Periodontal disease

Classification of Periodontal
Disease
The Periodontal Pocket
Extension of Inflammation from the Gingiva to
The Supporting Periodontal Tissues
Furcation Involvement
Bone Loss and Patterns of Bone Destruction
In Periodontal Disease
Trauma from Occlusion
Gingival Disease in Childhood
Juvenile Periodontitis
Epidemiology of Gingival and Periodontal
Disease

Classification of Periodontal Disease
Classification of Periodontal
Disease The term periodontal disease is used in a
general sense to encompass all diseases of the
periodontium.
 The most common disease is initiated by plaque
accumulation in the gingivodental area and is
basically inflammatory in character, termed marginal
periodontitis or more accurately chronic
destructive periodontitis.
 The periodontal tissues can also be involved by
other nosologic entities and many of these fall into
degenerative or neoplastic categories. They are
considered as periodontal manifestations of
systemic diseases

CHRONIC DESTRUCTIVE PERIODONTITIS
I. Periodontitis
A. Marginal periodontitis
1. Slowly progressing
2. Rapidly progressing
3. Refractory
B. Juvenile form of periodontitis
1. Generalized form
2. Localized form
C. Necrotizing Ulcerative Periodontitis
II. Trauma from occlusion*
III. Periodontal atrophy*
A. Presenile atrophy
B. Disuse atrophy

MARGINAL PERIODONTITIS
Clinical features: chronic inflammation of the
gingiva, pocket formation, and bone loss. Tooth
mobility and pathologic migration appear in
advanced cases.
Etiology: dental plaque
Types: slowly progressing periodontitis, rapidly
progressing periodontitis, refractory
periodontitis

Slowly progressing periodontitis
 Also called “adult type periodontitis” and is
associated with abundant plaque and calculus
 It is usually painless, but may be accompanied by
sensitivity of exposed roots, dull, deep pain caused by
forceful wedging of food into periodontal pockets,
acute symptoms caused by periodontal abscess
formation, and pulpal symptoms resulting from root
caries
 It is generalized or affects many teeth.

Rapidly progressing periodontitis
 associated with scantier amounts of
plaque and calculus
 seen most commonly in young adults in
their twenties, but can occur up to age 35,
extreme inflammation, hemorrhage,
proliferation of the marginal gingiva,
exudation, and rapid bone loss.

Refractory periodontitis
 refers to cases that do not respond to
therapy and/or recur soon after adequate
treatment for unknown reasons
 accdg. to Page, it is due to the ff.
mechanisms: abnormal host response,
resistant organisms, or untreatable
morphologic problems

2-4 mm 4-6 mm 7 mm ↑
Marginal periodontitis is also subclassified on the basis
of severity and degree of tissue destruction:

JUVENILE PERIODONTITIS
 Includes advanced destructive lesions in children and
adolescents
Generalized form: includes the whole dentition,
associated with systemic conditions as Papillon-Lefevre
syndrome, hypophosphatasia, agranulocytosis, Down’s
syndrome and others
Localized form: previously termed as periodontosis,
precocious advanced alveolar atrophy, juvenile atrophy,
juvenile paradentosis, and juvenile parodontopathia;
characterized by deep angular lesions localized in
the first molars and incisors.

TRAUMA FROM OCCLUSION
Clinical features:
1. Increased tooth mobility
2. Widening of the periodontal space, particularly
in the gingival region of the root (angular
destruction of bone.
 These changes are adaptation phenomena to
the increased function. It does NOT produce
gingival inflammation or the formation of
periodontal pockets.

PERIODONTAL ATROPHY
Atrophy: decrease in the size of the tissue or
organ or of its cellular elements after it has
attained its normal mature size
 Senile (physiologic atrophy) refers to
generalized reduction in the height of alveolar
bone, accompanied by recession of gingiva
with overt inflammation or trauma from
occlusion, occurring with increasing age.

Presenile atrophy
 reduction in the height of periodontium that is uniform
throughout the mouth and without apparent cause
Disuse atrophy
Results when the functional stimulation for the
maintenance of the periodontal tissues is markedly
diminished or absent.
 characterized by thinning of periodontal ligament,
thinning and reduction in the number of periodontal fibers
and disruption of fiber bundle arrangement, thickened
cementum, reduction in height of alveolar bone, and
osteoporosis

 A periodontal pocket is a
pathologically deepened sulcus: it
is one of the important clinical
features of periodontal disease.

1. Enlarged, bluish red marginal gingiva with a
“rolled” edge separated from the tooth surface
2. A reddish blue vertical zone extending from
the gingival margin to the attached gingiva
3. A break in the faciolingual continuity of the
interdental gingiva
4. Shiny, discolored, and puffy gingiva
associated with exposed root surfaces
5. Gingival bleeding6. Purulent exudate of the gingival margin or its
response to digital pressure on the lateral
aspect
7. Looseness, extrusion, and migration of
teeth.
8. The development of diastemata where none
existed.

SYMPTOMS:
1. Localized pain or a sensation of pressure
after eating, which gradually diminishes
2. A foul taste in localized areas.
3. A tendency to suck material from the
interproximal spaces.
4. Radiating pain “deep in the bone”
5. A “gnawing” feeling or feeling of itchiness in
the gums.

SYMPTOMS:
6. The urge to dig a pointed instrument into
the gums with relief obtained from the
resultant bleeding
7. Complaints that food sticks between teeth
or that the teeth feel loose or a preference
to eat on the other side.
8. Sensitivity to heat and cold; toothache in
the absence of caries.

CLASSIFICATION:
ACCDG. TO
MORPHOLOGY
ACCDG. TO NO. OF
SURFACES
INVOLVED
I. Gingival Pocket
II. Periodontal
Pocket
1.Suprabony
pocket
2.Infrabony
pocket
I. Simple
II. Compound
III. Complex

GINGIVAL POCKET
 Relative or false pocket
 formed by gingival enlargement without
destruction of the underlying periodontal
tissues.
 The sulcus is deepened because of
increased bulk of gingiva
ACCDG. TO
MORPHOLOG
Y

PERIODONTAL POCKET
 Absolute or true pocket
 Occurs with destruction of supporting periodontal
tissues
 Has two types:
1. Suprabony – bottom of the pocket is coronal to
the underlying alveolar bone
2. Infrabony – bottom of the pocket is apical to the
underlying alveolar bone
ACCDG. TO
MORPHOLOG
Y

1. SIMPLE – one tooth surface
2. COMPOUND – two or more surfaces
3. COMPLEX – a spiral type of pocket that
originates on one tooth surface and twists
around the tooth to involve one or more
additional surfaces; most common
ACCDG. TO NO.
OF SURFACES
INVOLVED

Deepening of the gingival
sulcus may occur by:
1. Movement of the gingival
margin in the direction of
the crown
2. Migration of the junctional
epithelium apically and its
separation from the tooth
surface
3. Combination of both
processes
PATHOGENESIS

Plaque
Gingival
inflammation
Pocket formation
More plaque formation

Period of quiescence:
Period of inactivity
reduced inflammatory
response and little or no
loss of bone and CT
attachment
Gram+ bacteria
proliferate and a more
stable condition is
established
PEROIODONTAL DISEASE ACTIVITY
Period of exacerbation:
Period of activity
There is build-up of
unattached plaque, with
gram-, motile, and
anaerobic bacteria
Bone and CT attachment
are lost and pocket deepens
Show bleeding and
greater amounts of exudate
May last for days, weeks
or months

CLINAL FEATURES HISTOPATHOLOGIC FEATURES
1. Varying degrees of bluish red
discoloration; flaccidity; smooth,
shiny surface; and pitting on
pressure
1. Circulatory stagnation;
destruction of gingival fibers and
surrounding tissues; atrophy of
epithelium; edema and
degeneration
2. Gingival wall may be firm and
pink
2. Fibrotic changes
3. Bleeding upon probing 3. Increased vascularity; thinning
and degeneration of epithelium
4. Inner aspect of pocket is painful
upon exploring
4. Ulceration of the inner aspect of
the pocket wall
5. Pus may be expressed by
applying digital pressure
5. Suppurative inflammation of the
inner wall

Microtopography of the Gingival Wall of Pocket
1. Area of relative quiescence
flat surface with minor depressions and mounds and occasional shedding of
cells
2. Area of bacterial accumulation
Abundant debris and bacterial clumps (cocci, rods, filaments, few spirochetes)
penetrating into enlarged intercellular spaces
3. Areas of emergence of leukocytes
Leukocytes appear through holes in eintercellular spaces
4. Areas of leukocyte-bacterial interaction
Leukocytes are covered by bacteria in an apparent process of phagocytosis
5. Areas of intense epithelial desquamation
Consist of semiattached and folded epithelial squames
6. Areas of ulceration
Exposed connective tissue
7. Areas of hemorrhage
Numerous erythrocytes

The Pocket Contents
Periodontal pockets contain debris consisting
principally of:
1. Microorganisms and their products
2. Dental plaque
3. Gingival fluid
4. Food remnants
5. Salivary mucin
6. Desquamated epithelial cells
7. leukocytes

The following structural changes in cementum are
seen:
1. Presence of pathologic granules (due to
degeneration of sharpey’s fibers in cementum)
2. Areas of increased mineralization (decreased
sensitivity)
3. Areas of demineralization (increased sensitivity,
caries and pulpitis may occur
• The dominant microorganism in root surface caries
is Actinomyces viscosus
The Root Surface
Wall

1. Cementum covered by calculus
2. Attached plaque
3. Unattached plaque
4. Junctional epithelium
5. Partially lysed CT fibers
6. Intact CT fibers

THE RELATIONSHIP OF THE PERIODONTAL
POCKET TO BONE
Suprabony pocket Infrabony pocket
Base of the pocket is coronal to
the crest of alveolar bone
Base of the pocket is apical to
the crest of alveolar bone
Horizontal pattern of bone
destruction
Vertical (angular) pattern of
bone destruction
Restored transseptal fibers are
arranged horizontally
Restored transseptal fibers are
arranged obliquely
On the facial and lingual
surfaces, the PDL fibers
beneath the pocket follow their
normal horizontal-oblique
course
On facial and lingual, the PDL
fibers follow the angular pattern
of the adjacent bone

A periodontal abscess (lateral or parietal
abscess) is a localized purulent inflammation in
the periodontal tissues.
CLASSIFICATION ACCDG. TO LOCATION:
1. Abscess in the supporting periodontal tissue
along the lateral aspect of the root
2. Abscess in the soft tissue wall of a deep
periodontal pocket
The
Periodontal
Abscess

The periodontal cyst is an uncommon lesion that
produces localized destruction of the periodontal tissues
along a lateral root surface, most often in the mandibular
canine-premolar area.
The following possible etiologies have been suggested:
1. Odontogenic cyst
2. Lateral dentigerous cyst
3. Primordial cyst
4. Stimulation of epithelial rests of PDL by infection from
a periodontal abscess or from the pulp through an
accessory canal
The Periodontal Cyst

 The extension of inflammation from the
marginal gingiva into the supporting periodontal
tissues marks the transition from gingivitis from
periodontitis
 The transition from gingivitis to periodontitis is
associated with changes in the composition of
bacterial plaque.
In advanced stages, the number of motile
organisms and spirochetes increases, whereas
the number of coccoid and rods decreases

Interproximally:
1. From gingiva into
the bone
2. From the bone
into the PDL
3. From the gingiva
into the PDL

Facially and lingually:
1. From gingiva
along the outer
periosteum
2. From the
periosteum into
the bone
3. From the gingiva
into the PDL

THE EFFECT OF TRAUMA FROM OCCLUSION
 Trauma from occlusion may cause the
inflammatory exudate to be channeled between
the transseptal fibers directly into the PDL which
may lead to vertical bone losses and infrabony
pocket formation.
 Excessive pressure affects alignment of
transseptal fibers so that they become angular
instead of horizontal
 Excessive tension causes stretching and
unraveling of the principal fiber bundles of the
PDL, reducing the barrier provided by the intact
bundles

CLINICAL ASPECTS OF INFLAMMATION IN THE
PDL
Tooth Mobility
 The inflammatory exudate reduces tooth support
by causing degeneration and destruction of the
principal fibers and a break in the continuity
between the root and the bone
Pain
 Superimposed acute inflammation may be the
cause of considerable pain

 Periodontitis is an infectious disease of the
gingival tissue, changes that occur in bone are
crucial because the destruction of bone is
responsible for tooth loss.
 The height and density of the alveolar bone
are normally maintained by an equilibrium,
regulated by local and systemic influences
between bone formation and bone resorption.

 The most common cause of bone destruction in
periodontal disease is the extension of inflammation
from the marginal gingiva into the supporting
periodontal tissues.
 The inflammatory invasion of the bone surface and
the initial bone loss that follows mark the transition
from gingivitis to periodontitis.
 The extension of inflammation to the supporting
structures of a tooth may be modified by the
pathogenic potential of plaque or the resistance of the
host.

Periodontal destruction occurs in an
episodic, intermittent fashion, with periods of
inactivity or quiescence.
The destructive periods result in loss of
collagen and alveolar bone with deepening
of the periodontal pocket. The reasons for
the onset of destructive periods have not
been totally elucidated.
Periods of
Destruction

1. Bacterial plaque products induce the
differentiation of bone progenitor cells into
osteoclasts and stimulate gingival cells to
release mediators that have the same
effect.
2. Plaque products and inflammatory
mediators can also act directly on
osteoblasts or their progenitors, inhibiting
their action and reducing their numbers.
Mechanisms of
Bone
Destruction

Bone Destruction Caused by Trauma from
Occlusion
Another cause of periodontal destruction is trauma
from occlusion.
 Trauma from occlusion can produce bone
destruction in the absence or presence of
inflammation.
When combined with inflammation, trauma from
occlusion aggravates the bone destruction caused by
the inflammation and causes bizarre bone patterns.

Bone Destruction Patterns in Periodontal
Disease
Horizontal Bone Loss
Bone Deformities (Osseous Defects)
• Vertical or Angular Defects
• Osseous Craters
• Bulbous Bone Contours
• Reversed Architecture
• Ledges

Horizontal Bone Loss
 Horizontal bone loss is the most common
pattern of bone loss in periodontal disease.
 The bone is reduced in height, but the bone
margin remains roughly perpendicular to the
tooth surface. The interdental septa and facial
and lingual plates are affected, but not
necessarily to an equal degree around the
same tooth.

Bone Deformities (Osseous defects)
Different types of bone deformities can result
from periodontal disease. These usually occur
in adults and have been reported in human
skulls with deciduous dentitions. Their
presence may be suggested on radiographs,
but careful
probing and surgical exposure of the areas is
required to determine their exact conformation
and dimensions.

Vertical and Angular Defects
 occur in an oblique direction, leaving a hollowed-
out trough in the bone alongside the root; the base of
the defect is located apical to the surrounding bone.
 In most instances, angular defects have been
accompanying infrabony pockets; such pockets
always have an underlying angular defect.
 Angular defects are classified on the basis of the
number of osseous walls.

Osseous craters
 are concavities in the crest of the
interdental bone confined within the facial
and lingual walls.
 Craters have been found to make up
about one third (35.2%) of all defects and
about two thirds (62%) of all mandibular
defects. They are twice as common in
posterior segments as in anterior segments.

Bulbous bone contours
 are bony enlargements caused by
exostosis, adaptation to function, or
buttressing bone formation. They are found
more frequently in the maxilla than in the
mandible.

Reversed architecture
 Reversed architecture defects are
produced by loss of interdental bone,
including the facial plates, lingual plates, or
both, without concomitant loss of radicular
bone, thereby reversing the normal
architecture. Such defects are more common
in the maxilla.

Ledges
 Ledges are plateau-like bone
margins
caused by resorption of thickened bony
plates

 The term furcation involvement refers to the
invasion of the bifurcation and trifurcation of
multirooted teeth by periodontal disease.
 The prevalence of furcation involved molars is
not clear. Whereas some reports indicate that
the mandibular first molars are the most
common sites and the maxillary premolars are
the least common, others have found higher
prevalence in upper molars.
 The number of furcation involvements
increases
with age.

Clinical Features:
1. The tooth may or may not be mobile and is
usually symptom free.
2. Tooth is sensitive to thermal changes
(caused by caries or lacunar resorption of the
root in furcation area)
3. Recurrent or constant throbbing pain (caused
by pulp changes)
4. Sensitivity to percussion (caused by acute
inflammatory involvement of the periodontal
ligament.

Possible Etiologies:
1. Trauma from occlusion
2. Presence of enamel projections in the
furcation
3. Proximity of furcation to cemento-enamel
junction
4. Presence of accessory pulpal canals in the
furcation area (may extend pulpal
inflammation to the furcation)

Diagnosis:
Furcation involvements have been classified as
Grades I, II, III, and IV according to the amount
of tissue destruction
 Grade I – incipient bone loss
 Grade II – partial bone loss
 Grade III – total bone loss with through-and-
through opening of the furcation
 Grade IV – similar to Grade III but with
gingival recession exposing the furcation to view.

 Trauma from occlusion refers to tissue
injury resulting from occlusal forces
exceeding the adaptive capacity of the
tissues.
 Trauma from occlusion is the tissue
injury – not the occlusal force.
 An occlusion that produces such injury
is called a traumatic occlusion.

Acute Trauma
 Acute trauma from occlusion results from
an abrupt change in occlusal force such as
that produced by biting on a hard object or
restorations and prosthetic appliances that
interfere with or alter the direction of
occlusal forces on the teeth.
The results are tooth pain, sensitivity to
percussion, and increased tooth mobility.

Chronic Trauma
 Chronic trauma from occlusion is more
common than acute form.
 It most often develops from gradual
changes in the occlusion produced by tooth
wear, drifting movement, and extrusion of
teeth, combined with parafunctional habits
such as bruxism and clenching, rather than
as a sequela of acute periodontal trauma.

Primary trauma from occlusion
 occurs if trauma from occlusion is considered the
primary etiologic factor in periodontal destruction and
if the only local alteration to which a tooth is
subjected is one of occlusion
Secondary trauma from occlusion
 occurs if trauma from occlusion is considered a
secondary cause of periodontal destruction; this is
the case when the adaptive capacity of the tissues to
withstand occlusal forces is impaired.
 Alveolar bone loss is the most common cause of
secondary trauma and may be difficult to remedy.

Stages of Tissue Response
The tissue response occurs in
three stages. The first is injury, the
second is repair, and the third is
adaptive remodelling of the
periodontium

Stage I : Injury
 produced by excessive occlusal forces
 Different lesions are produced by pressure and
tension.
Severe tension causes widening of the periodontal
ligament, thrombosis, hemorrhage, tearing of the
periodontal ligament, and resorption of alveolar bone
 Severe pressure causes necrosis of the periodontal
ligament and bone. The bone is resorbed from viable
periodontal ligament adjacent to necrotic areas and from
marrow spaces, a process called undermining resorption.
Stages of
Tissue
Response

Stage II : Repair
 Repair is constantly occurring in the periodontium.
The damaged tissues are removed, and new
connective tissue cells and fibers, bone, and cementum
are formed in an attempt to restore the injured
periodontium.
 When bone is resorbed by excessive occlusal forces,
nature attempts to reinforce the thinned bony trabeculae
with new bone.
 The attempt to compensate for lost bone is called
buttressing bone formation and is an important
feature of the reparative process.
Stages of
Tissue
Response

Stage III : Adaptive
remodeling of the Periodontium
 If the repair process cannot keep pace with the
destruction caused by the occlusion, the periodontium is
remodeled in an effort to create a structural relationship
in which the forces are no longer injurious to the tissues.
 This results in a thickened periodontal ligament, which
is funnel-shaped at the crest, and angular defects in the
bone, with no pocket formation. The involved teeth
become loose.
Stages of
Tissue
Response

Effect of insufficient Occlusal Force
 Insufficient stimulation causes
degeneration of the periodontium, manifested
by thinning of the periodontal ligament,
atrophy of the fibers, osteoporosis of the
alveolar bone, and reduction in bone height.
Hypofunction results from an open bite
relationship, an absence of functional
antagonists, or unilateral chewing habits that
neglect one side of the mouth.

Reversibility of Traumatic Lesions
 Trauma from occlusion is reversible.
 The injurious force must be relieved for
repair to occur.

The Influence of Trauma from Occlusion on the
Progression of Marginal Periodontitis
 The local irritants that initiate gingivitis and periodontal
pockets affect the marginal gingiva but trauma from
occlusion occurs in the supporting tissues and does not
affect the gingiva
 Trauma from occlusion does not cause periodontal
pockets or gingivitis, nor does it have any influence on
bacterial repopulation of pockets after scaling and root
planing.
 Occlusal stresses however increase the periodontal
destruction induced by periodontitis.

Clinical and Radiographic Signs of Trauma from
Occlusion
 The most common clinical sign of trauma to the
periodontium is increased tooth mobility.
 The radiographic signs include:
1. Increased width of periodontal space
2. Vertical destruction of interdental septum
3. Radioluscence and condensation of alveolar bone
4. Root resorption

PATHOLOGIC MIGRATION
 Pathologic migration refers to tooth
displacement that results when the balance
among the factors that maintain physiologic
tooth position is disturbed by periodontal
disease
 occurs most frequently in the anterior region
 Pathologic migration in the occlusal or
incisal direction is termed extrusion.

The perodontium of the deciduous dentition:
1. The gingival of deciduous dentitions is pale
pink, firm and either smooth or stippled(the
latter is found in 35 percent of children from 5
to 13 year of age).
2. The interdentally gingival is broad
faciolingually and tends to be relatively
narrow mesidestally,in formity with the
contour of the a proximal tooth surfaces.
3. The mean gingival sulcus depth for the
primary dentations is 2.1mm ± 0.2mm.

Physiologic Gingival Changes Associated
with Tooth Eruption
The following are physiological changes in the
gingival associated with tooth eruption:
1. pre-eruption bulge - before the crown
appears in the oral cavity , the gingival presents
a bulged that is firm , may be slightly blanched,
and conforms to the underlying crown contour of
the teeth.

2. Formation of the Gingival Margin - The
marginal gingival and sulcus develop as the crown
penetrates the oral mucosa. In the course of
eruption the gingival margin is usually edematous
,rounded, and slightly
Reddened
3. normal prominence of the gingival margin -
During the period of mixed dentition it is normal for
the marginal gingiva around the permanent teeth to
be quit promenant ,particulary in the maxillary
anterior region.

TYPES OF GINGIVAL DISEASE
1. Chronic Marginal Gingivitis
2. Localized Gingival Recession
3. Acute Gingival infections

Chronic Marginal Gingivitis
 This is the most prevalent type of gingival change
in childhood. The gingival exhibits all the change in
color, size, consistency, and surface texture
characteristic of chronic inflammation .
 a fiery red surface discoloration is often
superimposed on underlying chronic change.
 gingival color change and swelling appear to be
more common expressions of gingivitis in children
than are bleeding and increased pocket.

Etiology
 In children ,as in adult, the most common cause of
gingivitis is plaque. Local conditions such as materia
alba and poor oral hygiene favor its accumulation.
 in preschool children ,the gingival response to
bacterial plaque. Was found to be markedly reduced
from that in adult.
 dental plaque appears to form more rapidly in
children(age 8 to 12 years) than in adult.

Calculus
 Is uncommon in infants it occur in approximately 9
per cent of children between the age of 4 and 6
years, in 18 percent between 7 and 9 years, in 33 to
43 percent between 10 and 15 year age.
 in children with cystic fibrosis, calculus formation
is more common (occurring in 77 per cent ages 7 to
9 years, and in 90 per cent at age 10 to 15 years)
and more severe; this is probably related to
increased concentration of phosphate, calcium, and
protein in saliva.

 Gingivitis associated with tooth eruption is
frequent and has given rise to the term eruption
gingivitis.
 Tooth eruption eruption per se dose not cause
gingivitis. The inflammation result from plaque
accumulation around erupting teeth.
 Plaque retention around deciduous teeth facilities
plaque formation around permanent teeth.
 Partially exfoliated, loss deciduous teeth
frequently cause gingivitis.
 Other factors favoring plaque build-up are food
impaction and materia alba accumulation around
tooth partically destroyed by caries.

 Children frequently develop unilateral chewing
habits to avoid loss or carious teeth, aggravating
the accumulation of plaque on non-chewing side.
 Gingivitis occur more frequently and with greater
severity around malposed teeth because of
increase tendency to accumulate plaque and
materia alba.
 Severe changes include gingival enlargment,
bluish red discoloration, ulceration.
 Gingival health and contour are restored by
correction of malposition.

 Gingivitis is increased in children with excessive
overbite and overjet, nasal obstruction, and mouth
breathing habit.

LOCALIZED GINGIVAL RECESSION
 Gingival recession around individual teeth or
groups of teeth is a common source of concern.
 The gingival may be inflamed or free of disease,
depending on the presence or absence of local
irritants.
 In children the position of the tooth in the arch is
most important.
 Gingival recession occurs on teeth in labial
version or on those that are tilted or rotated so that
the root projection labials.

ACUTE GINGIVAL INFECTIONS
Acute herpetic gingivostomatitis
 this is most common type of acute gingival
infections in childhood
 it often occurs as a sequela of upper respiratory
tract infections.
Candidiasis
 This is mycotic infection of the oral cavity
caused by the fungus candida albicans. Most often
acute but may be chronic

ACUTE GINGIVAL INFECTIONS
Acute necrotizing ulcerative gingivitis
 The incidence of (ANUG) in childhood is low.
 In children living in area chronic malnutration is
common and in children with down’s sydrome, the
incidence and severity of ANUG seem to be
increased
 Acute herpetic gingivostomatitis, which is more
common childhood, is occasionally erroneously
diagnosed as ANUG

TRAUMATIC CHANGES IN THE PERIODONTIUM
 traumatic change may occur in the periodontal
tissue of deciduous teeth under several condition.
 In the process of shedding deciduous teeth,
resorption of teeth and bone weakens the
periodontal support ,so that the existing functional
forces are injyrious to the remaining supporting
tissue.

TRAUMATIC CHANGES IN THE
PERIODONTIUM
 Excessive occlusal forces may be produced by
malalignament, mutilation, loss or extraction of
teeth or by dental restoraton.
In the mixeddentition stage ,the periodontium of
permanent teeth may be traumatizing because the
permanent teeth bear increased occlusal load .
 The periodontal ligament of an erupting
permanent tooth may be injured by occlusal forces
transmitted through the deciduous tooth it is
replacing

The Oral Mucous Membrane in Childhood
Diseases
 Childhood disease present specific alteration in
the oral mucosa include gingival disease. Among
these are the communicable diseases such as :
-varicella(chickenpox)
-rubeola(measles)
-scarlatina(scarlet fever)
-diphtheria

 Juvenile periodontitis refers to cases of
severe, rapid periodontal destruction and
premature tooth loss in children and teenagers,
the etiology of which is not understood.
 These cases occur infrequently and can be
classified as
1. Those occurring in otherwise healthy
individuals (localized form)
2. Those associated with a variety of diseases
of other systems

GENERALIZED FORM
This type of juvenile periodontitis attacks
the whole dentition or a large part of it and is
associated with systemic disturbances
 Papillon-lefevre syndrome
 Down’s Syndrome
 Neutropenias
 Hypophosphatasia
 Acute and Subacute Leukemia
 Prepubertal periodontitis

Papillon-Lefevre Syndrome
 a syndrome characterized by hyperkeratotic
skin lesions, severe destruction of the
periodontium, and in some cases, calcification of
the dura
 Periodontal lesions consist of early
inflammatory involvement leading to bone loss
and exfoliation of teeth
By the age of 15 years, patients are usually
edentulous except for the third molars
 The syndrome is inherited and appears to
follow an autosomal recessive pattern of
inheritance
Generalize
d
form

Down’s Syndrome
 a congenital disease caused by a
chromosomal abnormality and characterized
by mental deficiency and growth retardation
 Periodontal disease in Down’s syndrome is
characterized by formation of deep periodontal
pockets associated with a substantial plaque
accumulation and moderate gingivitis
 these findings are usually generalized,
although they tend to be more severe in the
lower anterior region
Generalize
d
form

Neutropenia
 destructive generalized periodontal lesions have
been described in children with neutropenia
Hypophosphatasia
 a rare familial skeletal disease, which in some cases
results in loss of primary teeth, particularly the incosors
Acute and Subacute Leukemia
 these diseases in children are accompanied by
gingival changes
Generalize
d
form

Prepubertal periodontitis
 these cases are rare, and they start during or
immediately following eruption of the primary teeth
 An extremely acute inflammation and
proliferation of the gingival tissues, with rapid
destruction of bone, are found
 All primary teeth are affected, but the permanent
dentition may not be affected
Generalize
d
form

LOCALIZED FORM
 previously known as diffuse atrophy of the
alveolar bone, deep cementopathia, parodontitis
marginalis progressiva, paradontosis,
periodontosis
Disease of the periodontium occurring in an
otherwise healthy adolescent which is
characterized by a rapid loss of alveolar bone
about more than one tooth of the permanent
dentition

Age and Sex Distribution
 juvenile periodontitis affects both males and
females and is seen most frequently in the period
of puberty and the age of 25 years
Distribution of Lesions
 The classic distribution is in the region of the
first molars and incisors, with the least destruction
in the cuspid-premolar area
Localized
form

Clinical Findings
 The most striking feature of early juvenile
periodontitis is the lack of clinical inflammation in
the presence of deep periodontal pockets
 There is a small amount of plaque, forming a
thin film on the tooth and rarely mineralizing to
become calculus
 Clasically, one sees a distolabial migration of
the maxillary incisors, with diastema formation
Localized
form

Clinical Course
 The rate of bone loss is about three to four
times faster than that in typical periodontitis
Histopathology
 A thin, frequently ulcerated pocket epithelium,
infiltrated by numerous leukocytes covers large
areas of inflammatory cell accumulation
composed mainly of plasma cells and blast
cells, with lymphocytes and macrophages
present in small numbers
Localized
form

Histopathology
 Collagen and other tissuecomponents
constitute only a small proportion of the
diseased site as compared with the situation in
adult-type periodontitis
Bacteriology
 The two bacteria that have been considered
pathogens in juvenile periodontitis are
Actinobacillus actinomycetemcomitans and
Capnocytophaga
Localized
form

Disease
Dental epidemiology is the study of pattern
(distribution) and dynamics of dental diseases in
a human population
Pattern implies that certain people are selected
for attack by a disease and that the association
between a disease and an affected population
can be described as age, sex, racial or ethnic
group, occupation, social characteristics, place
of residence, susceptibility , and exposure to
specific agents, to name only a few
Disease

Disease
Dynamics refers a temporal pattern and is
concerned with trends, cyclic patterns, and the
time that elapses between the exposure to
inciting factors and the onset of the specific
disease
Epidemiologic indices are attempts to
quantitate clinical conditions on a graduated
scale, thereby facilitating comparison among
populations examined by the same criteria and
methods.

Disease
Prevalence is the proportion of persons
affected by a disease at a specific point in time
Incidence is defined as the rate of occurrence
of new disease in a population during a given
interval of time

Disease
INDICES USED TO STUDY PERIODONTAL
PROBLEMS
The indices that are discussed can be divided
according to the variable measured
1. The degree of inflammation of the gingival
tissues
2. The degree of periodontal destruction
3. The amount of plaque accumulated
4. The amount of calculus present

Disease
Indices Used to Assess Gingival Inflammation
1. Papillary-Marginal Attachment Index
2. Periodontal Index
3. Gingivitis Component of the Periodontal Disease
Index
4. Gingival Index
5. Indices of Gingival Bleeding
• Sulcus Bleeding Index
• Bleeding Points Index
• Interdental Bleeding Index
• Gingival Bleeding Index

Disease
Papillary-Marginal Attachment Index (Schour and
Massler)
 Originally the PMA index was used to count the
number of gingival units affected with gingivitis
 The developers of this index eventually added a
severity component for assessing gingivitis; the
papillary units (P) were scored on a scale of 0 to 5,
and the marginal (M) and attached (A) gingiva were
scored on a scale of 0 to 3.
Indices Used to Assess
Gingival Inflammation

Disease
Periodontal Index (Russel)
 The PI was intended to estimate the extent of
deeper periodontal disease than the PMA index by
measuring the presence or absence of gingival
inflammation and its severity, pocket formation, and
masticatory function
0 – negative
1 – mild gingivitis
2 – Gingivitis
6 – Gingivitis with pocket formation
8 – Advanced destruction with loss of masticatory
function

Disease
Gingivitis Component of the Periodontal Disease Index
(Ramfjord)
 The Periodontal Disease Index (PDI) is similar to the PI
in that both are used to measure the presence and
severity of periodontal disease
 The PDI does so by combining assessments of
gingivitis and gingival sulcus depth on six selected teeth
(#3, 9, 12, 19, 25, 28)
 A numerical score for the gingival status component of
the PDI is obtained by adding the values for all of the
gingival units and by dividing by the number of teeth

Disease
Gingival Index (Loe and Silness)
 The gingival index (GI) was developed solely for the
purpose of assessing the severity of gingivitis and its
location in four possible areas: the distofacial papilla,
the facial margin, the mesiofacial papilla, and the
entire lingual gingival margin.
 Totaling the scores around each tooth yields GI
score for the area.
0.1 – 1.0 Mild gingivitis
1.1 – 2.0 Moderate gingivitis
2.1 – 3.0 Severe gingivitis

Disease
Indices of Gingival Bleeding
 The Sulcus Bleeding Index (SBI) of
Muhlemman and Mazor uses bleeding on gentle
probing as the first criterion for indicating gingival
inflammation
 The Bleeding Points Index (Lenox and
Kopczyk) was developed to assess a patient’s
oral hygiene performance. It determines the
presence or absence of gingival bleeding
interproximally and on the facial and lingual
surfaces of each tooth

Disease
Indices of Gingival Bleeding
 The Interdental Bleeding Index (caton and
Polson) utilizes a triangle-shaped toothpick
made of soft, pliable wood to stimulate the
interproximal gingival tissue
 The Gingival Bleeding Index (GBI) of Ainamo
and Bay was developed as an easy and suitable
technique for the practitioner to assess a
patient’s progress in plaque control

Disease
Indices Used to Measure Periodontal Destruction
1. Gingival Sulcus Measurement Component of the
Periodontal Disease Index
2. Extent and Severity Index
3. Radiographic Approaches to Measuring Bone
Loss
• Gingival-Bone Count Index
• Periodontitis Severity Index
Indices Used to Measure
Periodontal Destruction

Disease
Gingival Sulcus Measurement Component of the
Periodontal Disease Index (Ramfjord)
 The technique developed by Ramfjord for
measuring gingival sulcus depth with a
calibrated periodontal probe involves measuring
the distance from the cemento-enamel junction
to the free gingival margin to the bottom of the
gingival sulcus or pocket
 The difference between the two measurements
yields the gingival sulcus depth, which
translates into gingival attachment

Disease
Extent and Severity Index (Carlos and
coworkers)
 The ESI was developed because of a lack of
satisfaction with previous indices of
periodontal disease
 It expresses the percentage of sites that
exhibit disease (E) and measures mean
attachment loss in millimeters (S). Hence
the ESI = (E, S)

Disease
Radiographic Approaches to Measuring Bone
Loss
 The Gingival-Bone Count Index, developed by
Dunning and Leach, records the gingival condition
and the level of the crest of alveolar bone
 The Periodontitis Severity Index (PSI) was
developed by Adams and Nystrom to assess the
presence or absence of periodontitis. The
presence of interproximal bone loss is determined
radiographically using a modified Schei ruler

Disease
Indices Used to Measure Plaque Accumulation
1. Plaque Component of the Periodontal Disease
Index
2. Simplified Oral Hygiene Index
3. Turesky-Gilmore-Glickman Modification of the
Quigley-Hein Plaque Index
4. Plaque Index
5. Modified Navy Plaque Index
6. Patient Hygiene Performance Index

Disease
Plaque Component of the Periodontal Disease
Index
 The plaque component of the PDI is used on the
six teeth selected by Ramfjord (#3, 9, 12, 19, 25,
and 28) after staining with Bismarck brown
solution
 The criteria measure the presence and extent of
plaque on a scale of 0 to 3, looking specifically at
all interproximal facial and lingual surfaces the
index teeth.
Plaque Accumulation

Disease
Simplified Oral Hygiene Index (Greene and
Vermillion)
 The OHI-S measures the surface area of the tooth
covered by debris and calculus
 It consists of two components: a Simplified
Debris-Index (DI-S) and a Simplified Calculus
Index (CI-S). Each component is assessed on a
scale of 0 to 3.
 The six tooth surfaces examined in the OHI-S are
the facial surfaces of the teeth #3, 8, 14, and 24
and the lingual surfaces of #19 and 30.
Plaque Accumulation

Disease
Turesky-Gilmore-Glickman Modification of the
Quigley-Hein Plaque Index
 Plaque was assessed on the facial and lingual
surfaces of all teeth after using a disclosing
agent
 A plaque score per person was obtained by
totaling all of the plaque scores and dividing by
the number of surfaces examined.
Plaque Accumulation

Disease
Plaque Index (Silness and Loe)
 The PlI is unique among the indices because it
ignores the coronal extent of plaque on the
tooth surface area and assess only the
thickness of plaque at the gingival area of
tooth
 It examines distofacial, facial, mesiofacial, and
lingual surfaces
 The PlI score for the area is obtained by
totaling the four plaque scores per tooth.
Plaque Accumulation

Disease
Modified Navy Plaque Index
 This index records the presence or absence of
plaque, by a score of 1 or 0 respectively, on
nine areas of tooth surface of the six index
teeth used by Ramfjord.
 A modified navy plaque index score per person
is obtained by totaling all nine of the
subdivision scores per tooth surface and
dividing by the number of tooth surfaces
examined
Plaque Accumulation

Disease
Patient Hygiene Performance Index (Podshadley
and Haley)
 The PHP index was the first index developed for
the sole purpose of assessing an individual’s
performance in removing debris after
toothbrushing instruction
 It records the presence or absence of debris as
1 or 0 respectively, using the six surfaces of the
six OHI-S teeth
Plaque Accumulation

Disease
Indices Used to Measure Calculus(Podshadley
and Haley)
1. Calculus component of OHI-S
2. Calculus component of PDI
3. Probe Method of Calculus Assessment
4. Calculus Surface Index
5. Marginal Line Calculus Index

Disease
Indices Used to
Measure Calculus
Calculus component of
OHI-S
0 = No calculus
1 = Supragingival
calculus covering not
more than 1/3 of root
surface
2 = Supragingival
calculus cover 1/3 - 2/3
3 = Supragingival
calculus cover more than
2/3

Disease
Calculus component of PDI (Ramfjord)
 The calculus component of the PDI assesses the
presence and extent of calculus on the facial and
lingual surfaces of six teeth on a numerical scale of
0 to 3.
Probe method of Calculus Assessment (Volpe
and associates)
 developed for longitudinal studies of the quantity
of of supragingival calculus formed
Indices Used to
Measure Calculus

Disease
Calculus Surface Index (Ennever and coworkers)
 The CSI is one of two indices that are used in short-
term clinical trials of calculus-inhibitory agents, to
determine rapidly whether a specific agent has any
effect on reducing or preventing supragingival or
subgingival calculus
Marginal Line Calculus Index (Muhlemann and Villa)
 This index was developed to assess the
accumulation of supragingival calculus on the
gingival 3rd of tooth or along the margin of the
gingiva
Indices Used to
Measure Calculus

Disease
Factors Affecting the Prevalence and Severity of
Gingivitis and Periodontitis
1. Age
-prevalence and severity of periodontal disease
increases directly with increasing age
2. Sex
- In general, males consistently have a higher
prevalence and severity of periodontal disease
3. Race
- Blacks had more periodontal disease than
whites

Disease
Factors Affecting the Prevalence and Severity of
Gingivitis and Periodontitis
4. Education and Income
-periodontal disease is inversely related to increasing
levels of education, as well as increasing levels of
income
5. Place of Residence
- prevalence and severity of periodontal disease are
slightly higher in rural than in urban areas
6. Geographic Area
- Children and youths living in South have slightly
higher PI scores than in Midwest and West accdg to
NHES

Disease
Etiological Factors of Gingival and Periodontal
Disease
1. Oral Hygiene
- the strong positive association that exists between
poor oral hygiene and gingival and periodontal
disease makes poor hygiene the primary etiologic
agent
2. Nutrition
- A secondary factor in the etiology of periodontal
disease
- The nutrients that have been specifically associated
with the periodontal tissues are vit. A, B complex, C,
and D and calcium and phosphorus

Disease
Etiological Factors of Gingival and Periodontal
Disease
3. Fluorides
- some investigators reported lower prevalence and
severity of gingival and periodontal disease in
optimally fluoridated areas
4. Adverse Habits
- tobacco smoking and betel nut chewing have been
associated with increased periodontal disease
5. Professional Dental Care
- The incidence and severity of periodontal disorders
are lower under in individuals having regular dental
care

Periodontal disease

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