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Page 1: Aggressive period
Page 2: Aggressive period

Prof Dr. Eman Abd El-Sattar Tella.

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Aggressive periodontitis generally affects systemically

healthy individuals less than 30 years old although

patients may be older.

Aggressive periodontitis may be distinguished from

chronic periodontitis by the age of onset, the rapid rate

of disease progression, the nature and composition of

the subgingival microflora, alterations in the host's

immune response and a familial aggregation of

diseased individuals.

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LOCALIZED AGGRESSIVE

PERIODONTITIS

Clinical Characteristics

Localized aggressive periodontitis (LAP) 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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A striking feature of LAP is the lack of clinical

inflammation despite the presence of deep

periodontal pockets. Furthermore, the amount of

plaque on the affected teeth is minimal and

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. Although the quantity

of plaque may be limited, it often contains elevated

levels of A actinomycetemcomitans and in some

patients, Porphyromonas gingivalis.

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- Localized aggressive periodontitis progresses rapidly.The rate of bone loss is about three to four times fasterthan in chronic periodontitis.

- Other clinical features of LAP may include:

* Distolabial migration of maxillary incisors withdiastema formation.

* Increasing mobility of first molars.

* Sensitivity of denuded root surfaces to thermal andtactile stimuli.

* Deep dull radiating pain during masticationbecause of irritation of the supporting structures bymobile teeth and impacted food.

* Periodontal abscesses.

* Regional lymph node enlargement.

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Radiographic Findings:

Vertical loss of alveolar bone around the first molars and

incisors, beginning around puberty in healthy teenagers,

is a classic diagnostic sign of LAP.

Radiographic findings may include an "arc-shaped loss

of alveolar bone extending from distal surface of second

premolar to mesial surface of second molar“.

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GENERALIZED AGGRESSIVE

PERIODONTITIS

Clinical Characteristics

Generalized aggressive periodontitis (GAP) usually affects individuals

under the age of 30 but older patients also may be affected.

Clinically, GAP is characterized by "generalized interproxirnal

attachment loss affecting at least three permanent teeth other

than first molars and incisors".

- As seen in LAP, patients with GAP have small amounts of

bacterial plague associated with

the affected teeth. Quantitatively, the amount of plaque seems

inconsistent with the amount of periodontal destruction.

Qualitatively, Porphyromonas gingivalis. A. actinomycetem-comitans and Bacteroides forsythus frequently are detected in

the plaque that is present. In contrast to LAP, individuals affected

with GAP produce a poor antibody response to the pathogens

present.

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The destruction occurs episodically with periods of

advanced destruction followed by stages of

quiescence of variable length (weeks to months or

years). Radiographs show bone loss that has

progressed since the previous evaluation.

In cases of GAP, the gingival tissue response 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 occurs in the destructive stage in

which attachment and bone are actively lost.

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In other cases, the gingival tissues may appear pink, free

of inflammation. However, deep pockets can be

demonstrated by probing. This tissue response coincide

with periods of quiescence in which the bone level

remains stationary.

In other cases, the gingival tissues may appear pink,

free of inflammation. However, 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 GAP may have systemic

manifestations such as weight loss, mental depression

and general malaise. They should receive medical

evaluations to rule out possible systemic involvement.

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The radiographic picture in GAP range from

severe bone loss associated with minimal number

of teeth to advanced bone loss affecting the

majority of teeth in the dentition.

Sites in GAP patients demonstrated osseous

destruction of 25 to 60 % during a 9-week period.

Despite this extreme loss, other sites in the same

patient showed no bone loss.

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RISK FACTORS FOR AGGRESSIVE

PERIODONTITIS

Microbiologic Factors

- Although several specific microorganisms are

detected in patients with LAP (A

actinomycetemcomitans (A. a.), Capnocytophaga sp.

Eikenella corrodens, Prevotella intermedia and

Campyiobacter rectus), A. a. is implicated as the primary

pathogen associated with this disease is based on the

following evidence:

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1- High frequency of A. a. (approximately 90%) in

lesions characteristic of LAP.

2- Elevated levels of A. a. were showed in sites

with evidence of disease progression.

3- Elevated serum antibody titers to A.

actinomvcetemcomitans is showed in many

patients with LAP.

4- A correlation between reduction in the

subgingival load of A. a. during treatment and

a» successful clinical response.

5- A. a. produces a number of virulence factors

that may contribute to the disease process.

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Immunologic Factors:

Some immune defects are implicated in the pathogenesis

of aggressive periodontitis.

The human leukocyte antigens (HLA), which regulate

immune responses, were evaluated as markers for

aggressive periodontitis. HLA-A9 and B15 antigens are

consistently associated with aggressive periodontitis.

Patients with aggressive periodontitis display functional

defects of PMNs which can impair either the chemotactic

attraction of PMN to the site of infection or their ability to

phagocytose and kill microorganisms.

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Genetic Factors

- All individuals are not equally susceptible to

aggressive periodontitis. A familial pattern of

alveolar bone loss have implicated genetic factors

in aggressive periodontitis.

- Genetic predisposition for LAP 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 can influence

the extent of destruction seen in young adults.

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TREATMENT OF AGGRESSIVE

PERIODONTITIS

Localized Aggressive Periodontitis

- Standard periodontal therapy:

Such therapy has included scaling and root planing, flap

surgery with and without bone grafts, root amputations,

hemisections, occlusal adjustment and strict plaque control.

However, response was unpredictable. Frequent maintenance

visits appear to be most important.

Lack of response of aggressive periodontitis to local therapy

alone is the result of the presence of A.actinomycetemcomitans in the tissues where it remains after

therapy to reinfect the pocket. Systemic use of antibiotics

eliminates bacteria from the tissues.

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Current Approach to Therapy. Patients who are

diagnosed as having an early form of aggressive

periodontitis may respond to standard periodontal

therapy. In almost all cases, systemic tetracycline (250

mg of tetracycline 4 times daily for at least 1 week)

should be given in conjunction with local mechanical

therapy. If surgery is indicated, systemic tetracycline

should be taken approximately 1 hour before surgery.

Doxycycline 100 mg/day may also be used.

Chlorhexidine rinses should also be prescribed and

continued for several weeks to aid healing and augment

plaque control.

In refractory localized aggressive periodontitis cases,

tetracycline- esistant Actinobacilfus species have been

suspected. After performing antibiotic susceptibility

tests, the clinician may consider a combination of

amoxicillin and metronidazole.

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