Periodontal Exam Guide

Prepared & Designed by: Muhammed M. Nasser
(Student at College of Dentistry)
PERIODONTICS
4th
stage

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Contents
No. Lecture Page
1 Periodontal Examination and Diagnosis 2
2 Periodontal instruments 14
3 Terms in periodontology & Gingiva 27
4 Periodontal Ligament (PDL) 41
5 Cementum 48
6 Alveolar process (AP) 56
7 Dental Plaque Biofilm 65
8 Microbiologic Specificity of Periodontal Diseases 77
9 Pathogenesis of Periodontal Disease 86
10 Host-Parasite Interactions 96
11 Classification of Diseases and Conditions Affecting the
Periodontium (Part.1)
107
12 Classification of Diseases and Conditions Affecting the
Periodontium (Part.2)
122
13 Dental Calculus & Other Local Predisposing Factors 136
14 Dental Stain 143
15 The Treatment Plan (Part.1) 156
19 Oral halitosis 229
20 Risk Factors for Periodontal Diseases 237
21 Smoking and Periodontal diseases 247
22 Impact of periodontal infection on systemic health 256
23 Gingival & periodontal pocket 261

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1Periodontal Examination and Diagnosis
Proper diagnosis is essential to intelligent treatment.
Periodontal diagnosis should first determine whether disease is present then identify its type,
extent, duration, distribution and severity.
Periodontal diagnosis is determined after careful analysis of the case history and evaluation the
clinical signs and symptoms, as well as the result of various tests (probing, mobility assessment,
radiographs, blood test, and biopsies).
The following is a recommended sequence of procedures for the diagnosis of periodontal
diseases.
Overall Appraisal of the patient
This includes consideration of the patient’s mental, emotional status, attitude and physiologic
age.
Medical History
The importance of the medical history should be explained to the patients because patients omit
information that they cannot relate to their dental problems. The patient should be made aware
of:
1. The presence of conditions that may require special precautions or modifications in treatment
procedure.
2. The possible role that some systemic diseases, conditions, may play in the cause of
periodontal disease.
3. The possibility that oral infections may have a powerful influence on the occurrence and
severity of certain systemic disease.

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The Medical history should include reference to the following:
• Is the patient under the care of a physician, and if so what is the problem? Its duration and
nature.
• Details on hospitalization and operation including diagnosis, kind of operation, and
complications.
• Medical problem hematologic, endocrine, infectious, cardiovascular
• The medications taking with special inquiry should be made regarding the dosage and duration
of therapy with anticoagulant and corticosteroids.
• History of allergy recorded like fever, asthma, sensitivity to food.
• Family medical history including bleeding disorders and diabetes or others.
• Abnormal bleeding tendencies such as nose bleeding, abnormal ecchymosis, prolonged
bleeding from minor cut and excessive menstrual bleeding.
Dental History
Current illness some patients may be unaware of any problem but many may report bleeding
gum; loose of teeth; spreading of the teeth with the appearance of spaces where none existed
before, foul test in the mouth, Sensitivity when chewing, sensitivity to cold & hot, and extreme
sensitivity to inhaled air.
A preliminary oral examination is done to explore the source of the patient’s chief complaint
and to determine if emergency treatment is required.
The Dental History should include reference to the following:
• A list of visit to the dentist, frequency, date of the last visit, nature of treatment and cleaning
by a dentist.
• The patient’s oral hygiene regimen including tooth brushing (frequency, method, type of tooth
brush and dentifrices), mouth wash, interdental brush, water irrigation and dental floss.
• Any orthodontic treatment, duration & termination date.
• Pain in the teeth or in the gingiva (nature, duration & how its relieved)
• Gingival bleeding (spontaneously, on brushing or eating)

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• A bad test in the mouth.
• Do the teeth feel “loose” or insecure? Is there difficulty in chewing? Any tooth mobility
should be recorded.
• The patient's general dental habits such as grinding or clenching of the teeth during the day or
at night. Do the teeth or jaw muscles feel “sore” in the morning? Are there other habits such as
tobacco smoking or chewing, nail biting, or biting on foreign objects?
• History of previous periodontal problems, including the nature of the condition and if
previously treated, the type of treatment received (surgical or nonsurgical) and approximate
period of termination of previous treatment
• Does the patient wear any removable prosthesis? Does the prosthesis enhance or is it a
detriment to the existing dentition or the surrounding soft tissues?
• Does the patient have implants replacing any of the missing teeth?
Radiographic Survey
The radiographic survey should consist of a minimum of 14 intraoral films and four posterior
bite-wing films. Panoramic radiographs are a simple and convenient method of obtaining a
survey view of the dental arch and surrounding structures. They are helpful for the detection of
developmental anomalies, pathologic lesions of the teeth and jaws, and fractures as well as
dental screening examinations of large groups. They provide an informative overall
radiographic picture of the distribution and severity of bone destruction in periodontal disease,
but a complete intraoral series is required for periodontal diagnosis and treatment planning.
Radiographic image tend to underestimate the severity of bone loss, the difference between the
alveolar crest height and the radiographic appearance range from 0-1.6mm mostly accounted for
x-ray angulation.
Casts
Casts from dental impressions are useful adjuncts in the oral examination.
They indicate:
• The position of the gingival margins (recession).
• The position and inclination of the teeth.

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• Proximal contact relationships, and food impaction areas.
• They provide a view of the lingual-cuspal relationships.
• Casts are important records of the dentition before it is altered by treatment. Finally, casts also
serve as visual aids in discussions with the patient and are useful for pretreatment and
posttreatment comparisons, as well as for reference at recall visits. They are also helpful to
determine the position of implant placement if the case will require their use.
Clinical Photographs
Color photographs are useful for recording the appearance of the tissue before and after
treatment.
Clinical Examination
Oral Hygiene
The extent of accumulated food debris, plaque, and tooth surface stains.
Disclosing solution may be used to detect plaque that would otherwise be unnoticed. The
amount of plaque detected, however, is not necessarily related to the severity of the disease
present. For example, aggressive periodontitis is a destructive type of periodontitis in which
plaque is minimal. Qualitative assessments of plaque are more meaningful, and their value in
diagnosis.
Oral Malodor
Oral malodor, also termed fetor ex ore, fetor oris, or halitosis, is foul or offensive odor
emanating from the oral cavity. Mouth odors may be of diagnostic significance, and their origin
may be either oral or extraoral. It may indicate patient with systemic diseases (Liver disease,
DM, tonsillitis, oropharynx & stomach).
Examination of Lymph Nodes
1. Because periodontal, periapical, and other oral diseases may result in lymph node changes,
the diagnostician should routinely examine and evaluate head and neck lymph nodes.

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2. Lymph nodes can become enlarged and/or indurated as a result of an infectious episode,
malignant metastases, or residual fibrotic changes.
3. Inflammatory nodes become enlarged, palpable, tender, and fairly immobile. The overlying
skin may be red and warm.
4. Patients are often aware of the presence of “swollen glands.” Primary herpetic
gingivostomatitis, necrotizing ulcerative gingivitis (NUG), and acute periodontal abscesses may
produce lymph node enlargement.
Examination of the Teeth and Implants
• The teeth are examined for caries, poor restorations, developmental defects, anomalies of
tooth form, wasting, hypersensitivity, and proximal contact relationships.
• The stability, position, and number of implants and their relationship to the adjacent natural
dentition is also examined.
Periimplantitis
• Can create pockets around implants. Probing is important in diagnosis.
• To prevent scratching the implant surface we should use plastic instrument.
Dental Plaque & Calculus
✓ Supragingival plaque and calculus can be directly observed.
✓ Detection of subgingival calculus each tooth surface is carefully checked to the level of
gingival attachment.
✓ Warm water is useful to deflect the gingiva and aid in visualization of calculus.
Wasting Disease of the Teeth
Wasting is defined as any gradual loss of tooth substance characterized by the formation of
smooth, polished surfaces. The forms of wasting are: Erosion, Abrasion, Attrition & Abfraction.

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Erosion:
• Also called corrosion, is a sharply defined wedge-shaped depression in the cervical area of the
facial tooth surface.
• The surfaces are smooth, hard, and polished. Erosion generally affects a group of teeth.
• In the early stages, it may be confined to the enamel, but it generally extends to involve the
underlying dentin, as well as the cementum.
• The etiology of erosion is not known. Decalcification by acidic beverages, or citrus fruits,
combined with the effect of acid salivary secretion are suggested causes.
Abrasion:
• Rrefers to the loss of tooth substance induced by mechanical wear other than that of
mastication.
• Abrasion results in saucer-shaped or wedge shaped indentations with a smooth, shiny surface.
• Abrasion starts on exposed cementum surfaces rather than on the enamel and extends to
involve the dentin of the root. A sharp “ditching” around the cemento-enamel junction appears
to be the result of the softer cemental surface, as compared with the much harder enamel
surface.
• Tooth brushing with an abrasive dentifrice, Aggressive tooth brushing and hard tooth brush
are the most common causes.
• Horizontal brushing at right angles to the vertical axis of the teeth results in the severest loss
of tooth substance.
Attrition:
• Is occlusal wear resulting from functional contacts with opposing teeth. Such physical wear
patterns may occur on incisal, occlusal, and approximal tooth surfaces.
• A certain amount of tooth wear is physiologic, but accelerated wear may occur when abnormal
anatomic or unusual functional factors are present.
• Occlusal or incisal surfaces worn by attrition are called facets.
• When active tooth grinding occurs, the enamel rods are fractured and become highly reflective
to light. Thus shiny, smooth, and curviplanar facets are usually the best indicator of ongoing
frictional activity.

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• If dentin is exposed, a yellowish brown discoloration is frequently present.
• Facets vary in size and location depending on whether they are produced by physiologic or
abnormal wear. Facets are usually not sensitive to thermal or tactile stimulation.
• Attrition has been correlated with age when older adults are considered.
• The angle of the facet on the tooth surface is potentially significant to the periodontium.
* Horizontal facets tend to direct forces on the vertical axis of the tooth, to which the
periodontium can adapt most effectively.
*Angular facets direct occlusal forces laterally and increase the risk of periodontal
damage.
Abfraction:
Results from occlusal loading surfaces causing tooth flexure and mechanical microfractures and
tooth substance loss in the cervical area.
Examination of the Periodontium
The periodontal examination should be systematic, starting in the molar region in either the
maxilla or the mandible and proceeding around the arch. This prevents overemphasis of unusual
findings at the expense of other conditions that although less striking, may be equally important.
It is important to detect the earliest signs of gingival and periodontal disease.
Gingiva
The gingiva is the keratinized mucosa that surrounds the teeth. It forms a collar around each
tooth. The gingiva is typically coral pink in color and can be readily distinguished from the
adjacent dark red alveolar mucosa by its lighter pink color. In dark-skinned persons the gingiva
may contain melanin pigment to a greater extent than the adjacent alveolar mucosa.
Localized gingival inflammation is confined to the gingiva in relation to a single tooth or group
of teeth.
Generalized gingival inflammation involves the entire mouth.
Features of the gingiva to consider are: color, size, contour, consistency, surface texture,
position, ease of bleeding, and pain.

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Color changes in the gingiva
The normal gingival color is coral pink.
Gingiva becomes redder when there is an increase in vascularization or the degree of epithelial
keratinization becomes reduced or disappears. Thus, chronic inflammation intensifies the red or
bluish red color; this is caused by vascular proliferation and reduction of keratinization owing to
epithelial compression by the inflamed tissue
Changes in the size of the gingiva
The normal size depends on the sum of the bulk cellular and intercellular elements, and their
vascular supply.
In disease, the size is increased, which can be termed as gingival enlargement. The factors
responsible for this are increase in fibers and decrease in cells as in the non-inflammatory type.
Whereas in the inflammatory type there will be increase in cells and decrease in fibers.
Changes in the consistency of the gingiva
Both chronic and acute inflammations produce changes in the normal firm, resilient consistency
of the gingiva. In chronic gingival inflammation both destructive (edematous) and reparative
(fibrotic) changes coexist, and the consistency of the gingiva is determined by their relative
predominance
Gingival Index (GI) (Loe, 1967)
Gingival Index (GI) (Loe, 1967) measures the degree of gingival inflammation.
Tissues surrounding each tooth divided into 4 gingival scoring units: distal facial papilla, facial
margin, mesial facial papilla, lingual gingival margin.
Score of gingival index
✓ Score 0 Normal gingiva.
✓ Score 1 Mild inflammation: slight change in color, slight edema. No bleeding on probing.
✓ Score 2 Moderate inflammation: redness, edema and glazing. Bleeding on probing,
✓ Score 3 Severe inflammation: marked redness and edema. Ulceration. Tendency to
spontaneous bleeding,

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The GI may be used for the assessment of prevalence and severity of gingivitis in populations,
groups and individuals.
Gingival bleeding
Gingival bleeding varies in severity, duration and the ease with which it is provoked. Bleeding
on probing is easily detectable clinically and therefore is of great value for the early diagnosis
and prevention of more advanced gingival inflammation. Gingival bleeding on probing is one of
the earliest visual signs of inflammation. It can appear earlier than color changes or any other
visual signs of inflammation. It also provides an additional advantage, by being a more
objective sign that requires less subjective estimation by the examiner. Gingival bleeding on
probing also helps us to determine whether the lesions are in an active or inactive state.
Bleeding on probing (BOP)
A periodontal probe is inserted to the bottom of the gingival/periodontal pocket by applying
light force and is moved gently along the tooth (root) surface. If bleeding is provoked upon
retrieval of the probe, the site examined is considered -BOP- positive and, hence, is inflamed.
Plaque Index
Clinical plaque indices are used to evaluate the level and rate of plaque formation on tooth
surfaces, and to test the efficacy of oral care products for removal and prevention of plaque
deposits from these surfaces. A number of different indices have been described:
• Which was introduced by Silness and Loe in 1964
✓ Used on all teeth (28, wisdom teeth are excluded) or selected teeth (6 teeth).
✓ No substitution for any missing tooth.
✓ Used on all surfaces (4) (M, B, D, L).
✓ This index measures the thickness of plaque on the gingival one third of the teeth.
• 0 No plaque
• 1 A film of plaque adhering to the free gingival margin and adjacent area of the tooth, which
can not be seen with the naked eye. But only by using disclosing solution or by using probe.

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• 2 Moderate accumulation of deposits within the gingival pocket, on the gingival margin and/
or adjacent tooth surface, which can be seen with the naked eye.
• 3 Abundance of soft matter within the gingival pocket and/or on the tooth and gingival
margin.
Calculus Index (CI)
Calculus is mineralized material on the tooth surface. The calculus index refers to the amount of
calculus on a tooth.
• CI 0 - No observable calculus.
• CI 1 - Supragingival calculus covering not more than 1/3 of the exposed tooth surface.
• CI 2 - Supragingival calculus covering more than 1/3 but not more than 2/3 of the exposed
tooth surface or presence of flecks of subgingival calculus.
• CI 3 - Supragingival calculus covering more than two-thirds of the exposed tooth surface or a
continuous heavy band of subgingival calculus around the cervical portion of the tooth.
Pockets
Depth of sulcus: The normal sulcus
depth usually 1–3 mm
Pockets: is defined as pathologically
deepened of gingival sulcus may
occur by coronal movement of the
gingival margin (gingival pocket), or
apical displacement of gingival
attachment (periodontal pocket) or
combination of the above.
Pockets are generally painless but may give rise to symptoms such as localized or sometimes
radiating pain or sensation of pressure after eating, which gradually diminishes. A foul taste in
localized areas, sensitivity to hot and cold, and toothache in the absence of caries is also
sometimes present. a “rolled” edge separating the gingival margin from the tooth surface; or an
enlarged, edematous gingiva, may suggest their presence. The presence of bleeding,
suppuration, and loose, extruded teeth may also denote the presence of a pocket
Fig.1 Illustration of
pocket formation that
indicates expansion in
two directions
(arrows) from the
normal gingival
sulcus (left) to the
periodontal pocket
(right).

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Gingival pocket: Also known as pseudopocket or false pocket, seen in gingivitis formed by
gingival enlargement (increased gingival bulk) without apical migration of the junctional
epithelium.
Periodontal pocket: true pocket seen in periodontitis, occurs with apical migration of
junctional epithelium and destruction to the supporting periodontal tissues. It can classify into:
✓ Suprabony pocket: bottom of the pocket is coronal to the underlying alveolar bone.
✓ Infrabony pocket: bottom of the pocket is apical to the crest of the alveolar bone.
Detection of Pockets
The only accurate method of detecting and measuring periodontal pockets is careful exploration
with a periodontal probe.
Pockets are not detected by radiographic examination. The periodontal pocket is a soft tissue
change. Radiographs indicate areas of bone loss in which pockets may be suspected, but they do
not show pocket presence or depth.
Assessment of probing pocket depth (PPD)
For effective treatment planning, the location, topography, and extent of periodontal lesions
must be recognized in all part of the dentition. It is, therefore, mandatory to examine all sites of
all teeth for the presence or absence of periodontal lesions. The probe should be inserted
parallel to the vertical axis of the tooth and “walked” circumferentially around each surface of
each tooth to detect the areas of deepest penetration.This turn means that single-rooted teeth
have to be examinated at four sites at least (e. g. mesial, buccal, distal, and oral) and multirooted
Fig.2 Different types of pockets.
(A) Gingival pocket. There is no
destruction of the supporting
periodontal tissues. (B) Suprabony
pocket. The base of the pocket is
coronal to the level of the
underlying bone. Bone loss is
horizontal. (C) Intrabony pocket.
The base of the pocket is apical to
the level of the adjacent bone. Bone
loss is vertical.

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teeth at six sites at least (e. g. mesiobuccal, buccal, distobuccal, distooral, oral, and mesio-oral)
The probing depth, that is the distance from the gingival margin to the bottom of the gingival
sulcus/pocket, is measured to the nearest millimetre by means of a graduated periodontal probe.
Clinical Attachment Level (CAL)
is a more accurate indicator of the periodontal support around the tooth than probing depth
alone.
CAL is measured from a fixed point on the tooth that doesn’t change, the CEJ.
To calculate CAL, two measurements are needed:
• In recession: probing depth + gingival margin to the CEJ (add).
• In tissue overgrowth: probing depth – gingival margin to the CEJ (subtract).
Changes in the level of attachment can be the result of gain or loss of attachment and afford a
better indication of the degree of periodontal destruction or gain.
Fig.3 Calculate CAL

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2Periodontal instruments
Periodontal instruments are designed for specific purposes, such as removing calculus, planning
root surfaces, curetting the gingival wall or removing disease tissues.
Periodontal instruments
composed of (Fig.1):
A. Blade
B. Shank
C. Handle
Classification of periodontal instruments
A. diagnostic instruments
1. Dental mirrors
Dental mirrors used for specific uses:
✓ Indirect vision
✓ Indirect illumination
✓ Transillumination
✓ Retraction
Nonspecific uses: Handles can be used for checking mobility, percussion.
2. Periodontal probes
Periodontal probes used to locate, measure and mark pockets as well as determine their course
on individual tooth surfaces. A typical probe is a tapered rod-like instrument calibrated in
millimeters with a blunt, rounded tip.
Fig.1 Parts of a typical periodontal instrument.

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Periodontal probes are used to measure the depth of the pocket and to determine their
configuration.
Types of periodontal probes:
• Color-coded
• Noncolor-coded
A. The Marquis color-coded probe (Fig.2): The calibrations are in 3 millimeter sections.
B. Williams probe (Fig.3):
Has both color and non-color coding with markings at 1,2,3,5,7,8,9 and 10 mm.
C. The Michigan “O” probe with markings: At 3, 6, and 8 mm.
D. The WHO probe (Fig.4):
It has a 0.5 mm ball at the tip and millimeter marking at 3.5, 8.5 and 11.5 mm and color coding
from 3.5 to 5.5 mm.
Fig.2
Fig.3 Fig.4

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3. Explorers
Are used to locate calculus deposits and caries.
They are also used to locate subgingival deposits in various areas, and to check the smoothness
of the root surfaces after root planing.
Explorers are designed with different shapes and angles for a variety of use.
B. Scaling, root planing, and curettage instruments
They are classified as follows:
A. For supra gingival scaling
Include: Sickle scalers, cumine, push scalers.
1. Sickle scalers (Fig.5)
Sickle scalers have a flat surface
and two cutting edges that
converge in a sharply-pointed tip.
The arch-shape of the instrument
makes the tip so strong that it will
not break off during use.
They appear triangular in cross-
section. The sickle scaler is
inserted under ledges of calculus
no more than 1 mm below the
gingival sulcus.
It is used with a pull stroke.
Sickles with straight shanks are
designed for use on anterior teeth
and premolars. Sickle scalers with
contra-angled shanks adapt to
posterior teeth.
Fig.5

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2. Cumine (Fig.6)
A hybrid (double ended)
instrument – one end is a “spoon”
curette -the other is a heavy duty
tooth scaler. It is hook-like
having a simple curved shape
without offset which tapers to a
sharp point.
Uses: Both ends can be used to dislodge thick calculus deposits to allow visualization of the
crown or prior to further scaling.
✓ Scaler end; to remove heavy supragingival calculus deposits from interproximal area.
✓ Curette end or spoon end ; gentle curettage of large sockets to remove the granulation
tissue (if present), removal of soft tissues from sites of bony pathology e.g. to clean out
the bony defect in debridement of bone cyst lesions. also used to clean labial and lingual
surfaces from calculus.
3. Pushing scaler (Fig.7)
These have been designed for the
proximal surfaces of teeth and
primarily used in the anterior areas.
Push stroke through interproximal
contact while maintaining contact with
tooth surface. Needs sufficient
interproximal space and care with
surrounding tissues.
B. For subgingival scaling
1. Hoe scaler (Fig.8)
Hoe scaler, are used to remove tenacious subgingival deposits, Hoe scalers are used for scaling
of ledges or rings of subgingival calculus. The blade is bent at a 99-degree angle; the cutting
edge is formed by the junction of the flattened terminal surface with the inner aspect of the
Fig.6
Fig.7

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blade. The blade has been reduced to
minimal thickness to permit access to the
roots without interference from the
adjacent tissues.
Hoe scalers are used in the following manner:
1. The blade is inserted to the base of
the periodontal pocket so that it makes
two point contact with the tooth
(Fig.9). This stabilizes the instrument.
2. The instrument is activated with a
firm pull stroke toward the crown, pull
action parallel to the long axis of the
tooth. Must be fully engaged with
every effort being made to preserve the
two point contact with the tooth
2. Curettes (Fig.10)
Curettes are used to plane the root
surface by removing altered cementum
and also, for scraping the soft tissue
wall of the periodontal pockets.
Curette can be adapted to provide
good access to deep pockets, with
minimal soft tissue trauma.
There are cutting edges on both sides
of the blade.
Fig.8
Fig.9
Fig.10

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Sonic and ultrasonic instruments
Used for removing plaque, scaling, curetting and removing stains.
Two types of ultrasonic units are:
• Magnetostrictive: Vibration of the tip is elliptical; hence all the sides can be used.
• Piezo-electric: Pattern of vibration of the tip is linear; only two sides of the tip are active.
Ultrasonic vibrations range from 20,000 to 45,000 cycles/second. They operate in a wet field
and have attached water outlets. Ultrasonic instrument tip must be cooled by fluid to prevent
overheating of the vibrating instrument tip. They have been shown to be as effective as hand
instruments in subgingival calculus removal, removal of attached and unattached subgingival
plaque, removal of toxins from root surfaces, and in reduction and maintenance of pocket depth.
The water lavage from ultrasonic instruments has three benefits on the treatment site.
• Flushing action–flushes calculus, blood, bacteria, plaque from treatment site.
• Cavitation.
• Acoustic streaming.
As the water exits from instrument tip, it forms a spray of tiny bubbles that collapses and
releases shock waves in a process known as cavitation. It causes disruption of bacterial
microflora.
Advantage of ultrasonic over hand Ins.:
1- Less effort, pressure, trauma and time.
2- Simple manipulation.
3- Water sprays clean debris.
Disadvantage of sonic & ultrasonic instrumentations:
1- Lack of tactile sensation because of light pressure during manipulation.
2- Heat generation, required coolant system.

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3- Impair of visibility because of water spray.
4- Aerosol contamination.
5- Damage restorative materials (porcelain, amalgam, gold, composite & Titanium implant
abutments).
Contraindication of ultrasonic device:
1 -Infectious diseases.
2-Cardiac pacemaker & hearing aids.
3 -Gag reflex
4 -young children
5- pain.
Plastic and Titanium Instruments for Implants:
Several different companies are manufacturing plastic and titanium instruments for use on
titanium and other implant abutment materials. It is important that plastic or titanium
instruments be used to avoid scarring and permanent damage to the implants.
C. Cleansing and polishing instruments
Rubber cups, brushes, dental tapes
Rubber cups (Fig.11)
Rubber cups consist of a rubber shell with or without webbed configurations in the hollow
interior. They are used in the handpiece with a special prophylaxis angle. The hand piece,
prophylaxis angle must be sterilized after each patient use, or a disposable plastic prophylaxis
angle and rubber cup may be used and then discarded. A good cleansing and polishing paste
that contains fluoride should be used and kept moist to minimize frictional heat as the cup
revolves. Polishing pastes are available in fine, medium, or coarse grits and are packaged in
small, convenient, single-use containers. Aggressive use of the rubber cup with any abrasive
may remove the layer of cementum, which is thin in the cervical area.

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Bristles brush (Fig.12)
Bristle brushes are available in wheel and cup shapes. The brush is used in the prophylaxis
angle with a polishing paste. Because the bristles are stiff, use of the brush should be confined
to the crown to avoid injuring the cementum and the gingiva.
Dental tape
Dental tape with polishing paste is used for polishing proximal surfaces that are inaccessible to
other polishing instruments. The tape is passed interproximally while being kept at a right angle
to the long axis of the tooth and is activated with a firm labiolingual motion. Particular care is
taken to avoid injury to the gingiva. The area should be cleansed with warm water to remove all
remnants of paste.
D. Surgical instruments
Excisional and incisional instruments, surgical curettes and periodontal elevators scissors and
nippers
Knives
Knives are basic instruments and can be obtained with both fixed and replaceable blades.
1. Kirkland knifes (Fig.13)
Typically used for gingivectomy. These knives are kidney shaped and can be obtained as either
double-ended or single-ended instruments.
Fig.11 Fig.12

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2. Interdental knives eg: Orban knife
(Fig.14)
These spear-shaped knives having
cutting edges on both sides and are
designed with either double-ended or
single-ended blade. useful for excising
interproximal tissue.
3. Surgical blades (Fig.15) eg: #12D, 15, 11.
Periodontal elevators (Fig.16)
These are needed to reflect and move the flap after the incision has been made for flap surgery.
Fig.14
Fig.15
Fig.16
Fig.13

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Tissues forceps (Fig.17)
Tissues forceps used to hold the flap during suturing and used to position and displace the flap
after reflection.
Scissors
Scissors are used in periodontal surgery for such purposes as removing tags of tissue during
gingivectomy, trimming the margins of flaps, enlarging incisions in periodontal abscesses, and
removing muscle attachments in mucogingival surgery.
Surgical nippers (Fig.18)
Serve same purpose as Scissors and they
are also used for contouring the
architectural form and for forming
interdental sluiceways
Needle holders (Fig.19)
Used to suture the flap at the desired position after surgical procedure has been complete.
Fig.18
Fig.19
Fig.17

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General principles
Effective instrumentation is governed by a number of general principles that are common to all
periodontal instruments. Proper position of the patient and the operator, illumination and
retraction for optimal visibility, instrument stability and sharp instruments are the fundamental
pre-requisites
Instrument stabilization
Stability of the instrument and the hand is the primary requisite for controlled-instrumentation,
stability and control is essential for effective instrumentation and to avoid injury to the patient
or clinician. The two factors that provide stability are, instrument grasp and finger rest.
Instrument Grasp
Grasping can be divided in to
1. pen grasp (Fig.20):
Index finger and thumb hold
instrument, middle finger under
instrument.usually provide less
tactile sensitivity & flexibility of
movement so it is not
recommended during periodontal
instrumentation.
2. modified pen grasp (Fig.21):
Index finger and thumb hold
instrument. Middle finger guides
instrument, as it rest on the pad of
middle finger so this will provide
tactile sensitivity. The ring-finger
acts as fulcrum/finger rest while the
little finger relaxed beside ring
finger.so it is recommended for all
periodontal instruments. This grasp
Fig.20
Fig.21

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allows precise control of the working end, permits a wide range of movements and facilitates
good tactile conduction.
3. palm and thumb grasp
(Fig.22):
Fingers wrapped around handle,
thumb used to stabilize instrument.
The palm and thumb grasp is useful
for stabilizing instruments during
sharpening and for manipulating air
and water syringes.
Correct grasp provides:
• Maximized stability during instrumentation.
• Minimized patient trauma and operator fatigue.
• Improved tactile sensitivity.
Finger Rest
The finger rest serves to stabilize the hand and the instrument by providing a firm fulcrum, as
movements are made to activate the instrument. A good finger rest prevents injury and
laceration of the gingival and surrounding tissues. The ring finger is preferred by most
clinicians for the finger rest. Maximal control is achieved when the middle finger is kept
between the instrument shank and the fourth finger. This built-up fulcrum is an integral part of
the wrist-forearm action that activates the powerful working stroke for calculus removal. Finger
rests may be generally classified as intraoral finger rests or extraoral fulcrums.
Condition of instruments (sharpness)
Prior to any instrumentation, all instruments should be inspected to make sure that they are
clean, sterile and in good condition. The working ends of pointed or bladed instruments must be
sharp to be effective.
Fig.22

26
Advantages of Sharpness:
1. Easier calculus removal.
2. Improved stroke control
3. Reduced number of strokes.
4. Increased patient comfort.
5. Reduced clinician fatigue.
Ideally, it is best to sharpen your instruments after autoclaving and then re-autoclave them prior
to patient treatment. Dull instruments may lead to incomplete calculus removal and unnecessary
trauma because of excess force applied.
For all instruments, the instrument is held in the non-dominant hand using a palm grasp.
The index finger and thumb should be near the junction of the functional shank and the top of
the handle such that they will counter balance the force produced at the opposite end of the
instrument once the stone is activated. For all stones, the lower half is held in the dominant
hand with the thumb on the edge closer to the operator and the fingers on the edge farther. The
entire arm will work in one fluid motion so the grasp is intended to stabilize the stone and make
such a motion comfortable to accomplish (Fig.23). The difference between the instruments is
found at the working end. These differences make sharpening technique a little different for
each instrument type.
Fig.23

27
3 Terms in periodontology & Gingiva
Terms in periodontology
The term periodontium arises from the greek word “Peri” meaning around and “odont” meaning
tooth, thus it can be simply defined as “the tissues investing and supporting the teeth”.
✓ The periodontium is composed of the following tissues namely:
• Alveolar bone.
• Root cementum.
• Periodontal ligament (Supporting tissues).
• Gingiva (investing tissue).
Fig.1 Tissues of the periodontium.

28
✓ The various diseases of the periodontium are collectively termed as periodontal
diseases.
✓ Periodontal therapy: is the treatment of periodontal diseases.
✓ Periodontology: the clinical science that deals with the periodontium in health and
disease.
✓ Periodontics: is the branch of dentistry concerned with prevention and treatment of
periodontal disease.
The Oral Mucosa
The oral mucosa consists of three zones:
1. Masticatory mucosa
2. Specialized mucosa
3. Lining mucosa
1. Masticatory mucosa:
it includes the gingiva and the covering of the hard palate.
The boundaries are from the free gingival margin to the mucogingival junction on the facial
and lingual surfaces.
The mucogingival junction is a distinct line between the attached gingiva apically and the
alveolar mucosa.
No mucogingival junction on the palatal side because both gingiva and alveolar mucosa are of
the same type which is masticatory mucosa.
The tissue is firmly attached to the underlying bone and covered with keratinized epithelium to
withstand the frictional forces of food during mastication.
2. Specialized mucosa:
it covers the dorsum of the tongue.

29
3. Lining mucosa:
is the oral mucous membrane that lines the reminder of the oral cavity. Examples for this type
are the tissue covering the lips, cheeks, floor of the mouth, inferior surface of the tongue, soft
palate and the alveolar mucosa.
Alveolar mucosa: is located apical to the attached gingiva and extends into the vestibule of the
mouth, it is darker red and movable because it has no elastic fibers.
Biology of the periodontal tissues / Introduction
Periodontium is the functional unit of tissues supporting the tooth including gingiva, the
periodontal ligament (PDL), the cementum and the alveolar process.
The tooth and the periodontium are together called the dentoperiodontal unit.
The main support of the tooth is provided by the periodontal ligament, which connects the
cementum of the root to the alveolar bone or tooth socket into which the root fits.

30
The gingiva
Macroscopic features
It is that part of the oral mucosa (masticatory mucosa) that covers the alveolar process of the
jaws and surrounds the neck of the teeth. The main function of the gingiva is to protect the
surrounding tissues from the oral environment.
Anatomically the gingiva is divided into:
1. Marginal gingiva (free or un-attached gingiva).
2. Attached gingiva.
3. Interdental gingiva.
Marginal gingiva (free or un-attached gingiva):
It is the terminal edge or border of the gingiva surrounding the tooth in a collar-like fashion. It
is well adapted to the tooth surface but it is not attached to it. It is separated from the tooth by a
fine space called the gingival sulcus.
The marginal gingiva is separated from the attached gingiva by the free gingival groove which
is (a shallow linear depression on the faciolingual surface that roughly corresponds to the base
Fig.2 Diagram illustrating anatomic landmarks of the gingiva.

31
off the gingival sulcus). The free gingival groove is about 1mm wide and it is only present in
about 30-40% of adults.
Gingival sulcus (Fig.3):
is defined as the space or shallow
crevice between the tooth and the
free gingiva, which extends apical
to the junctional epithelium.
It is V-shaped and barely permits
the entrance of periodontal probe.
Under ideal condition it is about
0mm which is seen only in germ
free animal.
The probing depth of normal
gingival sulcus is 2-3mm. in
histological section the depth is
about 1.8mm.
Attached gingiva:
It is that part of the gingiva which is firm, resilient and tightly bound to the cervical portion of
the tooth and underlying periosteum of the alveolar bone by the gingival fibers and the
junctional epithelium.
It is demarcated coronally from the free gingiva by the free gingival groove, and extends
apically to the mucogingival junction where it becomes continuous with the alveolar mucosa.
(the junction between the attached gingiva and the alveolar mucosa is called the mucogingival
line or junction).
The width of attached gingiva is the distance between the mucogingival junction and the
projection of the external surface of the bottom of the gingival sulcus or the periodontal pocket.
The width of attached gingiva is greater in maxilla than mandible. Least width in the
mandibular 1st premolar area and the greatest width are in the maxillary incisors region. The
width of attached gingiva increases with age and supra-erupted teeth.
Fig.3

32
Interdental gingiva:
It occupies the gingival embrasure. It is of two
shapes (Col and Pyramidal). Col is a valley-like
depression that connects the facial and lingual
papilla. It is covered by thin non-keratinized
epithelium representing the most frequent site for
initiation of disease process.
The lateral border and tip of the Interdental
papilla are formed by continuation of marginal
gingiva and the intervening portion by the
attached gingiva.
In the presence of diastema the Interdental papilla
will be absent.
The shape of Interdental gingiva
depends on:
• The contact relationship
between the teeth.
• The width of the proximal
tooth surfaces.
• The course of the
cemento-enamel junction.
Microscopic features
The gingiva consists of a central core of connective tissue covered by stratified squamous
epithelium.
The gingival epithelium (Fig.5)
Three types of epithelium exist in the gingiva:
1. The oral or outer epithelium (Keratinized epithelium).
Fig.4 Col
Fig.5 Proximal View.

33
2. The sulcular epithelium.
3. The junctional epithelium (Non-keratinized epithelium).
The oral epithelium:
It covers the crest and the outer surface of the marginal and attached gingiva. On average, the
oral epithelium is 0.2-0.3 mm in thickness. It is keratinized or parakeratinized or combination of
both
Keratinization varies in different areas in the following order:
• Palate (Most keratinized)
• Gingiva
• Ventral aspect of the tongue
• Cheek (least keratinized)
Fig.5

34
The boundary between the oral epithelium and the underlying connective tissue has a wavy
course. The projections of epithelial cells into the connective tissue are known as “Rete Pegs”
while the intervening connective tissue portions which project into the epithelium are called
connective tissue papillae. This alternating pattern of depression and protuberances of the
connective tissue papillae and epithelial rete pegs is thought to give the attached gingiva the
stippled appearance.
The oral epithelium has the following cell layers (Fig.6):
1. Basal layer (stratum basale or stratum
germintivum): the basal cells are either
cuboidal or cylindrical and posses the ability
to divide. It is called stratum germintivum
because it is where the epithelium renewed.
The basal cells are separated from the
connective tissue by a basement membrane.
2. Spinous layer (Stratum spinosum):
consists of large cells with short cytoplasmic
processes resembling spines.
3. Granular layer (stratum granulosum):
electron dense keratohyalin bodies begin to
occur. These granules are believed to be
related to synthesis of keratin.
4. Keratinized cell layer (stratum
Corneum): This is the most superficial layer and where both para and ortho-keratinization
occur.
Types of cells in the oral epithelium:
1. Keratinocytes cell: it is the principal cell type of oral epithelium comprises about 90% of the
total cell population, responsible for the production of keratin which contributes to the
protective function of the epithelium. These cells undergo continuous proliferation and
differentiation from basal cell to the surface of epithelium. It takes about 3-4 weeks for the
keratinocyte to reach the outer surface where it becomes desquamated from stratum corneum.
Fig.6

35
2. Melanocyte cells: responsible for the production of melanin pigment and can be found in the
basal cell layer.
3. Langerhans cell: they play a role in defense mechanism of the oral epithelium. They have an
immunological function by recognizing and processing antigens.
4. Merkel cells: they are located in the deeper layers of epithelium, they have nerve ending and
have been identified as tactile receptors.
The epithelial cells are joined together by structure known as desmosome, which is composed
of two hemidesmosomes separated from each other by granulated material (GM)
Each hemidesmosome is composed from (Fig.7):
• The outer leaflets (OL):
of cell membrane of two adjoining cells.
• The inner leaflet (IL):
is the thicker leaflet of cell membrane.
• The attachment plaque (AP):
which represent granular and fibrillar material in the
cytoplasm.
The sulcular epithelium:
It lines the gingival sulcus and is thin; nonkeratinized stratified squamous epithelium without
rete pegs. It extends from the coronal limit of the junctional epithelium to the crest of the
gingival margin. Although it contains Keratinocytes they do not undergo Keratinization. Partial
Keratinization may occur in response to physical stimulation.
The sulcular epithelium is extremely important because it may act as a semi permeable
membrane through which injurious bacterial products pass into the gingival and tissue fluid
from the gingiva seeps into the sulcus.
The junctional epithelium (JE):
The epithelium that attaches the gingiva to the surface of the tooth. It forms the base of the
sulcus.
Fig.7

36
The junctional epithelium is attached to the tooth surface by internal basal lamina and
hemidesmosome and to the gingival connective tissue by external basal lamina and
hemidesmosome.
The attachment of the JE to the tooth is reinforced by the gingival fibers; hence, the JE and the
gingival fibers are considered a functional unit, referred to as the dentogingival unit.
The JE consists of a collar like band of stratified squamous non keratinized epithelium.
Thickness varies from 2-3 Layers in early life and increases with age up to 15-20 layers at the
base of the gingival sulcus. The length of junctional epithelium ranges from 0.25 to 1.35mm.
The cells are arranged in basal and suprabasal layer.
The JE assumes a key role in maintenance of periodontal health, it creates the firm epithelial
attachment that connects the soft tissue to the tooth surface. It is quite permeable and thus
serves as a pathway for diffusion of the bacterial plaque products to the connective tissue. There
is also a diffusion of host defense substances in the opposite direction moving towards the
sulcus.
Differences between the three types of gingival epithelium:
• The size of the cells in the junctional epithelium is relatively larger than the oral epithelium.
• The intercellular spaces are wider in the junctional epithelium than the oral epithelium.
• The number of desmosome is fewer in the junctional epithelium than the oral epithelium, this
could explain the JE susceptibility to tear during probing and its greater permeability to migrate
cells and fluids.
• No Keratinization, a no rete pegs in the sulcular and junctional epithelium, so they are thinner
than oral epithelium
• Turnover rate is very high in junctional epithelium (4-6 days) compared to oral epithelium (6-
12 days or up to 40 days).
• Junctional epithelium forms the attachment of the gingiva to the tooth surface while oral and
sulcular epithelium have no attachment to tooth surface.
Epithelial connective tissue interface:
Basement membrane forms a continuous sheet that connects the epithelium and connective
tissue. Electron microscope reveals a faintly fibrillar structure, called as the basal lamina which
is a part of the basement membrane. This structure has

37
• Lamina lucida adjacent to the basal epithelial cell.
• Lamina densa which is located beneath the lamina lucida from this structure and there are
anchoring fibrils that project into the connective tissue.
The gingival connective tissue (CT)
The connective tissue supporting the oral epithelium is termed as lamina properia and can be
divided into two layers:
• The superfacial papillary layer: This has papillary projections between the epithelial rete
pegs.
• The deep reticular layer: that lies between the papillary layer and the underlying structures.
The lamina properia consists of cells, fibers, blood vessels embedded in amorphous ground
substances.
Cells of the connective tissue:
• Fibroblast: the most predominant cells of the CT (65%). They synthesize collagen, elastic
fibers and the connective tissue matrix, and they regulate collegen degredation.
• Mast cells: it is responsible for the production of certain components of the matrix, and they
produces vasoactive substances which may control the flow of blood through the tissue.
• Macrophages: They have a phagocytic action and involved in the defense mechanism.
• Inflammatory cells: they have different immunological functions such as polymorphonuclear
leukocytes, lymphocytes and plasma cells.
The connective tissue fibers:
which are formed by the fibroblasts cells
• Collagen fibers: which is the most predominant type of fibers
• Reticulin fibers
• Oxytalan fibers
• Elastin fibers

38
The functions of gingival fibers:
1. It braces the marginal gingiva firmly against the tooth.
2. It helps to withstand the forces exerted by mastication
3. It unites the free gingiva to the root cementum and the adjacent attached gingiva.
The arrangement of the gingival fibers is described as principal group fibers (Fig.8) which
are:
1. Dentogingival fibers: they project from the
cementum in a fanlike conformation towards the
crest and outer surface of the marginal gingiva.
They provide support to the gingiva by attaching
it to the tooth.
2. Alveolar gingival fibers: they extend from the
periosteum of the alveolar crest coronally into
the lamina properia. Their function is to attach
the gingiva to the alveolar bone.
3. Dentoperiosteal fibers: they arise from the
cementum near the cementoenamel junction and
insert into the periosteum of the alveolar bone
and protect the periodontal ligament.
4. Circular fibers: they surround the tooth in a
cuff or ring like fashion and course through the
connective tissue of the marginal and attached
gingiva.
5. Trans-septal fibers: they are located
interproximally, they extend from cementum of
one tooth to the cementum of neighbouring tooth. They protect the interproximal bone and
maintain tooth to tooth contact.
Connective tissue ground substances:
It is produced by fibroblast, followed by mast cells and other components derived from the
blood. The matrix is the medium in which the connective tissue cells are embedded and is
Fig.8

39
essential for the maintenance of the normal function of the connective tissue. Thus, the
transportation of water, electrolytes, nutrients, metabolites etc.. to and from the individual
connective tissue cells occurs within the matrix.
The main constituents are proteoglycans and glycoproteins.
Blood supply and nerves:
Gingival tissue has rich vascular supply from internal maxillary artery.
Blood supply is from:
• Supraperiosteal arteriols.
• Vessels of periodontal ligaments.
• Arterioles emerging from the crest of the Interdental septa.
Nerve supply is derived from the terminal branches of the maxillary and mandibular branches
of the trigeminal nerve.
Clinical descriptive criteria of clinically healthy gingiva and inflamed one:
1. Gingival color
The normal color of gingiva is coral pink with some variations depending on:
• The amount of melanin in the tissues.
• The thickness of the epithelium.
• The degree of the Keratinization.
• The vascularity of the connective tissue.
Dark skinned people often exhibit dark blue or brown color. Melanin, a non-hemoglobin-
derived brown pigment, is responsible for the normal pigmentation of the skin, gingiva and
remainder of the oral mucous membrane. It is present in all normal individuals, often not in
sufficient quantities to be detected clinically but in black individuals it is prominent in the oral
cavity.

40
The color of inflamed gingiva may vary from red to bluish red due to vasodilatation which leads
to bleeding tendency.
2. Gingival contour
The gingiva usually ends coronally in knife edged margins and scalloped in contour.
In inflamed gingiva, the contours are often rounded and enlarged because of vascular stagnation
and increases formation of collagen fibers.
3. Gingival consistency
The gingiva is usually resilient, firm and bound down to the underlying bone because of the
dense collagenous nature of the gingival connective tissue.
In inflamed gingiva, the consistency may be soft and spongy because of the vascular stagnation
and decrease in the amount of gingival collagen fibers or extremely firm because of excessive
formation of collagen (fibrosis), this is in case of chronic inflammation.
4. Gingival surface texture
Gingiva may have either stippled or smooth and shiny surface, the attached gingiva is stippled,
while the free gingiva is smooth.
In inflamed gingiva, reduction or lack of stippling is not an indicator of health nor is the
absence of stippling an indicator of disease. Hence, stippling frequently begins to disappear in
old age.
5. Size
The size of the gingiva corresponds with the sum total of the bulk of cellular and intercellular
elements and their vascular supply.
Alteration in size is a common feature of gingival disease.

41
4Periodontal Ligament (PDL)
Definition
PDL is a connective tissue structure that surrounds the root and connects it with the bone.
Structure
the periodontal ligament space has the shape of an hourglass and is narrowest at the mid root
level. The width of PDL is approximately 0.25+ 50 percent.
Cellular composition
Cells of PDL are categorized as:
1. Synthetic cells
a. Osteoblast
b. Fibroblast
c. Cementoblasts
2. Resorpative cells
a. Osteoclasts
b. Cementoclasts
c. Fibroblasts
3. Progenitor cells
4. Epithelial rest of malassez

42
5. Connective tissue cells (mast cells and macrophages)
Synthetic cells:
1. Osteoblasts: covers the periodontal surface of the alveolar bone. They are responsible for the
formation of alveolar bone.
2. Fibroblasts: the most prominent connective tissue cells (65%). The main function of the
fibroblasts is the production of various types of fibers (collagen fibers, Reticulin fibers,
Oxytalan fibers and Elastin fibers). Fibroblasts are also instrumental in the synthesis of
connective tissue matrix.
3. Cementoblasts: are seen lining the cementum and are responsible for cementum deposition.
Resorpative cells:
1. Osteoclasts: these are the cells that resorb the bone and tend to be large and multinucleated.
2. Fibroblasts: they synthesize collagen and also possess the capacity to resorb and degrade the
old callogen fibers.
3. Cementoclasts: cementum is not remodeled in the fashion of alveolar bone and periodontal
ligament but that it undergoes continual deposition during life. However resorption of
cementum occurs in certain circumstances by cementoclasts.
Progenitor cells:
they differentiate into functional type of connective tissue cells.
Epithelial rest of Malassez:
they are found close to cementum. When certain pathologic conditions are present, cells of
epithelial rest can undergo rapid proliferation and can produce a variety of cysts and tumors of
the jaws.
Connective tissue cells
Mast cells: they play a role in inflammatory reaction.

43
Macrophages: they are capable of phagocytosis.
Extracellular components
1. Fibers
a. Collagen
b. Oxytalan
2. Ground substances
a. Proteoglycans
b. Glycoproteins
Periodontal fibers:
The most important elements of the periodontal ligament are the principal fibers. They are
collagenous in nature and are arranged in bundles following a wavy course.
The terminal portion of these principal fibers that insert into the cementum and bone are termed
Sharpey’s fibers.
The principal fibers of the PDL are arranged in five groups (Fig.1):
Alveolar crest fibers: they extend obliquely from the cementum just beneath the junctional
epithelium to the alveolar crest.
Function: retain tooth in socket and resist lateral movement.
Horizontal group: extends from cementum to the alveolar bone at right angle to the long axis
of the tooth.
Oblique group: they are the largest group extending coronally in an oblique direction from the
cementum to the bone.
Function: they resist axial directed forces.

44
Apical group: they radiate from the cementum of root apex to the bone.
Function: it prevents tooth tipping, resists luxation, and protects blood, lymph and nerve supply
of the tooth.
Inter-radicular fibers: Extends from cementum of bifurcation areas, splaying from apical into
furcal bone.
Function: it resists luxation and also tipping and torquing.
Ground substance:
The ground substance is made up of two major groups of substances:
• Glycosaminoglycans: such as hyaluronic acid, proteoglycans.
• Glycoproteins: such as fibronectin and laminin It also has high water content (70%).
Fig.1

45
Development of principal fibers of PDL (Fig.2)
It will be as follows
1. Small, fine brush like fibrils are detected arising from the root
cementum and projecting into the PDL space.
2. Small fibers are seen on the surface of the bone but only in thin,
small numbers.
3. The number and thickness of fibers originating from the bone
increase and elongate. They radiate towards the loose connective
tissue in the mid portion of the periodontal ligament.
4. The fibers originating from the cementum also increase in length
and thickness and fuses with the fibers originating from the alveolar
bone in the periodontal ligament space.
5. Following tooth eruption, the principal fibers become organized in
bundles and run continuously from bone to cementum.
Structures present in the connective tissue
1. Blood vessels (Fig.3): periodontal ligament is
supplied by branches derived from three sources
dental, inter-radicular and interdental arteries.
2. Lymphatics: lymphatic vessels follow the path
of blood vessels in the periodontal ligament.
3. Nerve intervention: periodontal ligament is
mainly supplied by dental branches of the alveolar
nerve. The periodontal ligament has
mechanoreceptors providing sense of touch,
pressure, pain and proprioception during
mastication.
4. Cementicles: calcified masses adherent to or
detached from the root surface.
Fig.2
Fig.3

46
Functions of the PDL
1. Physical
2. Formative and remodeling
3. Nutrional and sensory function
Physical function
A. Provide soft tissue “casing’' to protect the vessels and nerves from injury by mechanical
forces.
B. Transmission of occlusal forces to the bone.
C. Attaches the teeth to the bone.
D. Maintains the gingival tissues in their proper relationship to the teeth.
E. (shock absorption) Resists the impact of occlusal forces
Formative and Remodeling function
Cells of the periodontal ligament have the capacity to control the synthesis and resorption of the
cementum, ligament and alveolar bone. Periodontal ligament undergoes constant remodeling;
old cells and fibers are broken down and replaced by new ones.
Nutritive functions
Since PDL has a rich vascular supply, it provides nutrition to the cementum, bone, and gingiva.
Sensory functions
The PDL is supplied with sensory nerve fibers which transmit sensation of touch, pressure and
pain to higher centers.

47
Clinical consideration
✓ The width of PDL space varies with age, location of tooth, degree of stress to which the
tooth was subjected.
✓ In compliance with the physiologic mesial migration of the teeth the PDL is thinner on
the mesial root surface than on the distal surface.
✓ A tooth in hyperfunction may have a wider PDL space and a tooth in hypofunction may
have a narrow PDL space.
✓ The width of PDL space is about 0.25mm in normal functions. It is widest at the cervical
and apical portions of the root and narrowest at the middle.
✓ The most interesting features of the PDL are its adaptability to rapidly changing applied
force and its capacity to maintain its width at constant dimensions throughout its lifetime.

48
5Cementum
It is a thin specialized calcified tissue covering the roots surfaces of the teeth.
It has many features similar to the bone tissue but differs from bone in the following aspects:
✓ It is microscopic organization.
✓ Has no innervation
✓ Has no blood or lymph vessels.
✓ Does not undergo physiological remodeling (resorption and deposition), but it is
characterized by continuous deposition throughout life.
Functions of cementum
✓ Anchorage of the tooth in the alveolus
✓ To attach the PDL fibers to the teeth
✓ To contribute to the process of repair after damage to the root surface and following
regenerative periodontal surgical procedures.
Cemento-enamel junction (C.E.J) (Fig.1)
Three types of relationships involving the cementum may exist at the C.E.J:
✓ Cementum overlaps the enamel (60%-65%)
✓ Edge-to edge (butt joint (30%)
✓ Cementum and enamel fail to meet (5%-10%)
* In the last condition, there is a possibility of gingival recession which may result in
sensitivity because the dentin is exposed.

49
Types of cementum
There are two types of cementum:
1. Primary (acellular cementum)
2. Secondary (cellular cementum)
Fig.1
Fig.2 Types of cementum.

50
1. Primary (acellular cementum):
Is the first to be formed in conjunction with root formation and tooth eruption, it does not
contain cells and sharpey's fibers make up most of its structure.
Generally it covers the cervical third of the root.
2. Secondary (cellular cementum):
Which is formed after tooth eruption and in response to functional demands, therefore it grows
faster and over a thin layer of acellular cementum at the apical third of the root and furcations of
multirooted teeth. This type of cementum contains cells (cementocytes), but sharpey's fibers
occupy a smaller portion of this type of cementum.
Cellular cementum is less calcified than the acellular type.
Both acellular cementum and cellular cementum are arranged in lamellae separated by
incremental lines parallel to the long axis of the root. These lines represent “rest periods” in
cementum formation and they are more mineralized than the adjacent cementum.
Structures of cementum
Cementum consist of:
• Fibrous elements (collagen fibers) which is composed of type I (90%) and type III (about
5%) collagens.
• Cellular elements.
Fig.3 incremental lines.

51
• Calcified interfibrillar matrix.
1. Fibrous elements:
There are two types:
a. Extrinsic fibers (sharpey's fibers):
which are the embedded portion of the principal
fibers of the PDL and are formed by the fibroblast
cells . Sharpey's fibers make up most of the
structure of acellular cementum and they are
inserted at right angles to the root surface and
penetrate deep into the cementum.
b. Intrinsic fibers:
These fibers are produced by cementoblast cells and
are oriented more or less parallel to the long axis of
the root and form a cross banding arrangement with
sharpey's fibers
2. Cellular elements:
The cells associated with cementum are few and generally resides within the PDL.
a. Cementoblast cells:
responsible for the formation of both cellular and acellular cementum.
b. Cementocyte cells:
are found only in cellular cementum, they are located within spaces (lacunae) that communicate
with each other through canaliculi for transportation of nutrients through the cementum and
contribute to the maintenance of the vitality of this tissue.
Fig.4 (E) Extrinsic fibers & (I)
Intrinsic fibers.

52
C. Fibroblast cells:
These cells belong to the PDL where they are responsible for synthesis of principal fibers but
since these fibers become embedded in cementum, fibroblasts indirectly participate in the
formation of cementum.
d. Cementoclast cells:
these cells are responsible for extensive root resorption that lead to primary teeth exfoliation.
Permenant teeth do not undergo physiologic resorption but localized cemental resorption may
occur which appears as concavities in the root surface and may be caused by local or systemic
causes. local conditions include, trauma from occlusion, orthodontic movement, cyst and occur
on mesial surfaces in association with mesial drift. Among systemic conditions are calcium
deficiency and hypothyroidism.
Reversal line: The newly formed cementum is demarcated from the root by a deeply staining
irregular line which delineates the border of the previous resorption.
Incremental lines: Both acellular cementum and cellular cementum are arranged in lamellae
separated by incremental lines parallel to the long axis of the root. These lines represent “rest
periods” in cementum formation and they are more mineralized than the adjacent cementum.
Fig.5 Fig.6

53
Trauma from occlusion: Forces that exceed the adaptive capacity of the periodontium and
produce injury.
Interfibrillar matrix:
These are proteoglycans, glycoproteins and phosphoproteins formed by cementoblast cells.
Proteoglycans are most likely to play a role in regulating cell-cell and cell-matrix interactions
both during normal development and during the regeneration of cementum.
Mineralization of cementum
Occurs by the deposition of hydroxyapatite crystals, first within the collagen fibers, later upon
the fiber surface and finally in the interfibrillar matrix.
Cellular cementum is less calcified than acellular cementum and cementum mineralizalion is
less than that of the bone, enamel and dentin.
Permeability of cementum
In very young animals, acellular cementum and cellular cementum are very permeable and
permit the diffusion of dyes from the pulp and external root surface. The canaliculi in cellular
cementum is some areas are contagious with the dentinal tubule. The permeability of cementum
diminishes with age.
Exposure of cementum to the oral environment
Cementum becomes exposed to the oral environment in cases of gingival recession and as a
result of the loss of attachment in pocket formation.
The cementum is sufficiently permeable to be penetrated in these cases by organic substances,
organic ions and bacteria.
Bacterial invasion of the cementum occurs frequently in individuals with periodontal disease,
and cementum caries can develop.

54
Development of cementum
Both cellular and acellular cementum are produced by cementoblast cells.
Cementoid is first formed which is a non-calcified tissue containing collagen fibrils distributed
in matrix.
Cementum is characterized by continuous deposition and increase in thickness throughout life.
A thin layer of cementum noted on recently erupted tooth will tend to increase thickness with
age.
Cementum formation is most rapid in the apical regions to compensates for tooth eruption and
attrition.
The thickness of cementum is more pronounced in the apical third and in the furcation areas
than the cervical portion.
Cementum is thicker in distal than in mesial surfaces because of functional stimulation from
mesial drift over time.
Hypercementosis
Refers to a prominant thickening
of the cementum.
It is largely an age-related
phenomenon and it may be
localized to one tooth e.g. tooth
without antagonists or with
periapical lesion, and sometimes
affect the entire dentition that may
occur in patients with paget's
disease.
It could pose a problem if an
affected tooth requires extraction.
Fig.7 Hypercementosis

55
Cemental aplasia or hypoplasia
Refers to an absence or paucity of cellular cementum.
Ankylosis (Fig.8)
Fusion of the cementum and alveolar bone with
obliteration of the PDL. It results in resorption of
the cementum and its gradual replacement by bone
tissue and it may develop after chronic periapical
inflammation and occlusal trauma. Clinically,
ankylosed teeth lack the physiologic mobility of
normal teeth as well as proprioception is lost
because pressure receptors in the PDL. are deleted
or do not function correctly. Furthermore, the
physiologic drifting and eruption of teeth can no
longer occur.
When implants are placed in the jaw, healing results in bone that is formed in direct apposition
to the implant without intervening CT, this may be interpreted as a form of ankyloses.
Fig.8

56
6Alveolar process (AP)
Is the portion of the maxilla and mandible that
forms and supports the tooth sockets (alveoli).
It develops in conjunction with the formation of
and during the eruption of the teeth and is
gradually resorbed if the teeth are lost, thus it is
tooth dependent structure
Functions of alveolar process
1.comprises the attachment apparatus and the supporting tissue of the teeth together with root
cementum and PDL fibers.
2. provide the osseous attachment to the PDL fibers
3.distribute and resorb forces generated by mastication and other tooth contacts
Parts of the alveolar process
1. Alveolar bone proper:
it is a thin layer of compact bone forming the inner socket wall (lines the alveolus), which is
seen as the lamina dura in radiographs. A great number of sharpey's fiber bundles are embedded
into this layer of bone which is adjacent to the PDL therefore it is called ((bundle bone))
Histologically this bone contains many small holes or openings called ((volkmann's canals))
through which blood ve ssels, lymphatics and nerves link the PDL with the cancellous bone thus
it is called ((cribriform plate))
Fig.1
Alveolar
process

57
2. An external plate of cortical bone.
3. Cancellous trabeculae or spongy bone:
which is located in the space between the external cortical plate and alveolar bone proper, they
meet and fuse to form the alveolar crest. cancellous bone, which act as supporting alveolar
bone, with cortical bone surround the alveolar bone proper (ABP).
Fig.2
Fig.3

58
Alveolus: is the space in the alveolar bone that accommodates the roots of the teeth.
Basal bone: is the portion of the jaw located apically but unrelated to the teeth (Fig.4).
Lamina dura: the layer of ABP appears as white line surrounding the root of the tooth on
radiographs (Fig.5).
The alveolar processes are subdivided according to their anatomical relationships to the
teeth:
1. Interproximal bone (interdental septum): The bone located between the roots of adjacent
teeth
2. Inter radicular bone: the bone located between the roots of multirooted teeth.
3. Radicular bone: the alveolar process located on the facial, lingual or palatal surfaces of the
roots of teeth.
The distance between the crest of the alveolar bone and the cementoenamel junction increases
with age to an (average of 2.81mm). The thickness of alveolar process varies from one region to
another depends on the position of the teeth in the arch and their relationship to one another,
e.g. teeth that are labially positioned in the arch will have thin labial radicular bone and thicker
lingual radicular bone.
Fig.4 Fig.5

59
Bone marrow
The cavities of all bones of new-born are occupied by red marrow while in the adult jaw
occupied by fatty or yellow type of marrow, however foci of red bone marrow are seen in the
jaw which may be visible radiographically as zones of radiolucency.
Common locations are the maxillary and mandibular molar and premolar areas.
Periosteum and Endosteum (Fig.7)
Periosteum: it is a layer of tissue covering the outer surface of bone, it contains collagen fibers
and cells (osteoblasts) with blood vessels, nerves and fibroblasts.
Endosteum: the marrow spaces inside the bone are lined by endosteum, this tissue contains
cells (osteoblasts).
Fig.6

60
Anatomical defects of bone (Fig.8)
1.Fenestration (window):
This bony defect include isolated areas in which the root is not covered with bone but covered
only by periosteum and overlying gingiva and it does not extend to the marginal bone.
2. Dehiscence:
This bony defect include the denuded areas which extend to the bone margin, exposing the root
surface. The defects may extend to the middle of the root or farther.
Such defects occur on approximately 20% of the teeth, they occur more often on the facial bone
than on the lingual bone are more common on anterior than on posterior teeth.
The cause of these defects is not clear, but may be related to some factors such as, prominent
root, malposition or labial protrusion of the root with thin bony plate.
Fig.7

61
Haversian system or Osteon (Fig.9)
It is an internal mechanism that
bring a vascular supply to bones,
consists of central canal called
(Haversian canal) which in their
center contains the blood vessel.
These blood vessels surrounded by
bone lamellae which arranged in
concentric layers constitute the
center of an osteon.
The blood vessels in haversian canal
are connected with each other by
anastomoses running in the
Volkmann's canals, so the nutrition
of bone is secured by the
incorporation of blood vessels in the
bone tissue.
Fig.8
Fig.9

62
Bone cells
1. Osteoblast cells (bone forming cells):
Is responsible for the production of an organic matrix of bone which is consisting primarily of
collagen fibers called (osteoid), this bone matrix undergoes mineralization by the deposition of
minerals such as calcium and phosphate, which are subsequently transformed to hydroxyl
apatite
2. Osteoclast cells:
These are large multinucleated cells found in concavities on the bone surface called (howship's
lacunae) these cells responsible for bone resorption.
3. Osteocyte cells (Fig.10):
Osteoblast cells that become trapped in the bone matrix and later on in the mineralized bone
tissue, we call them osteocyte cells, they are located in the lacunae and are connected with the
one another by extending processes into canaliculi through which they get nutrients and
removes metabolic waste products.
Fig.10

63
Resorption of bone
The sequence of events in the resorptive process as follows:
1. attachment of osteoclasts to the mineralized surface of bone.
2. creation of a sealed acidic environment, which demineralizes bone and exposes the
organic matrix.
3. degradation of the exposed organic matrix to its constituent amino acids via the action
of released enzymes (e.g.,acid phosphates, cathepsin).
4. Sequestering of mineral ions and amino acids within the osteoclast.
Composition of the bone
Bone consists of 2/3 inorganic matter and 1/3 organic matrix.
✓ The inorganic matter is composed principally of the minerals calcium and phosphate,
along with hydroxyl, carbonate, citrate, and lactate, trace amounts of other ions such as
sodium, magnesium and fluorine. The mineral salts are in the form of hydroxy apatite
crystals.
✓ The organic matrix consists mainly of collagen type I fibers (90%), with small amounts
of non collagenous proteins such as osteocalcin and osteonectin.
* Bone contains 99% of the body’s calcium ions and therefore is the major source for calcium
release when the calcium blood levels decrease, this is monitored by the parathyroid gland.
Remodeling of alveolar bone (Fig.11)
Alveolar bone undergoes constant physiologic remodeling (resorption and formation) in
response to external forces specially occlusal forces.
Teeth erupts and tend to move mesially throughout life to compensate for wearing in the
proximal contact areas with age which become flat, this referred to as physiologic mesial
migration, thus osteoclast cells and bone resorption occur in areas of pressure on the mesial
surface and osteoblast cells with new bone formed in areas of tension on the distal surface. This
process of resorption and formation of bone is called bone remodeling and it is important in the
orthodontic treatment (Fig.12).

64
Remodeling of alveolar bone is regulated by local influences include functional requirements on
the tooth and age related changes in bone cells while, systemic influences are probably
Hormonal (e.g., parathyroid hormone, or vitamin D3).
Fig.11
Fig.12

65
7Dental Plaque Biofilm
Oral biofilms are functionally and structurally organized polymicrobial communities that are
embedded in an extracellular matrix of exopolymers on mucosal and dental surfaces.
Dental plaque is defined clinically as a structured resilient yellow-grayish biofilm that adheres
firmly to the intraoral hard surfaces, including removable and fixed restorations. The tough
extracellular matrix makes it impossible to remove plaque by rinsing or the use of sprays.
Plaque can thus be differentiated from other deposits that may be found on the tooth surface
such as materia alba and calculus.
Materia alba refers to soft accumulations of bacteria, food deposit, and tissue cells that lack the
organized structure of dental plaque and are easily displaced with a water spray.
Calculus is formed as a hard mineralized deposit of dental plaque and is generally covered by a
layer of unmineralized plaque.
Differences between bacterial deposits
Materia alba Dental plaque Claculus
1 White cheese-like
accumulations
Resilient clear to yellow
grayish
Hard deposits formed by
mineralization of dental
plaque
2 A soft accumulation of
salivary proteins
Primarily composed of
bacteria in a matrix of
salivary proteins
3 Lack of organized structure
(not complex) as dental
plaque)
Considered as a biofilm Generally covered by a
layer of un-mineralized
dental plaque
4 Easily displaced by a water
spray
Removed only by
mechanical rinsing (tooth
brushing)

66
Microorganisms represent the main component of dental plaque, with approximately 1011
bacteria contained in one gram of plaque (wet weight). The number of bacteria in supragingival
plaque on a single tooth surface can exceed 109
. In a periodontal pocket, counts can range from
103
bacteria in a healthy crevice to > 108
bacteria in a deep pocket.
Using highly sensitive molecular techniques for microbial identification, it has been estimated
that more than 500 distinct microbial phenotypes can be present as natural inhabitants of dental
plaque. Any individual may harbor 150 or more different species. Non- bacterial
microorganisms that are found in plaque include archaea, yeasts, protozoa, and viruses.
Dental plaque is broadly classified as supragingival or subgingival based on its position on the
tooth surface toward the gingival margin
✓ Supragingival plaque is found at or above the latter; when in direct contact with the
gingival margin it is referred to as marginal plaque.
✓ Subgingival plaque is found below the gingival margin between the tooth and the
gingival pocket epithelium.
Supragingival plaque typically demonstrates a stratified organization of a multilayered
accumulation of bacterial morphotypes. Gram-positive cocci and short rods predominat at the
tooth surface, whereas gram-negative rods and filaments, as well as spirochetes, predominate in
the outer surface of the mature plaque mass.
Fig.1 Clinical picture of 10-day-old
supragingival plaque. Balck rows indicate
early signs of gingival inflammation.
Fig.2 Supragingival calculus is depicted on
the buccal surface of maxillary molars
adjacent to the orifice for the parotid duct.

67
In general, the subgingival microbiota differs in composition from the supragingival plaque,
primarily because of the local availability of blood products and a low reduction-oxidation
(redox) potential, which characterizes the anaerobic environment.
The environmental parameters of the subgingival region differ from those of the supragingival
region. The gingival crevice or pocket is bathed by the flow of crevicular fluid, which contains
many substances which bacteria may use as nutrients. Host inflammatory cells and mediators
are likely to have considerable influence on the establishment and growth of bacteria in the
subgingival region. Both morphologic and microbiologic studies of subgingival plaque reveal
distinctions between the tooth-associated and soft tissue-associated regions of subgingival
plaque.
The tooth-associated cervical plaque, adhering to the root cementum, does not markedly differ
from that observed in gingivitis. At this location, filamentous microorganisms dominate, but
cocci and rods also occur. This plaque is dominated by gram positive rods and cocci, including
S. mitis, S. sanguinis, Actinomyces oris. However, in the deeper parts of the pocket, the
filamentous organisms become fewer in numbers, and in the apical portion they seem to be
virtually absent. Instead, the microbiota is dominated by smaller organisms without a particular
orientation. The apical border of the plaque mass is separated from the junctional epithelium by
a layer of host leukocytes, and the bacterial population of this apical tooth-associated region
shows an increased concentration of gram-negative rods.
The layers of microorganisms facing the soft tissue lack a definite intermicrobial matrix and
contain primarily gram-negative rods and cocci as well as large numbers of filaments,
flagellated rods, and spirochets. Host tissue cells (e.g., white blood cells and epithelial cells)
may also be found in this region. Bacteria are also found within the host tissues, such as in the
soft tissues and within epithelial cells, as well as in the dentinal tubules.
Fig.3 Scanning
electron
micrograph of
bacteria within
dentinal tubules.

68
The composition of the subgingival plaque depends on pocket depth; the apical part is more
dominated by spirochetes, cocci and rods, whereas in the coronal part more filaments are
observed.
The site specificity of plaque is significantly associated with diseases of the periodontium.
Marginal plaque, for example, is of prime importance in the initiation and development of
gingivitis. Supragingival plaque and tooth-associated subgingival plaque are critical in calculus
formation and root caries; whereas tissue associated subgingival plaque is important in the
tissue destruction that characterizes different forms of periodontitis.
Biofilms also form on artificial surfaces exposed to the oral environment such as prostheses and
implants.
Accumulation of a Dental Plaque Biofilm
The process of plaque formation can be divided into several phases
1- The formation of the pellicle on the tooth surface.
2- Initial adhesion/attachment of bacteria.
3- Colonization/plaque maturation.
Formation of the Pellicle
All surfaces in the oral cavity including hard and soft tissues, are coated with a layer of organic
material known as the acquired pellicle. The pellicle on tooth surface consists of more than 180
peptides, proteins, and glycoproteins including keratins, mucins, proline-rich proteins,
phosphoproteins (e.g., statherin), histidine-rich proteins, and other molecules that can function
as adhesion sites (receptors) for bacteria. Salivary pellicle can be detected on clean enamel
surfaces within 1 minute after introduction into the mouths of volunteers. By two hours, the
pellicle is essentially in equilibrium between adsorption and detachment, although further
pellicle maturation can be observed for several hours. Consequently, bacteria that adhere to
tooth surfaces do not contact the enamel directly but interact with the acquired enamel pellicle;
however, the pellicle is not merely a passive adhesion matrix.

69
Many proteins retain enzymatic activity when incorporated into the pellicle, and some of these,
such as peroxidases, lysozyme and α-amylase, may affect the physiology and metabolism of
adhering bacterial cells.
Initial Adhesion/Attachment of Bacteria
Tooth brushing removes most but not all bacteria from the exposed surfaces of teeth. However,
recolonization begins immediately and bacteria can be detected within 3 minutes of introducing
sterile enamel into the mouth.
The initial steps of transport and interaction with the surface are essentially nonspecific (i.e.,
they are the same for all bacteria). The proteins and carbohydrates that are exposed on the
bacterial cell surface become important once the bacteria are in loose contact with the acquired
enamel pellicle. It is the specific interactions between microbial cell surface “adhesin”
molecules and receptors in the salivary pellicle that determines whether a bacterial cell will
remain associated with the surface. Only a relatively small proportion of oral bacteria possess
adhesins that interact with receptors in the host pellicle, and these organisms are generally the
most abundant bacteria in biofilms on tooth enamel shortly after cleaning. Over the first 4 to 8
hours, 60% to 80% of bacteria present are members of the genus Streptococcus. Other bacteria
commonly present at this time include species that cannot survive without oxygen (obligate
aerobes), such as Haemophilus spp. and Neisseria spp., as well as organisms that can grow in
the presence or absence of oxygen (facultative anaerobes) including Actinomyces spp. and
Veillonella spp. These species are considered the “primary colonizers” of tooth surfaces.
The primary colonizers provide new binding sites for adhesion by other oral bacteria.
The metabolic activity of the primary colonizers modifies the local microenvironment in ways
that can influence the ability of other bacteria to survive in the dental plaque biofilm. For
example, by removing oxygen, the primary colonizers provide conditions of low oxygen tension
that permit the survival and growth of obligate anaerobes.
Colonization and Plaque Maturation
The primary colonizing bacteria adhered to the tooth surface provide a new receptors for
attachment by other bacteria in a process known as “coadhesion.” Together with growth of
adherent microorganisms, coadhesion leads to the development of micro colonies and
eventually to a mature biofilm.
Different species or even different strains of a single species have distinct sets of coaggregation
partners. Fusobacteria coaggregate with all other human oral bacteria while Veillonella spp.,

70
Capnocytophaga spp. and Prevotella spp. bind to streptococci and/or actinomyces. Each newly
cell becomes itself a new surface and therefore, may act as a coaggregation bridge to the next
potentially accreting cell type that passes by.
Well-characterized interactions of secondary colonizers with early colonizers include the
coaggregation of F. nucleatum with S. sanguinis, Prevotella loescheii with A. oris, and
Capnocytophaga ochracea with A. oris. Streptococci show intrageneric coaggregation, allowing
them to bind to the nascent monolayer of already bound streptococci.
Secondary colonizers, such as Prevotella intermedia, Prevotella loescheii, Capnocytophaga
spp., F. nucleatum, and P. gingivalis do not initially colonize clean tooth surfaces but adhere to
bacteria already in the plaque mass.
The transition from
early supragingival
dental plaque to
mature plaque
growing below the
gingival margin
involves a shift in the
microbial population
from primarily gram-
positive organisms to
high numbers of
gram- negative
bacteria. Therefore, in
the later stages of
plaque formation
coaggregation
between different
gram-negative species
is likely to
predominate.
Examples of these
types of interactions
are the co aggregation
of F. nucleatum with
P. gingivalis or T.
denticola.
Fig.4 Diagrammatic representation of initial plaque formation.

71
Overview of Primary and Secondary Colonizers in Dental Plaque
Primary colonizers Secondary colonizers
✓ Streptococcus gordonii
✓ Streptococcus intermedius
✓ Streptococcus mitis
✓ Streptococcus oralis
✓ Streptococcus sanguinis
✓ Actinomyces gerencseria
✓ Actinomyces israelii
✓ Actinomyces naeslundii
✓ Actinomyces oris
✓ Aggregatibacter
actinomycetemcomitans serotype a
✓ Capnocytophaga gingivalis
✓ Capnocytophaga ochracea
✓ Capnocytophaga sputigena
✓ Eikenella corrodens
✓ Actinomyces odontolyticus
✓ Veillonella parvula
✓ Campylobacter gracilis
✓ Campylobacter rectus
✓ Campylobacter showae
✓ Eubacterium nodatum
✓ Aggregatibacter
actinomycetemcomitans serotype b
✓ Fusobacterium nucleatum ssp
nucleatum
✓ Fusobacterium nucleatum ssp vincentii
✓ Fusobacterium nucleatum ssp
polymorphum
✓ Fusobacterium periodonticum
✓ Parvimonas micra
✓ Prevotella intermedia
✓ Prevotella loescheii
✓ Prevotella nigrescens
✓ Streptococcus constellatus
✓ Tannerella forsythia
✓ Porphyromonas gingivalis
✓ Treponema denticola
Factors Affecting Supragingival Dental dental plaque formation
Clinically, early undisturbed plaque formation on teeth follows an exponential growth curve
when measured planimetrically. During the first 24 hours starting from a clean tooth surface,
plaque growth is negligible from a clinical viewpoint (<3% coverage of the vestibular tooth
surface, which is an amount nearly undetectable clinically). This “lag time” is due to the fact
that the microbial population must reach a certain size before it can be easily detected by the
clinician. During the following 3 days, coverage progresses rapidly to the point where, after 4
days, on average 30% of the total coronal tooth area will be covered with plaque.
Several reports have shown that the microbial composition of the dental plaque will change
with a shift toward a more anaerobic and a more gram-negative flora including an influx of

72
fusobacteria, filaments, spiral forms, and spirochetes. This was in this beautifully illustrated in
experimental gingivitis studies ecologic shift within the biofilm, there is a transition from the
early aerobic environment characterized by gram-positive facultative species to a highly
oxygen-deprived environment in which gram negative anaerobic microorganisms predominate.
Bacterial growth in older plaque is much slower than in newly formed dental plaque
presumably because nutrients become limiting for much of the plaque biomass.
Topography of Supragingival Plaque
Early plaque formation on teeth follows a typical topographic pattern with initial growth along
the gingival margin and from the interdental space (areas protected against shear forces). Later,
a further extension in the coronal direction can be observed. This pattern may fundamentally
change when the tooth surface contains irregularities that offer a favorable growth path. Plaque
formation can also start from grooves, cracks, or pits. By multiplication, the bacteria
subsequently spread out from these starting up areas as a relatively even monolayer. Surface
irregularities are also responsible for the so-called “individualized plaque growth pattern, which
is reproduced in the absence of optimal oral hygiene. This phenomenon illustrates the
importance of surface roughness in plaque growth, which should lead to proper clinical
treatment options.
Surface Micro roughness
Rough intraoral surfaces (e.g. crown margins, implant abutments, and denture bases)
accumulate and retain more plaque and calculus in terms of thickness, area, and colony-forming
units.
Fig.5 Irregular plaque growth patterns follow tooth surface irregularities.

73
Ample plaque also reveals an increased maturity/pathogenicity of its bacterial components,
characterized by an increased proportion of motile organisms and spirochetes and/or a denser
packing of them.
Smoothing an intraoral surface decreases the rate of plaque formation.
Individual Variables Influencing Plaque Formation
The rate of plaque formation differs significantly between subjects, differences that might
overrule surface characteristics.
A distinction is often made between “heavy” (fast) and “light” (slow) plaque formers. It has
shown that the clinical wettability of the tooth surfaces, the saliva-induced aggregation of oral
bacteria, and the relative salivary flow conditions around the sampled teeth explained 90% of
the variation. Moreover, the saliva from light plaque formers reduced the colloidal stability of
bacterial suspensions of, for example, S. sanguinis.
Variation within the Dentition
Within dental arch large differences in plaque growth rate can be detected.
In general early plaque formation occurs faster: in the lower jaw (when compared to the upper
jaw); in molar areas; on the buccal tooth surfaces when compared to palatal sites (especially in
the upper jaw); and in the interdental regions when compared to the buccal or lingual surfaces.
Impact of Gingival Inflammation and Saliva
Several studies clearly indicate that early in vivo plaque formation is more rapid on tooth
surfaces facing inflamed gingival margins than on those adjacent to healthy gingival. These
studies suggest that the increase in crevicular fluid production enhances plaque formation.
Probably, some substance(s) from this exudate (e.g. minerals, proteins, or carbohydrates) favor
both the initial adhesion and/or the growth of the early colonizing bacteria.
Additionally, it is known that during the night, plaque growth rate is reduced by some 50%.
This seems surprising, since one would expect that reduced plaque removal and the decreased
salivary flow at night would enhance plaque growth.
The fact that the supragingival plaque obtains its nutrients mainly from the saliva appears to be
of greater significance than the antibacterial activity of saliva.

74
The Impact of Patient’s Age
Although older studies were contradictory, more recent papers clearly indicate that a subject’s
age does not influence de novo plaque formation.
The developed plaque in the older patient group resulted however, in a more severe gingival
inflammation, which seems to increased susceptibility to gingivitis with aging.
Spontaneous Tooth Cleaning
Many clinicians still believe that plaque is removed spontaneously from the teeth such as during
eating. However, based on the firm attachment between bacteria and surface, this seems
unlikely. Even in the occlusal surfaces of the molars, plaque remains, even after chewing
fibrous food carrots, apples, or chips.
Characteristics of Biofilm Bacteria (Life in “Slime City”)
Metabolism of Dental Plaque Bacteria
The majority of nutrients for dental plaque bacteria originate from saliva or GCF, although the
host diet provides an occasional but nevertheless important food supply.
Fig.6 No reduction of 100 hours old dental plaque before dinner (A), and after dinner (B)
with eating fibrous food

75
The transition from gram positive to gram negative microorganisms observed in the structural
development of dental plaque is paralleled by a physiologic transition in the developing plaque.
The growth of P. gingivalis is enhanced by metabolic byproducts produced by other
microorganisms, such as succinate from Capnocytophaga ochrecea and protoheme from
Campylobacter rectus. Overall, the total plaque population is more efficient than any one
constituent organism at releasing energy from the available substrates.
Metabolic interactions occur also between the host and plaque microorganisms. Increases in
steroid hormones are associated with significant increases in the proportions of P. intermedia
found in subgingival plaque. These nutritional inter-dependencies are probably critical to the
growth and survival of microorganisms in dental plaque and may partly explain the evolution of
highly specific structural interactions observed among bacteria in plaque.
Communication between Biofilm Bacteria
Bacterial cells do not exist in isolation. In a biofilm, bacteria have the capacity to communicate
with each other.
One example of this is quorum sensing, in which bacteria secrete a signaling molecule that
accumulates in the local environment and triggers a response such as a change in the expression
of specific genes once they reach a critical threshold concentration. The threshold concentration
is reached only at a high-cell density, and therefore bacteria sense that the population has
reached a critical mass, or quorum.
There is some evidence that intercellular communication can occur after cell-cell contact and in
this case, may not involve secreted signaling molecules.
Two types of signaling molecules have been detected from dental plaque bacteria: peptides
released by gram-positive organisms during growth and a “universal” signal molecule
autoinducer 2(AI-2). Peptide signals are produced by oral streptococci and are recognized by
cells of the same strain that produced them. Responses are induced only when a threshold
concentration of the peptide is attained, and thus the peptides act as cell density, or quorum,
sensors.
Biofilms and Antimicrobial Resistance
Bacteria growing in microbial communities adherent to a surface do not “behave” the same way
as bacteria growing suspended in a liquid environment (in a planktonic or unattached state). For
example, the resistance of bacteria to antimicrobial agents is dramatically increased in the

76
biofilm. Almost without exception, organisms in a biofilm are 1000 to 1500 times more
resistant to antibiotics than in their planktonic state.
The mechanisms of this increased resistance differ from species to species, from antibiotic to
antibiotic, and for biofilm growing in different habitats.
It is generally accepted that the resistance of bacteria to antibiotics is affected by their
nutritional status, growth rate, temperature, pH, and prior exposure to sub-effective
concentrations of antimicrobial agents. Variations in any of these parameters will thus lead to a
varied response to antibiotics within a biofilm. An important mechanism of resistance appears
to be the slower rate of growth of bacterial species in a biofilm, which makes them less
susceptible to many but not all antibiotics. The biofilm matrix, although not a significant
physical barrier to the diffusion of antibiotics, does have certain properties that can retard
antibiotic penetration.
In addition, extracellular enzymes such as β-lactamases, formaldehyde lyase, and formaldehyde
dehydrogenase may become trapped and concentrated in the extracellular matrix, thus
inactivating some antibiotics (especially positively charged hydrophilic antibiotics).
Recently, “super-resistant” bacteria were identified within a biofilm. These cells have multidrug
resistance pumps that can extrude antimicrobial agents from the cell. Since these pumps place
the antibiotics outside the outer membrane, the process offers protection against antibiotics that
target, for example, cell wall synthesis. The penetration and efficacy of antimicrobials against
biofilm bacteria are critical issues for the treatment of periodontal infections.
Antibiotic resistance may be spread through a biofilm by intercellular exchange of DNA. The
high density of bacterial cells in biofilm facilitates the exchange of genetic information among
cells of the same species and across species and even genera. Conjugation (the exchange of
genes through a direct interbacteria connection formed by a sex pilus), transformation
(movement of small pieces of DNA from the environment into the bacterial chromosome),
plasmid transfer, and transposon transfer have all been shown to occur in biofilms.

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