared tooth
surface.
Sources of marginal roughness include-
 grooves and scratches in the surface of carefully

polished acrylic resin, porcelain, or gold

restorations, separation of the restoration margin and
luting material from the cervical finish line, thereby
exposing the rough surface of the prepared
tooth ,dissolution and disintegration of the luting
material between the preparation and the restoration,
leaving a space and inadequate marginal fit of the
restoration.
 Subgingival margins typically have a gap of 20 to
40 microns between the margin of the restoration
and the unprepared tooth. Colonization of this
gap by bacterial plaque undoubtedly contributes
to the detrimental effect of margins placed in a
subgingival environment.
 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.
 Food impaction is the forceful wedging of food
into the periodontium by occlusal forces.
 As the teeth wear down, their originally convex
proximal surfaces become flattened and the
wedging effect of the opposing cusp is exaggerated.
 Cusps that tend to forcibly wedge food into
interproximal embrasures are known as plunger
cusps.
 MATERIALS

 DESIGN OF RPDs

 RESTORATIVE DENTISTRY
PROCEDURES
Inflammed Gingiva assocoated
with Acrylic RPD
 Irregular alignment of teeth
 Failure to replace missing posterior teeth
 Tongue thrusting
 Mouth breathing
 Restorations that do not conform to the
occlusal pattern
Irregular alignment of
teeth causing recession
on the labial aspect of
mandibular incisor
Tongue thrust
and
periodontal
destruction
 Plaque Retention and Composition.
 Gingival Trauma and Alveolar Bone Height.
 Tissue Response to Orthodontic Forces.
Orthodontic therapy and periodontal
problems
Gingival trauma and
bone height
Tissue response to
orthodontic forces
Toothbrush trauma
and chemical injury
 Associated with the prevalence of necrotizing ulcerative gingivitis
(NUG) as early as 1947.

 smokers have greater attachment loss and bone loss, an increased

number of deep pockets and amount of calculus formation.

 However, smokers demonstrate varied levels of plaque and

inflammation with a bias toward decreased inflammation.

 A diminished response to nonsurgical therapy has been reported

for smokers.
 Smokers who were treated with surgical
periodontal therapy and subsequently followed
with maintenance care exhibited less probing
depth reduction, smaller gains in clinical
attachment levels, less gain in bone height than
nonsmokers.
 Heavy cigarette smoking decreases the amount of
root coverage obtainable with thick free gingival
grafts
 Smokers exhibit depressed numbers of helper T -lymphocytes, which are important
to stimulate B-cell function for antibody production.

 Neutrophils from smokers with refractory periodontitis exhibit impaired

phagocytosis,diminished chemotaxis,or both

 Nicotine has been shown to decrease gingival blood flow.

 Periodontal wound healing may be adversely affected by exposure to tobacco or

nicotine, which may impair revascularization
 Radiation therapy has cytotoxic effects on both normal cells and malignant
cells.

 Radiation treatment induces an obliterative endarteritis that results in soft

tissue ischemia and fibrosis while irradiated bone becomes hypovascular and
hypoxic.

 Dermatitis and mucositis of the irradiated area

 Xerostomia

 Periodontal attachment loss and tooth loss was greater in cancer patients who
were treated with high-dose unilateral radiation as compared with the
nonradiated control side of the dentition