48312031 aggressive period on tit is kalps ppt

8/6/2019 48312031 Aggressive Period on Tit Is Kalps Ppt

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AGGRESSIVE PERIODONTITIS

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y LOCALIZED AGGRESSIVE PERIODONTITIS

Historical Background

Clinical Characteristics

Radiographic Findings

y GENERALIZED AGGRESSIVE PERIODONTITIS


Radiographic Findings

y RISK FACTORS FOR AGGRESSIVE PERIODONTITIS

Microbiologic Factors Immunologic Factors

Genetic Factors

Environmental Factors

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AGGRESSIVE vs CHRONIC

The rapid rate of disease progression,

The nature and composition of the associated

subgingival microflora, Alterations in the host's immune response,

Familial aggregation of diseased individuals.

Aggressive periodontitis generally affectssystemically healthy individuals less than 30

years old, although patients may be older.

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Aggressive periodontitis describes three of the

diseases formerly classified as early onset

periodontitis.

LJP

GJP

RPP

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Localized aggressive periodontitis was

formerly classified as localized juvenile

periodontitis (LJP).

Generalized aggressive periodontitis

encompasses the diseases previously

classified as

Generalized juvenile periodontitis (GJP)

Rapidly progressive periodontitis (RPP)

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LOCALIZED AGGRESSIVE PERIODONTITIS

y Historical Background

y In 1923, Gottlieb called diffuse atrophy o f the alveolar bone anddeep cementopathia

y In 1938, Wannenmacher described incisor-first molar involvement

and called the diseaseparodontitis marginalis progressivay In 1966 the World Workshop in Periodontics concluded that the

concept of periodontosis as a degenerative entity wasunsubstantiated and that the term should be eliminated fromperiodontal nomenclature.

y

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LOCALIZED AGGRESSIVE

PERIODONTITIS The termjuvenile periodontitis was introduced byChaputand colleagues in 1967 and by Butler' in1969.

In 1971, Baer' defined it as "a disease of theperiodontium occurring in an otherwise healthyadolescent which is characterized by a rapid lossof alveolar bone about more than one tooth ofthe permanent dentition.

The amount of destruction manifested is notcommensurate with the amount of localirritants."

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LOCALIZED AGGRESSIVE

PERIODONTITIS In 1989 the World Workshop in ClinicalPeriodontics categorized this disease as localized

juvenile periodontitis (LJP), a subset of the broad

classification of early onset periodontitis (EOP). Under this classification system, age of onset and

distribution of lesions were of primaryimportance when making a diagnosis of LJP

Most recently, disease with the characteristics ofLJP has been renamed localized aggressive

periodontitis.

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CLINICAL CHARACTERISTICS

Localized aggressive periodontitis usually has

an age of onset around puberty.

Clinically, it is characterized as having"localized first molar/incisor presentation with

interproximal attachment loss on at least two

permanent teeth, one of which is a first molar,

and involving no more than two teeth other

than first molars and incisors .

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WHY INCISORS & FIRSTMOLARS

The localized distribution of lesions in

localized aggressive periodontitis is

characteristic but as yet unexplained.

The following possible reasons for the

limitation of periodontal destruction to certain

teeth have been suggested:

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1. After initial colonization of the first permanentteeth to erupt (the first molars and incisors),Actinobacillus actinomycetemcomitans evades

the host defenses by differentmechanisms, production of polymorphonuclear leukocyte

chemotaxis-inhibiting factors,

endotoxin,

collagenases,

leukotoxin,

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y These factors allow the bacteria to colonize the pocketand initiate the destruction of the periodontal tissues.

y After this initial attack, adequate immune defenses are

stimulated to produce opsonic antibodies to enhancethe clearance and phagocytosis of invading bacteria andneutralize leukotoxic activity.

y In this manner, colonization of other sites may beprevented.

y A strong antibody response to infecting agents is onecharacteristic of localized aggressive periodontitis.

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2. Bacteria antagonistic to A.

actinomycetemcomitans maycolonize the

periodontal tissues and inhibit A.

actinomycetemcomitans from further

colonization of periodontal sites in the mouth.

This would localize A. actinomycetemcomitans

infection and tissue destruction."

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3.A. actinomycetemcomitans may lose its

leukotoxin producing ability for unknown

reasons.

If this happens, the progression of the disease

may become arrested or retarded and

colonization of new periodontal sites averted.

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4. The possibility that a defect in cementum

formation may be responsible for the localization

of the lesions.

Root surfaces of teeth extracted from patients

with localized aggressive periodontitis have been

found to have hypoplastic or aplastic cementum.

This was true not only of root surfaces exposedto periodontal pockets but also of roots still

surrounded by their periodontium.

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A striking feature of localized aggressive

periodontitis is the lack of clinical inflammation

despite the presence of deep periodontal pockets

Furthermore, in many cases the amount of

plaque on the affected teeth is minimal, which

seems inconsistent with the amount of

periodontal destruction present . The plaque that is present forms a thin biofilm on

the teeth and rarely mineralizes to form calculus."

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Although the quantity of plaque may be

limited, it often contains elevated levels ofA.

actinomycetemcomitans, and in some

patients, Porphyromonas gingivalis.

Localized aggressive periodontitis progresses

rapidly.

The rate of bone loss is about three to four

times faster than in chronic periodontitis.

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Other clinical features of localized aggressiveperiodontitis may include

Distolabial migration of the maxillary incisors

with concomitant diastema formation . Increasing mobility of the first molars,

Sensitivity of denuded root surfaces to thermaland tactile stimuli, and

Deep, dull, radiating pain during mastication,probably because of irritation of the supportingstructures by mobile teeth and impacted food.

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Periodontal abscesses may form at this stage,

and regional lymph node enlargement may

occur.

It should be noted that not all cases of

localized aggressive periodontitis progress to

the degree described previously.

In some patients, the progression of

attachment loss and bone loss may be self-

arresting.

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RADIOGRAPHIC FINDINGS

Vertical loss of alveolar bone around the first

molars and incisors, beginning around puberty

in otherwise healthy teenagers, is a classic

diagnostic sign of localized aggressive

periodontitis.

Radiographic findings may include an "arc-

shaped loss of alveolar bone extending fromthe distal surface of the second premolar to

the mesial surface of the second molar

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GENERALIZED AGGRESSIVE

PERIODONTITIS


Generalized aggressive periodontitis usually

affects individuals under the age of 30, butolder patients also may be affected.

In contrast to localized aggressive

periodontitis, evidence suggests that

individuals affected with generalized

aggressive periodontitis produce a poor

antibody response to the pathogens present.

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PERIODONTITIS

Clinically it is characterized by Generalized

interproximal attachment loss affecting at

least three permanent teeth other than first

molars and incisors"

The destruction appears to occur episodically

with periods of advanced destruction followed

by stages of quiescence of variable length(weeks to months or years).

Radiographs often show bone loss that has

progressed since the previous evaluation22


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PERIODONTITIS

As seen in localized aggressive periodontitis,

patients with generalized aggressive

periodontitis often have small amounts of

bacterial plaque associated with the affected

teeth .

Quantitatively, the amount of plaque seems

inconsistent with the amount of periodontaldestruction.

Qualitatively, P. gingivalis, A.

actinomycetemcomitans, and Bacteriodes23


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PERIODONTITIS

Two gingival tissue responses can be found in

cases of generalized aggressive periodontitis.

One is a severe, acutely inflamed tissue, oftenproliferating, ulcerated, and fiery red

Bleeding may occur spontaneously or with

slight stimulation.

Suppuration may be an important feature.

This tissue response is considered to occur in

the destructive stage, in which attachment

and bone are activel lost.24


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PERIODONTITIS

y In other cases, the gingival tissues may appear

pink, free of inflammation, and occasionally with

some degree of stippling, although the last

feature may be absent

yHowever, despite the apparently mild clinical

appearance, deep pockets can be demonstrated

by probing.y This tissue response coincide with periods of

quiescence in which the bone level remains

stationary.

y Some atients with eneralized a ressive25


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PERIODONTITIS Patients with a presumptive diagnosis ofgeneralized aggressive periodontitis must

have their medical histories updated and

reviewed.

These patients should receive medical

evaluations to rule out possible systemic

involvement.

As seen with localized aggressive

periodontitis, cases of generalized aggressive

periodontitis may be arrested spontaneously26


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RADIOGRAPHOC FINDINGS

The radiographic picture in generalized

aggressive periodontitis can range from severe

bone loss associated with the minimal number

of teeth, as described previously, to advanced

bone loss affecting the majority of teeth in the

dentition

Despite this extreme loss, other sites in thesame patient showed no bone loss.

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RISK FACTORS FOR AGGRESSIVE

PERIODONTITIS

MICROBIOLOGICAL FACTORS

IMMUNOLOGICAL FACTORS

GENETIC FACTORS ENVIRONMENTAL FACTORS

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PERIODONTITIS

yMicrobiologic Factors

yAlthough several specific microorganisms

frequently are detected in patients with localized

aggressive periodontitis

y A. actinomycetemcomitans,

y Capnocytophaga sp.,

y Eikenella corrodens,y Prevotella intertnedia, and

y Campylobacter rectus),

yA. actinomycetemcomitans has been implicated as

the rimar atho en associated with this29


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PERIODONTITIS

As summarized by Tonetti and Mombelli, this

link is based on the following evidence:

(1)A. actinomycetemcomitans is foundin highfrequency (approximately 90%) in lesions

characteristic of localized aggressive

periodontitis,

(2) sites with evidence of disease progression

often show elevated levels ofA.

actinomycetemcomitans,

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PERIODONTITIS

y (3) many patients with the clinicalmanifestations of localized aggressiveperiodontitis have significantly elevated serum

antibody titers to A. actinomycetemcomitans,y (4) clinical studies show a correlation between

reduction in the subgingival load ofA.actinomycetemcomitans during treatment anda successfulclinical response, and

y (5)A. actinomycetemcomitans produces anumber of virulence factors that may

contribute to the disease process31


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IMMUNOLOGIC FACTORS

Some immune defects have been implicated in

the pathogenesis of aggressive periodontitis.

The human leukocyte antigens (HLA), whichregulate immune responses, have been

evaluated as candidate markers for aggressive

periodontitis.

HLA-A9 and B15 antigens are consistently

associated with aggressive periodontitis

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IMMUNOLOGIC FACTORS

Patients with aggressive periodontitis display

functional defects of polymorphonuclear

leukocytes (PMNs), monocytes, or both.

These defects can impair either the

chemotactic attraction of PMN to the site of

infection or their ability to phagocytose and

kill microorganisms.

Current studies have also demonstrated a

hyper responsiveness of monocytes from

localized aggressive periodontitis patients33


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IMMUNOLOGIC FACTORS

This hyperresponsive phenotype could lead to

increased connective tissue or bone loss due

to excessive production of these catabolic

factors.

Additionally, poorly functional inherited forms

of monocyte FcyRII, the receptor for human

IgG2 antibodies, have been shown to bedisproportionately present in patients with

localized aggressive periodontitis.

These PMN and monocyte defects may be34


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Autoimmunity

yAutoimmunity has been considered to have a role

in generalized aggressive periodontitis ,antibodies

to collagen, DNA, and immunoglobulin G (IgG).

y Possible immune mechanisms include

yAn increase in the expression of type II major

histocompatibility complex (MHC) molecules, HLA

DR43 ,yAltered helper or suppressor T-cell function,

y Polyclonal activation of B cells by microbial

plaque, and 35


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Genetic Factors

Results from several studies support the

concept that all individuals are not equally

susceptible to aggressive periodontitis

Currently, specific genes have not been

identified that are responsible for these

diseases.

However, segregational analyses and linkage

analyses of families with a genetic

predisposition for localized aggressive

periodontitis suggest that a major gene plays a36


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Environmental Factors

The amount and duration of smoking are

important variables that can influence the

extent of destruction seen in young adults .

Patients with generalized aggressive

periodontitis who smoke have more affected

teeth and more loss of clinical attachment

than nonsmoking patients with generalizedaggressive periodontitis.

However, smoking may not have the same

impact on attachment levels in younger37


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Palmar and plantar hyperkeratosis associated

with Papillon-Lefevre syndrome.

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Radiograph of patient with Papillon-

Lefevre syndrome

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Patient with Papillon-Lefevre

syndrome

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Probe extends deep into pocket on mesial of

molar. Gingiva is healthy looking(LJP)

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Radiograph demonstrating deep localized circumferential bone

loss on first molar in 18-year-old.

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Radiograph showing semilunar bone defect on

mesial of first molar in a patient with LJP

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Rapidly progressive adult periodontitis in

a 28-year-old

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Rapidly progressive adult periodontitis in a 28-year-

old female, pocket depth recordings.

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Rapidly progressive adult periodontitis in

a 28-year-old female, radiographs

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Rapidly progressive adult periodontitis in a

29-year-old

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Rapidly progressive adult periodontitis in a 29-year-

old female.

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Prepubertal periodontitis: 13-year-old boy

with agranulocytosis.

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Prepubertal periodontitis: 13-year-old

boy with agranulocytosis

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Prepubertal periodontitis: 10-year-old boy with

S cyclic neutropenia.

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Prepubertal periodontitis: 10-year-old boy with

agammaglobulinemia and cyclic neutropenia.

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LJP IN 19 YR OLD

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LJP IN 19 YR OLD

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LJP IN 19 YR OLD

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Radiograph of a case of juvenile periodontitis

showing typical molar-incisor lesions.

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Lingual view of the left mandibular molar are in a

patient with juvenile periodontitis.

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Lingual view of the left mandibular molar are in a patient with

juvenile periodontitis., after flap elevation

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48312031 aggressive period on tit is kalps ppt

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