Prof.Dr. Mohamed El-Shahat - Delta Univdeltauniv.edu.eg/.../uploads/Aggressive-Periodontitis.pdfV. Necrotizing periodontal diseases a. Necrotizing ulcerative gingivitis (NUG) b. Necrotizing

Prof.Dr. Mohamed El-Shahat



Aggressive Periodontitis

Dr. Mohamad Al-ShahatProfessor of Oral Medicine & Periodontology



The bone height is within 2 millimeters of the cemento-enamel junction (CEJ)

The crestal bone is a continuation of the lamina dura of the teeth, and is continuous from tooth to tooth

Between the anterior teeth, the alveolar crest is pointed

Between the posterior teeth, the lamina duraand the crestal bone form a box, with sharp angles





I. Gingival diseasesa. Plaque-induced gingival diseasesb. Non-plaque-induced gingival diseases

II. Chronic periodontitisa. localizedb. Generalized

III. Aggressive periodontitisa. localizedb. Generalized

IV. Periodontitis as a manifestation of systemic diseases

Types of Periodontal Diseases


V. Necrotizing periodontal diseasesa. Necrotizing ulcerative gingivitis (NUG)

b. Necrotizing ulcerative periodontitis (NUP)

VI. Abscess of the periodontiuma. Gingival

b. Periodontalc. Pericoronal

VII. Periodontitis associated with endodontic lesions

a. Endodontic-periodontal lesion

b. Periodontal-endodontic lesionc. Combined lesion

VIII. Developmental or acquired deformities and conditions

a. Localized tooth-related factors

b. Mucogingival conditionsc. Occlusal trauma



Localized erosions of the marginal boneThinning of crestal lamina dura Loss of sharp border with the lamina dura

of the adjacent teeth Loss of spiking in the anterior Slight loss of bone height (<1/3)





Generalized form demonstrates horizontalbone loss

Localized defects include vertical bone lossand loss of buccal and lingual cortices

Loss of buccal or lingual cortex is difficultto view radiographically. It may be seenas decreased density over the root surface




Bone loss seen on radiographs is anindicator of past disease activity

Once periodontal treatment is initiatedand the disease is in remission, bone levels will not increase.

Therefore, clinical examination is necessary to determine the current disease status of the periodontium



Patient may have horizontal or vertical bone loss, or a combination of generalized horizontal bone loss with localized vertical defects

Bone level is in the apical 1/3 of the root Clinically, the teeth may be shifting, tipping,

or drifting Bone loss may be more extensive than is

apparent on the radiographs




It generally affects systemically healthy individuals less than 30 years old.

It is distinguished from chronic periodontitisby:

- Age of onset- Rapid rate of disease progression- Nature and compositions of the associated

subgingival microflora- Alterations in the host’s immune response -Familial aggregation of diseasedindividuals.


Formerly known as “Early-onset Periodontits” Classified into:

- Localized aggressive periodontitis(formerly known as Localized Juvenile Periodontits – LJP)

- Generalized aggressive periodontitis(formerly included Generalized Juvenile Periodontits “GJP” and Rapidly Progressive Periodontitis “RPP”)


Age of onset at about puberty. Difinition:

“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”



Overall Prevalence: 0.53%

21 times more likely to be seen in African

Americans than whites.

Prevalence in Hispanics: 1.7%


Patients will/may have bone loss, and possibly tooth loss by age 20.

Defective PMNs functions. LAP occurs in healthy adolescents: Colonization of Actinobacillus actinomycetemcomitans

(Aa). Minor inflammation of the gingival tissues The disease is detected by periodontal probing or x-rays,

which show localized, deep (vertical) bone loss, commonly limited to the first molars and incisors.

Bone loss progresses faster than in adult periodontitis, often at a rate of 3 to 4 μm/day.



• Actinobacillus actinomycetemcomitans very strongly associated with LAP

• A.a is not found in health individuals or in healthy sites of LAP patients

• A.a is very aggressive and causes a marked antibody response

• A.a invades the tissues thus to eradicate it, one must take systemic antibiotics or resect the tissue

• Most patients with A.a have a depressed neutrophilchemotaxis there is a lower level of neutrophilreceptors, mainly C5a




Disease is based on 3 factors:

Bacteria (certain kind)

Host response

Possibly genes

Bacteria: A.a Host Response: Impaired PMNs (phagocytosis,

chemotaxis and decreased receptors) Genes: may be AD inheritance


Gram negative, facultative anaerobic,

coccobacillus

Produce leukotoxin kills macrophages

Why is A.a the culprit?

None or low levels of A.a found at non diseased

sites

Extermination of A.a = Clinical Success

Presence of A.a after treatment resulted in

progressive attachment loss


Lost Teeth:

Over a 6 year period

▪ Untreated 43% lose teeth

35% if cases of untreated LAP lead to Generalized Aggressive Periodontitis

Compared to controls, those with LAP have 3.5 times greater attachment loss


Age of onset: About puberty Distribution of interproximal attachment loss:

Localized 1st molar/incisor presentation 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.

Rate of bone loss is 3 – 4 times faster than in chronic periodontitis.

Amount of local factors (plaque and calculus) are not in proportion to the amount and rate of tissue destruction.


Distolabial migration of maxillary incicorswith diastema formation that was not existing before.

Increasing mobility of the affected teeth. Increased sensitivity of the denuded root

surfaces. Dull deep radiating pain during mastication. Later, periodontal abscess formation.


Labio-distal migration of the incisors in LAP


An “arc-shaped loss of alveolar bone extending from the distal surface of the second premolar to the mesial surface of the second molar”




(1) - Initial colonization of the first erruptedteeth (incisors and 1st molars) by Aa which evades the host defense mechanism (PMN chemotachxis-inhibiting factor, collagenases, leukotoxin) leading to destructions at colonization sites.

This initial attack stimulate adequate immune response which prevent colonization and subsequent destruction of other sites.


(2) – Initial colonization by Aa may stimulate Bacterial Antagonistic to Aa which inhibit Aafrom further colonization of other periodontal sites.


(3) - Loss of leukotoxins produced by Aa for unknown reasons so the progression of the diseases may become arrested or impaired with no further colonization of new sites.


(4) – Defect in cementum formation of these teeth. Root surfaces of the extracted teeth from patients with LAP showed hypoplasticor aplastic cementum.


Keep in mind:

In order to control the disease, A.a must be eradicated or minimized

SRP NEVER removes 100% of bacteria

Without maintenance, disease will proceed

Disease has a high recurrence rate after first year therapy


SRP and Good OH will not eliminate A.a Subgingival gels, irrigation and antibiotics will not

eliminate A.a Best Bet: Systemic Antibiotics.

Surgery to remove granulation tissue in which A.a fester. Antibiotics: Metronidazole and Amoxicillin.


OHI, patient education

Gross calculus debridement if indicated

Surgical treatment of pockets > 5 mm, root planing and

curettage of pockets < 5mm. Chlorhexidine 1-2 weeks

post.

Surgery and interproximal brushing

Antibiotic therapy concurrent with surgery and/or root

planning

Post surgery evaluation 4-6 weeks: success measured

by good OH, decreased pockets, no BOP, gain in

attachment


Retreatment of deep, bleeding pockets

Maintenance every 3 months

Radiographs as needed

Reinforce OH

Prophylaxis/RP











GAP generally affect individuals under the age of 30, but older individuals also may be affected.

Generalized interproximal attachment loss affecting at least three permanent teeth other than first molars and incisors.

Episodic destruction usually takes place with periods of advanced destruction followed by stages of quiescence (weeks or months or years).


The amount of dental plaque seems inconsistent with the amount of periodontal destruction.

Qualitatively: Porphyromonus ginivalis (P.g.), Agricatibacter actinomycetemcomitans(A.a.), and Tannerella forsythia (T.f.) are detected in plaque of the affected periodontal sites.



Destructive phase Quiescence phase

- Gingiva appears severely inflamed, proliferated, ulcerated and fiery red. - Bleeding with stimulation

or spontaneously may occur.- Increased suppuration- This destructive phase is associated with active attachment and bone loss

- Gingiva appears pink, free of inflammation and even stippling may be present.

- No bleeding or suppuration from the deep pockets.


Range from severe bone loss associated with minimal number of teeth to advanced bone loss affecting the majority of teeth.

Radiographs taken at different times illustrate the aggressive nature of this disease




Aa has been implicated as the primary pathogen based on the following evidence:

1. Aa is found in high frequency (90%) in lesions characteristic of GAG.

2. Sites with evidence of disease progression often show elevated levels of Aa.

3. Many patients with GAG have significantly elevated serum antibody titers to Aa.

4. Reduction in the Aa is correlated to successful clinical response.

5. Aa produce a number of virulence factors that may contribute to disease process.


1. Patients with aggressive periodontitis show functional defects of PMN, monocytes or both.

2. PMN defects may be impaired chemotaxisto infected sites or in phagocytosis.

3. Monocytes show hyperresponsiveness with production of prostaglandin E2 (PGE2) with increased destruction of connective tissue and bone loss.


All individuals are not equally susceptible to aggressive periodontitis.

Studies have described a familial pattern of alveolar bone loss and have implicated genetic factors in aggressive periodontitis.


Amount and duration of smoking are important variables that can influence the extent of periodontal destruction.

Patients with GAP who smoke may have more affected teeth and more CAL than non-smoking.




A genetic disease with mutation in the cathepsin C gen.

The affected child has advanced periodontal disease of both primary and permanent dentitions.

Many patients become edentulous while in their teens.

Palmer-planter keratodermas (palmo-planter hyperkeratosis) affect the palms of the hands and the planter surface of the feet.








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Prof.Dr. Mohamed El-Shahat - Delta Univdeltauniv.edu.eg/.../uploads/Aggressive-Periodontitis.pdfV. Necrotizing periodontal diseases a. Necrotizing ulcerative gingivitis (NUG) b. Necrotizing