aggressive periodontitis kalps ppt
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AGGRESSIVE PERIODONTITISLOCALIZED AGGRESSIVE PERIODONTITIS
Historical Background Clinical Characteristics Radiographic Findings
GENERALIZED AGGRESSIVE PERIODONTITIS Clinical Characteristics Radiographic Findings
RISK FACTORS FOR AGGRESSIVE PERIODONTITIS Microbiologic Factors Immunologic Factors Genetic Factors Environmental Factors
AGGRESSIVE vs CHRONICThe 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 affects
systemically healthy individuals less than 30 years old, although patients may be older.
AGGRESSIVE PERIODONTITISAggressive periodontitis describes three of
the diseases formerly classified as early onset periodontitis.
LJPGJPRPP
AGGRESSIVE PERIODONTITISLocalized 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)
LOCALIZED AGGRESSIVE PERIODONTITISHistorical BackgroundIn 1923, Gottlieb“ called diffuse atrophy o f the
alveolar bone and deep cementopathia In 1938, Wannenmacher described incisor-first molar
involvement and called the disease parodontitis marginalis progressiva
In 1966 the World Workshop in Periodontics concluded that the concept of periodontosis as a degenerative entity was unsubstantiated and that the term should be eliminated from periodontal nomenclature.
LOCALIZED AGGRESSIVE PERIODONTITISThe term juvenile periodontitis was introduced
by Chaput and colleagues in 1967 and by Butler' in 1969.
In 1971, Baer' defined it as "a 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.
The amount of destruction manifested is not commensurate with the amount of local irritants."
LOCALIZED AGGRESSIVE PERIODONTITISIn 1989 the World Workshop in Clinical
Periodontics 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 primary importance when making a diagnosis of LJP
Most recently, disease with the characteristics of LJP has been renamed localized aggressive periodontitis.
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” .
WHY INCISORS & FIRST MOLARS
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:
WHY INCISORS & FIRST MOLARS
1. After initial colonization of the first permanent teeth to erupt (the first molars and incisors), Actinobacillus actinomycetemcomitans evades the host defenses by different mechanisms,
production of polymorphonuclear leukocyte chemotaxis-inhibiting factors,
endotoxin, collagenases, leukotoxin,
WHY INCISORS & FIRST MOLARS
These factors allow the bacteria to colonize the pocket and initiate the destruction of the periodontal tissues.
After this initial attack, adequate immune defenses are stimulated to produce opsonic antibodies to enhance the clearance and phagocytosis of invading bacteria and neutralize leukotoxic activity.
In this manner, colonization of other sites may be prevented.
A strong antibody response to infecting agents is one characteristic of localized aggressive periodontitis.
WHY INCISORS & FIRST MOLARS
2. Bacteria antagonistic to A. actinomycetemcomitans may colonize 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."
WHY INCISORS & FIRST MOLARS
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.
WHY INCISORS & FIRST MOLARS
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 exposed to periodontal pockets but also of roots still surrounded by their periodontium.
CLINICAL CHARACTERISTICSA 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."
CLINICAL CHARACTERISTICSAlthough the quantity of plaque may be
limited, it often contains elevated levels of A. 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.
CLINICAL CHARACTERISTICSOther clinical features of localized aggressive
periodontitis may include Distolabial migration of the maxillary incisors
with concomitant diastema formation .Increasing mobility of the first molars, Sensitivity of denuded root surfaces to thermal
and tactile stimuli, andDeep, dull, radiating pain during mastication,
probably because of irritation of the supporting structures by mobile teeth and impacted food.
CLINICAL CHARACTERISTICSPeriodontal 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.
RADIOGRAPHIC FINDINGSVertical 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 from the distal surface of the second premolar to the mesial surface of the second molar“
GENERALIZED AGGRESSIVE PERIODONTITISClinical CharacteristicsGeneralized aggressive periodontitis usually
affects individuals under the age of 30, but older 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.
GENERALIZED AGGRESSIVE PERIODONTITISClinically 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 evaluation
GENERALIZED AGGRESSIVE PERIODONTITISAs 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 periodontal destruction.
Qualitatively, P. gingivalis, A. actinomycetemcomitans, and Bacteriodes forsythus frequently are detected in the plaque that is present.
GENERALIZED AGGRESSIVE PERIODONTITISTwo gingival tissue responses can be found in
cases of generalized aggressive periodontitis. One is a severe, acutely inflamed tissue, often
proliferating, 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 actively lost.
GENERALIZED AGGRESSIVE PERIODONTITISIn 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
However, despite the apparently mild clinical appearance, deep pockets can be demonstrated by probing.
This tissue response coincide with periods of quiescence in which the bone level remains stationary.
Some patients with generalized aggressive periodontitis may have systemic manifestations such as weight loss, mental depression, and general malaise
GENERALIZED AGGRESSIVE PERIODONTITISPatients with a presumptive diagnosis of
generalized 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 spontaneously or after therapy, whereas others may continue to progress inexorably to tooth loss despite intervention with conventional treatment
RADIOGRAPHOC FINDINGSThe 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 the same patient showed no bone loss.
RISK FACTORS FOR AGGRESSIVE PERIODONTITISMICROBIOLOGICAL FACTORSIMMUNOLOGICAL FACTORSGENETIC FACTORSENVIRONMENTAL FACTORS
RISK FACTORS FOR AGGRESSIVE PERIODONTITISMicrobiologic FactorsAlthough several specific microorganisms
frequently are detected in patients with localized aggressive periodontitis A. actinomycetemcomitans, Capnocytophaga sp., Eikenella corrodens, Prevotella intertnedia, and Campylobacter rectus),
A. actinomycetemcomitans has been implicated as the primary pathogen associated with this disease.
RISK FACTORS FOR AGGRESSIVE PERIODONTITISAs summarized by Tonetti and Mombelli, this
link is based on the following evidence: (1) A. actinomycetemcomitans is found in
high frequency (approximately 90%) in lesions characteristic of localized aggressive periodontitis,
(2) sites with evidence of disease progression often show elevated levels of A. actinomycetemcomitans,
RISK FACTORS FOR AGGRESSIVE PERIODONTITIS(3) many patients with the clinical
manifestations of localized aggressive periodontitis have significantly elevated serum antibody titers to A. actinomycetemcomitans,
(4) clinical studies show a correlation between reduction in the subgingival load of A. actinomycetemcomitans during treatment and a successful clinical response, and
(5) A. actinomycetemcomitans produces a number of virulence factors that may contribute to the disease process
IMMUNOLOGIC FACTORSSome immune defects have been implicated
in the pathogenesis of aggressive periodontitis.
The human leukocyte antigens (HLA), which regulate immune responses, have been evaluated as candidate markers for aggressive periodontitis.
HLA-A9 and B15 antigens are consistently associated with aggressive periodontitis
IMMUNOLOGIC FACTORSPatients 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 patients with respect to their production of PGE 2 in response to lipopolysaccharide (LPS).
IMMUNOLOGIC FACTORSThis 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 be disproportionately present in patients with localized aggressive periodontitis.
These PMN and monocyte defects may be induced by the bacterial infection or may be genetic in origin.
AutoimmunityAutoimmunity has been considered to have a role
in generalized aggressive periodontitis ,antibodies to collagen, DNA, and immunoglobulin G (IgG).
Possible immune mechanisms include An increase in the expression of type II major
histocompatibility complex (MHC) molecules, HLA DR43 ,
Altered helper or suppressor T-cell function,Polyclonal activation of B cells by microbial plaque,
and Genetic predisposition.
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 a role in this disease, which is transmitted through an autosomal dominant mode of inheritance
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 generalized aggressive periodontitis.
However, smoking may not have the same impact on attachment levels in younger patients with localized aggressive periodontitis.
Palmar and plantar hyperkeratosis associated
with Papillon-Lefevre syndrome.
Radiograph of patient with Papillon-Lefevre syndrome
Patient with Papillon-Lefevre syndrome
Probe extends deep into pocket on mesial of molar. Gingiva is healthy looking(LJP)
Localized juvenile periodontitis in a 16-year-old male. Maxillary and mandibular incisors have severe bone loss causing them to spread.
Radiograph demonstrating deep localized circumferential bone loss on first molar in 18-year-old.
Radiograph showing semilunar bone defect on mesial of first molar in a patient with LJP
Rapidly progressive adult periodontitis in a 28-year-old
Rapidly progressive adult periodontitis in a 28-year-old female, pocket depth recordings.
Rapidly progressive adult periodontitis in a 28-year-old female, radiographs
Rapidly progressive adult periodontitis in a 29-year-old
Rapidly progressive adult periodontitis in a 29-year-old female.
Prepubertal periodontitis: 13-year-old boy with agranulocytosis.
Prepubertal periodontitis: 13-year-old boy with agranulocytosis
Prepubertal periodontitis: 10-year-old boy with S cyclic neutropenia.
Prepubertal periodontitis: 10-year-old boy with agammaglobulinemia and cyclic neutropenia.
LJP IN 19 YR OLD
LJP IN 19 YR OLD
LJP IN 19 YR OLD
Radiograph of a case of juvenile periodontitis showing typical molar-incisor lesions.
Lingual view of the left mandibular molar are in a patient with juvenile periodontitis.
Lingual view of the left mandibular molar are in a patient with juvenile periodontitis., after flap elevation