Periodontics I/Lecture3

Etiology of periodontal diseases

Dental Plaque

 Definition

It is an adherent intercellular matrix consisting primarily of proliferating microorganisms, along

with a scattering of epithelial cells, leukocytes and macrophages.

It can also be defined as the soft deposits that form the biofilm adhering to the tooth surface or
other hard surfaces in the oral cavity, including removable and fixed restorations. Dental Plaque is a
host-associated biofilm.

 Types Of Dental Plaque

Based on its relationship to the gingival margin, plaque is differentiated into two categories,
supragingival and subgingival plaque.

Supragingival plaque is further differentiated into:

Coronal plaque, which is in contact with only the tooth surface, and Marginal plaque, which is
associated with the tooth surface at the gingival margin.

Subgingival plaque can be further differentiated into:

 Attached plaque (can be tooth, epithelium and/or connective tissue associated)

 Unattached plaque

 Supragingival plaque

It can be detected clinically only after it has reached a certain thickness. Small amounts of plaque
can be visualized by using disclosing agents. The color varies from grey to yellowish-grey to yellow.
The rate of formation and location of plaque vary among individuals and is influenced by diet, age,
salivary factors, oral hygiene, tooth alignment, systemic diseases and host factors.

 Subgingival plaque

It is usually thin, contained within the gingival sulci or periodontal pocket and thus cannot be
detected by direct observation. Its presence can be identified only by running the end of probe around
gingival margin.

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 Differences between supragingival and subgingival plaque
Supragingival plaque Subgingival plaque
1. Matrix 50% Matrix Little or no matrix
2. Flora Mostly Gram-positive Mostly Gram-negative
3. Motile bacteria Few Common
4. Anaerobic/Aerobic Aerobic unless thick Highly anaerobic areas present
5. Metabolism Predominantly carbohydrates Predominantly proteins

 Tooth-associated Subgingival Plaque

The structure is similar to the supragingival plaque. The flora is dominated by Gram-positive cocci,
rods, filamentous bacteria and some/few Gram-negative cocci and rods. This flora is associated with
calculus formation, root caries and root resorption.

 Epithelium-associated Subgingival plaque

This type of plaque is loosely adherent because it lacks the interbacterial matrix and is in direct
association with the gingival epithelium, extending from the gingival margin to the junctional
epithelium. This plaque predominantly contains Gram-negative rods and cocci, as well as a large
number of flagellated bacteria and Spirochetes.

Characteristic of subgingival plaque

No. Tooth-associated subgingival plaque Epithelium-associated plaque
1. Gram-positive bacteria predominates Gram-positive and gram-negative bacteria.
2. Does not extend to junctional epithelium Extends to junctional epithelium.
3. May penetrate cementum May penetrate epithelium and connective tissue.
4. Associated with calculus formation and Associated with gingivitis and periodontitis.
root caries

 Connective Tissue-associated Plaque

It is usually demonstrated in ANUG and localized aggressive periodontitis patients. The clinical
significance is unclear.

The unattached plaque can be seen anywhere. Thus, the tooth-associated subgingival plaque is
most important in calculus formation, root caries and slowly progressive periodontal destruction,
whereas unattached bacterial components are associated with rapid periodontal destruction.

 Composition Of Dental Plaque

Bacteria + Intercellular matrix = Dental plaque

Bacteria make up approximately 70 to 80 percent of total material. One mg of dental plaque is estimated
to contain 250 million bacteria. Other than bacteria, mycoplasma, fungi, protozoa and viruses may be

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present. The material among the bacteria in dental plaque is termed as intermicrobial/cellular matrix. It
contains organic and inorganic portion. The organic matrix is composed of protein-polysaccharide
complex produced by microorganisms. Carbohydrates in the form of levans (fructans) provide mainly
energy while glucans (dextran) provide not only energy, but also act as the organic skeleton of plaque.
Other carbohydrates are galactose and rhamnose. Glycoproteins provide the protein component and
small amounts of lipids are also present. Inorganic components include, primarily calcium, phosphorus
with small amounts of magnesium, potassium and sodium.

 Formation/Development Of Dental Plaque

Pellicle is the initial organic structure that forms on the surfaces of the teeth and artificial
prosthesis. The first stage in pellicle formation involves adsorption of salivary proteins to apatite
surface. This result from the electrostatic ionic interaction between hydroxyapatite surfaces which has
negatively charged phosphate groups that interacts with opposite charged groups in the salivary
macromolecules.
The mean pellicle thickness varies from 100 nm at 2 hours to 500 to 1,000 nm.

The transition from pellicle to dental plaque is extremely rapid. The first components include mainly
cocci with small number of epithelial cells and PMNL's, they form a monolayer within a few hours, and
the attached bacteria proliferate and form small colonies of cocci. With time other types of
microorganisms proliferate and form different micro colonies.

Hence, in dental plaque development, two adhesion processes are required. First, bacteria must
adhere to the pellicle surface and become sufficiently attached to withstand oral cleansing forces.
Second, they must grow and adhere to each other to allow plaque accumulation.

 Growth and Accumulation of Bacteria

Once the bacteria are adhered to the pellicle, subsequent growth leads to bacterial accumulation
and increased plaque mass. Dental plaque growth depends on:

a. Growth via adhesion of new bacteria

b. Growth via multiplication of attached bacteria

The initial bacteria that colonize the pellicle surface are mostly gram-positive facultative
microorganisms such as Actinomyces viscosus and Streptococcus sanguis, as the plaque matures
secondary colonization of Prevotella intermedia, Capnocytophaga, Porphyromonas gingivalis takes
place. This ability of bacteria to adhere to different species and genera of microorganisms is known as
co aggregation.

 Clinical Significance Of Plaque

The microbial aggregation on the tooth surface if prevented from maturing may become
compatible with gingival health. Supragingival plaque if allowed to grow and mature may induce

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gingivitis and can lead to the formation of a microenvironment that permits the development of
subgingival plaque. Therefore, supragingival plaque strongly influences the growth, accumulation and
pathologic potential of subgingival plaque, especially in the early stages of gingivitis and periodontitis.

Subgingival plaque

In association with the presence of supragingival plaque, there are inflammatory changes that
modify the anatomic relationships of the gingival margin and tooth surface.
This result in enlarged gingiva which increases the space for bacterial colonization and also protects
bacteria from normal cleansing mechanisms.
They derive nutrients from gingival crevicular fluid. Many of these microorganisms lack the adherence
ability and utilize supragingival plaque bacteria as a means of colonization of the subgingival area.

 What Makes Plaque Pathogenic?

The following are the possible pathogenic mechanisms by which the plaque microorganisms can
cause periodontal disease.

a. Physical nature of plaque.

b. Invasion of tissue by bacteria.
c. Release of toxic and inflammatory substances.
d. Role of bacterial specificity.

Calculus

 Definition
Dental calculus is an adherent, calcified or calcifying mass that forms on the surface of teeth and
dental appliances. It is covered on its external surface by vital, tightly adherent, nonmineralized
plaque.

 Types
Depending upon the position of calculus in relation to the marginal gingiva it is classified as:
1. Supragingival calculus.
2. Subgingival calculus

 Supragingival calculus
It is tightly adherent calcified deposit that forms on the clinical crowns of the teeth above the free
gingival margin. Hence, it is clinically visible. It is also called as salivary calculus because it
forms from the saliva.

 Subgingival Calculus
As the name implies, it is that calcified deposit that is formed on the root surfaces below the free

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 marginal gingiva. It is believed to be formed from the gingival exudate and hence called serumal
calculus.

 Structure
The deposits of supragingival calculus are usually whitish-yellow in color and can get stained by
tobacco or food pigments, consistency is hard and clay-like. Since they derive the mineral salts
from salivary secretions, they are most abundant on the lingual surfaces of lower anterior teeth,
opposite Wharton's duct and Bartholin's duct and buccal aspects of maxillary molars opposite the
Stenson's duct.
Subgingival calculus is usually dark-brown or greenish-black in color and the deposits are firmly
attached to the tooth surface. Since they are hard and firm, it cannot be removed easily. Unlike
supragingival calculus, subgingival calculus can be found on any root surface with a periodontal
pocket. Morphologically, it can appear in different forms, most commonly ring-like or ledge-like
formations crusty, spiny or nodular deposits. Less frequently it can be seen as finger-like and
fern-like formations.

 Composition
It consists of inorganic and organic components. Trace amounts of zinc, strontium, bromine,
copper, manganese, gold and aluminium are also seen. At least, two-thirds of inorganic
component is crystalline in structure. The main crystal forms are: Hydroxyapatite, Mangnesium
whitlockite, Octacalcium phosphate and Brushite.

 Organic components
Mixture of protein, lipids, polysaccharide complexes, desquamated epithelial cells, leukocytes
and various microorganisms. Carbohydrate (consists of glucose, galactose, rhamnose, and
mannose).

Differences between supragingival and subgingival calculus

Supragingival subgingival
Location Above the gingival margin Deposits present below the margins of the gingiva

Color White, yellow in color Brown or greenish-black

Source Derived from salivary secretions Formed from gingival exudates

Composition -More brushite and octacalcium phosphate -Conversely less brushite and octacalcium phosphate
-more magnesium whitlockite
-less magnesium whitlockite -They are absent
-Salivary proteins are present -Sodium content increases with the depth of the pocke
-Sodium content is lesser

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  Formation of calculus

Calculus is nothing but, dental plaque that has undergone mineralization. It is formed by the
precipitation of mineral salts, which can start between 1st and 14th day of plaque formation. In two days
plaque can be 50 percent mineralized and 60 to 90 percent gets mineralized in 12 days. Calcification
starts in separate foci on the inner surface of the plaque. These foci of mineralization gradually increase
in size and coalesce to form a solid mass of calculus.

Calculus formation continues until it reaches maximum levels in about 10 weeks and 6 months,
after which there is a decline in its formation, due to mechanical wear from food and from the lips,
cheeks and tongue. This decline is referred to as reversal phenomenon.

 Pathogenic Potential of Calculus in Periodontal Diseases

Before 1960s the belief was that calculus was the principle etiologic factor in periodontal
diseases. However, the current view is that the initial damage to the gingival margin in the periodontal
disease is due to the pathogenic effects of microorganisms in plaque. However, the effect could get more
pronounced by calculus accumulation because it further provides retention of more plaque
microorganisms.

Hence, there is no doubt that, the mineralized deposits can:

1) Bring the bacterial deposits more closely to the supporting structures.
2) Interfere with the local self-cleansing defense mechanisms.

Iatrogenic Factors

Faults in the dental restorations and prosthesis referred to as iatrogenic factors are common
causes of gingival inflammation and periodontal destruction.

 Faulty Restorations

Six characteristics of restorations are important from periodontal point of view:

1. Margins of restorations
2. Contours and overhanging dental restorations
3. Occlusion
4. Dental materials
5. Design of removable partial dentures
6. Restorative procedures themselves.

Biologic width: is defined as the dimension of the soft tissue, which is attached to the portion
of the tooth coronal to the crest of the alveolar bone. The biologic width is commonly stated to be
2.04 mm, which represents the sum of epithelial and connective tissue measurements. Hence,

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encroachment of the biologic width frequently leads to gingival inflammation, clinical loss of
attachment and bone loss.

1) Margins of restorations:
Subgingival restorations can contribute to periodontal diseases by:
- Providing ideal locations for the accumulation of plaque.
- Changing the ecological balance of the gingiva to one that favors the growth of the disease
associated organisms, at the expense of the health-associated organisms.
- It was also demonstrated that subgingival restorations are plaque retentive areas that are
inaccessible to scaling instruments, hence greater chance of severe gingivitis and deeper pockets.

2) Contour of restoration/artificial crowns:

Over-contoured or improperly-contoured restorations tend to accumulate plaque and possibly
prevent the self-cleansing mechanisms of the adjacent cheek, lips and tongue. Proper contours of
the artificial crown are necessary for maintaining gingival health. Overhanging dental restoration
has been considered to be a contributing factor to gingivitis and possible periodontal attachment
loss. Many authors have demonstrated radiographic bone loss adjacent to posterior teeth with
overhanging restorations. The placement of the subgingival overhangs result in the changes in
the associated micro flora to that of one resembling the flora seen in chronic periodontitis. Hence
overhangs not only increase plaque mass but also increase the specific periodontal pathogens in
the plaque.

3) Occlusion:
poorly-constructed restoration will cause occlusal disharmonies that may be injurious to the
supporting normal periodontal tissues. This type of tissue injury is called (primary trauma from
the occlusion). Some of the examples are:
- Insertion of a high filling.
- Insertion of prosthesis, replacement that creates excessive forces on abutment or
antagonistic teeth.
- The drifting movement or extrusion of the teeth into spaces created by unreplaced
missing teeth.
- The orthodontic movement of teeth into functionally unacceptable position.

4) Dental materials:
In general, restorative materials are not by themselves injurious to the periodontal tissues.
It is the rough, unpolished surfaces that favor plaque accumulation and contributes to periodontal
diseases. Compared to all restorative materials that are available to the clinician, glass ionomer
restorations and porcelain seems to retain less plaque and thus are more acceptable from the

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 periodontal point of view. Fluoride constantly leaking from the glass ionomer cement prevents
the attachment of the bacteria to the pellicle and it also interferes with the metabolism and
growth of bacteria, whereas highly-polished surface of porcelain inhibits plaque formation and
permits its rapid removal too.

5) Design of removable partial dentures:

Several studies have shown that after the insertion of partial dentures, there is an increase in the
mobility of the abutment teeth within gingival inflammation and periodontal pocket formation.
This is due to the increased plaque accumulation. The presence of removable partial dentures not
only induces quantitative changes in plaque, but also qualitative changes by promoting the
development of most pathogenic bacteria. Hence, from periodontal point of view, fixed
prosthesis is more acceptable than the removable one.

6) Restorative procedures themselves:

It is can also cause destruction of periodontium. The use of the rubber dam clamps, copper
bands, matrix bands and disks in such a manner as to lacerate the gingiva, results in the varying
degrees of gingival inflammation.

 Periodontal Problems Associated with Orthodontic Therapy:

Orthodontic therapy may affect the periodontium by:
1) Favoring plaque retention and also modifying the gingival ecosystem.
2) Directly injuring the gingiva as a result of overextended bands which may also lead to forceful
detachment of gingiva from tooth causing gingival recession.
3) Creating excessive and/or unfavorable forces on the supporting tooth structures causes
necrosis of the periodontal ligament and adjacent alveolar bone; excessive forces also increase
the risk of apical root resorption.

Stains

Pigmented deposits on tooth surface are called stains. Dental stains may lead to tissue irritation
by creating a rough tooth surface, which contributes to plaque accumulation and retention.

Discoloration of teeth can occur in three different ways:

 Stains adhering directly to tooth surface.

 Stains contained within the calculus and soft deposits.
 Stains incorporated within the tooth structure or restorative material.

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 Classification of Stains
Based on location
1. Extrinsic stains: They occur on the external surface of the tooth and may be removed by
procedures like tooth-brushing, scaling and/or polishing.
2. Intrinsic stains: They occur within the tooth substance and cannot be removed by scaling and
polishing.

Based on source

1. Exogenous: They develop or originate from sources outside the tooth. They are may be extrinsic
and stay on the outer surface of tooth or intrinsic and become incorporated within the tooth.
2. Endogenous: They develop or originate from within the tooth. They are always intrinsic and
usually are discolorations of dentin reflected through enamel.

 Extrinsic stains
1. Brown stain: it is seen as thin, translucent, acquired, usually bacteria free, pigmented pellicle. It
is seen in individuals who do not brush adequately or who use dentifrice with inadequate
cleansing action. It is commonly seen on the buccal surface of maxillary molars and lingual
surface of mandibular anterior teeth. The brown color is due to presence tannin.

2. Tobacco stain: it is seen as tenacious dark brown or black deposit accompanied by brown
discoloration of tooth substance. It is commonly seen on the lingual surfaces of teeth. Staining
result from coal tar combustion products and from penetration of pits and fissures, enamel and
dentin by tobacco by-products. The degree of staining is not necessarily proportional to amount
of tobacco consumed, but depends to a considerable degree on pre-existent acquired coatings.

3. Black stain: it occurs as a thin black line on the facial and lingual surfaces of teeth along the
gingival margin and as diffuse patches on proximal surfaces. It is firmly attached and tends to
recur after removal. It is seen more common in women, children and individuals with excellent
oral hygiene. It is caused by chromogenic bacteria namely actinomyces species, prevotella
melaninogenicus.

4. Green stain: Green or greenish yellow stain is commonly seen in children. It is considered to be
stained remnants of enamel cuticle. It is commonly seen on gingival half of maxillary anterior
teeth. It is more frequent in boys (65%) than girls (63%).it is caused by fluorescent bacteria and
fungi.

5. Orange stain: It is seen on both facial and lingual surfaces of anterior teeth. It is caused by
chromogenic bacteria: Serratia marcescens and Flavobacterium.

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6. Metallic stains: Metallic stains are caused by incorporation of metals and metallic salts and their
products into acquired coatings. It is seen in industrial workers due to inhalation of metal
containing dust. Commonly seen are copper stains seen as green stain; iron dust cause brown
stain, manganese cause black stain , mercury cause greenish black stain, nickel causes green
stain and silver causes black stains.

7. Chlorhexidine stains: Brown color staining of teeth and tongue has been noted following the use
of chlorhexidine mouth rinse. Intensity of staining does not depend on concentration of
chlorhexidine rinse.

Following mechanisms have been suggested to cause staining:

 Degradation of chlorhexidine resulting in the formation of parachloraniline
 Catalysis of browning reaction of carbohydrates and amino acids by chlorhexidine
 Denaturation of proteins resulting in the formation of sulphides
 Precipitation of anionic dietary chromogens.

 Intrinsic Stains

Stains that occur within the tooth can be caused by:

Exogenous sources

1. Restorative materials
 Silver amalgam imparts grayish hue to the tooth
 Copper amalgam produces bluish-green color
2. Drugs
 Stannous fluoride produces brown stain
 Ammonical silver nitrate produces dark brown to black stain.

Endogenous sources

Example: Nonvital tooth

 Tetracycline administration during various stages of tooth development

 Developmental anomalies namely amelogenesis imperfect, dentinogenesis
imperfect
 Enamel hypoplasia
 Dental fluorosis
 Erythroblastosis fetalis.

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 Malocclusion

Depending on its nature, malocclusion exerts varied effect on the etiology of gingivitis and periodontal
diseases

1) Irregular alignment of teeth: Makes plaque control difficult.

2) Spacing between teeth: Same sequelae following loss of proximal contact can occur.
3) Facially-displaced teeth: Can lead to gingival recession.
4) Occlusal disharmony: Results in injury to periodontium.
5) Deep bite: Inflammation of palatal mucosa.
6) Open bite: Leads to accumulation of plaque and periodontal atrophy.

Habits

1) Mouth breathing:
It leads to localized gingival inflammation that is usually confined to the labial gingiva of the
maxillary anterior teeth. The tissue becomes reddened and swollen and it bleeds easily. The
surface of the gingiva is shiny. Gingival change associated with mouth breathing are:
A. Localized gingival inflammation in the maxillary anterior region.
B. Crowding of teeth with gingivitis.

2) Tongue thrusting:
It is the persistent, forceful wedging of the tongue against the teeth. Instead of the dorsum of the
tongue being placed against the palate with the tip behind the maxillary teeth during swallowing,
the tongue is thrust forward against the anterior teeth.
Tongue thrusting causes excessive lateral pressure, which may be traumatic to the periodontium.
It also causes spreading and tilting of the anterior teeth.
Numerous secondary sequelae may develop from tongue thrusting. They include, change in
direction of the functional forces so that lateral pressure against the crowns is increased.
Also interferes with food excursion and favors the accumulation of the food debris at the
gingival margin. Tongue thrusting is an important contributing factor in the pathologic tooth
migration.

3) Use of tobacco:
The following oral changes may occur in the smokers:
1. Brownish, tar-like deposits and discoloration of tooth structure. (Due to the nicotine and its
major metabolite, cotinine are deposited on the root surfaces).
2. Diffuse grayish discoloration and leukoplakia of the gingiva may occur.
3. "Smokers palate" (nicotinic stomatitis), characterized by prominent mucous glands with
inflammation of the orifices and a diffuse erythema.
4. Predisposition to acute necrotizing ulcerative gingivitis.

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5. Delayed postsurgical healing.
6. Marked increase in gingival crevicular fluid flow.
7. More severe gingivitis and periodontitis have been reported in smokers. Special type of
gingivitis, termed gingivitis toxica characterized by destruction of the gingiva and alveolar bone
has been attributed to the chewing of tobacco.
8. Oral polymorphonuclear cells from smokers show reduced ability to phagocytose particles.

4) Toothbrush trauma:
Acute or chronic gingival changes.
Acute changes are:
1. Sloughing of the epithelial surface occurs along with denudation of the underlying connective
tissue to form a painful gingival bruise.
2. Punctuate lesions are produced by the penetration of the gingiva by the toothbrush bristles.
3. Painful vesicle formation in the traumatized areas is also seen.
4. Diffuse erythema and denudation of the attached gingiva throughout the mouth may be the
striking sequelae of the overzealous brushing. The acute gingival changes noted can commonly
occur when the patient uses a new brush.
5. Tooth bristles forcibly embedded and retained in the gingiva are common cause of the acute
gingival abscess.

Chronic toothbrush trauma results in:

1. Gingival recession with denudation of root surface

2. Often the gingival margin is enlarged and appears to be ''piled up'', as if it were molded in
conformity with the strokes of the toothbrush.

5) Bruxism:
Is clenching or grinding of the teeth when the individual is not chewing or swallowing. It has
been estimated that during clenching or grinding the individual might impose a load of over 20
kg on a tooth over a period of 2.5 seconds each time. This is far in excess of normal functional
stresses and cause increased flow within the viscoelastic periodontal ligament and distortion of
alveolar bone. It also causes attrition of teeth.

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