Chronic and Aggressive Periodontitis

• CHRONIC AND AGGRESSIVE PERIODONTITIS

• PRESENTED BY : SUNNY JANNU

CHRONIC PERIODONTITIS

Formerly known as “ ADULT PERIODONTITIS “ or “ CHRONIC ADULT PERIODONTITIS “

1. Slowly progressing disease .

2. Progress aggressively in patients having diabetes, smoking, stress and thyroid conditions.

3. Can also occur in children and adolescents in response to plaque and calculus,

this is the reason it is no more termed as adult periodontitis.

4. Recently, defined as “ an infectious disease “ , resulting :

a) In inflammation within the supporting tissues of the teeth.

b) Progressive attachment loss.

c) Bone loss.

d) Presence of periodontal pocket of varying depths.

CLINICAL FEATURES1. Accumulation of supragingival and subgingival plaque and calculus.

2. Gingival inflammation.

3. Pocket formation.

4. Loss of attachment and bone.

5. Presence of inflammatory swelling.

6. Color ranging from pale red to magenta (purplish red).

7. Loss of stippling.

8. Blunted or rolled gingival margin.

9. Blunt or flattened interdental papilla.

10. All the signs of inflammation may not always be present.

11. Only sign may be bleeding on probing the pocket.

12. Increase gingival fluid exudation.

13. Purulent exudate may be present.

14. Signs of inflammation may be masked because of the fibrotic changes.

15. Horizontal and vertical bone loss.

16. Progressive increase in the mobility of the teeth involved.

17. Can be clinically diagnosed by:

a) Presence of deepened gingival sulcus (pocket).

b) Vertical zone of inflammatory changes from the marginal gingiva to the extent of attached gingiva involved.

c) Loss of clinical attachment:

i. Diagnosed radiographically.ii. Evidence of bone loss.

Differential diagnosis is based on :

1. Age of the patient.2. Rate of disease progression.3. Familial nature of aggressive disease.4. Can be correlated with the amount of plaque and calculus present.

DISEASE DISTRIBUTION

Chronic periodontitis is :

5. Site specific.6. Present only at the sites where there is plaque and calculus.7. Present only on the surfaces which show plaque and calculus

accumulation.

Can be localized or generalized

1. LOCALIZED PERIODONTITIS :

When < 30 % of teeth show attachment loss .

2. GENERALIZED PERIODONTITIS :When > 30 % of teeth show attachment loss .

The pattern of bone loss observed in chronic periodontitis are :

3. Vertical .4. Horizontal .

5. VERTICAL BONE LOSS :

a) When loss of attachment and bone loss is more in one tooth surface than the adjacent surfaces.

b) Associated with angular bony defects and intrabony pocket formation .c) Seen in advanced periodontitis .

2. HORIZONTAL BONE LOSS :

a) When attachment loss proceeds at a uniform rate on all the tooth surfaces.b) Associated with suprabony pockets.c) Bone loss is usually horizontal .

DISEASE SEVERITY :

Described as being :

1. Slight ( mild ) .2. Moderate .3. Severe.

These terms describe the disease severity of :

4. The entire mouth .5. A part of the mouth, such quadrant or sextant .6. The disease status of an individual tooth .

1. Slight (mild ) periodontitis :

1 - 2 mm of clinical attachment loss .

2. Moderate periodontitis :

3 – 4 mm of clinical attachment loss .

3. Severe periodontitis :

5 mm or more clinical attachment loss.

SYMPTOMS :

4. Usually painless .5. Sometimes localized dull pain, radiating deep into the jaw .6. Sensitivity to hot and cold or both due to root exposure .7. Areas of food impaction cause discomfort .8. Itchiness in gingiva .

DISEASE PROGRESSION

1. Slow rate but may be modified by systemic and / or environmental and behavioral factors .

2. Onset can occur any time in the presence of plaque and calculus .3. Usually becomes more evident in the mid - 30s therefore has accumulative

effect .4. Does not progress at an equal rate in all affected sites .5. Some areas may remain static .6. More rapid progress in interdental areas .

PREVALENCE

7. Increase in prevalence and severity with age .8. Affects both sexes equally .9. Age associated disease , not age related and occurs depending on disease

duration .

RISK FACTORS FOR DISEASE

Prior history of periodontitis :

1. Not a true risk factor but rather a disease predictor .

2. Prior history of periodontitis would suggest that patient to be vulnerable to the disease .

3. Patient has to take more care for maintenance of oral hygiene and regular scalings .

4. Proper monitoring required .

The risk factors that contribute to patient susceptibility are :

2. Local Factors .

2. Systemic Factors .

3. Environment and Behavioral Factors .

4. Genetic Factors .

1. LOCAL FACTORS :

a) Plaque accumulation on tooth and gingival surfaces is considered primary etiologic agent .

b) Increase in the proportion of gram – ve organisms in the subgingival plaque biofilm like Bacteroides gingivalis, Bacteroides forsythus, and Treponema denticola .

c) These microorganisms are associated with attachment and bone loss in chronic periodontitis and known as RED COMPLEX .

d) These bacteria impart a local effect on :

i. The cells of inflammatory response.ii. Cells and tissues of the host .iii. Results in a local site specific disease process .

e) PLAQUE RETENTIVE FACTORS :

i. Important in the development and progression of periodontitis .ii. They retain plaque microorganisms in close proximity to the periodontal tissues .iii. Provide an ecologic niche for plaque growth and maturation .

f) Calculus is the most important plaque retentive factor because of its ability to retain and harbor plaque of chronic bacteria on its rough surface .

g) Other factors that retain plaque or prevent its removal are :

i. Subgingival and / or overhanging margins of restorations .ii. Furcations exposed by loss of attachment and bone .iii. Crowded or malaligned teeth .iv. Root grooves and concavities .

2. SYSTEMIC FACTORS :

a) The rate of periodontal destruction is increased in patient suffering from systemic disease .

b) Diabetes is a systemic condition that increase the severity and extent of periodontal disease in an affected patient .

c) Type 1 or Insulin dependent diabetes mellitus ( IDDM ) is observed in children, teenagers, and young adults may lead to increased periodontal destruction when it is uncontrolled .

3. ENVIRONMENT AND BEHAVIORAL FACTORS :a) Smoking increase the severity and extent of periodontal disease .b) Smokers with chronic periodontitis have :

i. More attachment and bone loss .ii. More furcation involvements .iii. Deeper pockets .

c) Smokers form more supragingival and less subgingival calculus .d) They demonstrate less bleeding on probing than nonsmokers .

4. GENETIC FACTORS :

e) Periodontal destruction seen among family members and across different generations within family.

f) Recent studies demonstrate a familial aggregation of localized and generalized aggressive periodontitis.

g) Studies of monozygotic twins suggest a genetic component to chronic periodontitis .

h) More aggressive periodontal breakdown in response to plaque and calculus accumulation may exist .

i) Recent data indicates a genetic variation or polymorphism in the genes encoding interleukin 1 - alpha and interleukin 1- beta .

j) These are associated with an increased susceptibility to a more aggressive form of chronic periodontitis.

k) Smokers demonstrating the composite IL – 1 genotype are at greater risk for severe diseases.

l) Heavy smokers and IL- 1 genotype increase risk of tooth loss by 2.9 times .m) The combined effect of IL- 1genotype and smoking increased the risk of tooth loss

by 7.7 times .

AGGRESSIVE PERIODONTITIS

OBJECTIVES

DEFINITION CLASSIFICATION ETIOLOGY CLINICAL FEATURES DIAGNOSIS TREATMENT

DEFINITION

A bacterial disease of the teeth and gingiva that manifests before age 35, often in prepubescent children. It is caused primarily by the bacterium Actinobacillus actinomycetemcomitans, leading to rapid tissue deterioration.

Rapidly progressive adult periodontitis in a 29-year-old female

CLASSIFICATION

Aggressive PeriodontitisAggressive Periodontitis

Localized Aggressive Localized Aggressive Generalized AggressiveGeneralized Aggressive

ETIOLOGY

CAUSATIVE ORGANISM:– Actinobacillus actinomycetemcomitans is a

bacterial species including Gram negative, nonmotile, capnophilic short rods.

– It is considered as one of the most prominent pathogenic micro organism associated with periodontal diseases, mostly aggressive periodontitis.

COMMON FINDINGS

– Client otherwise clinically healthy, usually < 30 years of age

– Characterized by rapid bone & attachment loss (inconsistent with amount of destruction)

– Absence of large amounts of plaque & calculus– Family history – genetic trait

SEVERE BONE LOSS

OTHERS:– A.a. found in diseased sites– Host response abnormalities (phagocytosis,

chemotaxis)– Hyperactive macrophages

Produce excess amounts of prostaglandins, interleukin – 1

– Disease may be self-arresting

CLINICAL FEATURES OF LOCALIZED PERIODONTITIS

Circumpubertal onset of disease. Maxillary incisors migrate in distolabial

direction diastema Increasing mobility of affected teeth Periodontal abscess formation Sensitive root surfaces

Localized JUVENILE ONSET PERIODONTITIS

Migration of teeth associated with pockets and relatively healthy gingiva in another young patient with aggressive periodontitis

13 YEAR BOY

Elevated levels of A.a. found in active sites (low numbers in healthy sites)

Incidence of A.a. found to be greater in younger persons compared to older clients

Younger clients experience more destruction in a shorter period of time

The clinical photo and the X-Ray of this 28 year-old man show the advanced alveolar bone loss in the absence of significant

gingival inflammation, typical of the localized aggressive periodontitis

Radiographic Evaluation

Vertical bone loss affecting:– Usually bilateral affecting first permanent molars

& incisors, – Vertical loss of bone in an “arc-shape”

extending from the distal of the 2nd premolar to the mesial of the 1st molar

These X-rays show localized aggressive periodontitis affecting first molars

CLINICAL FEATURES OF GENERLISED PERIODONTITIS

Usually affects persons 30 years & younger but can affect older persons

Bone & attachment loss affects at least 3 teeth other than first molars & incisors

Often plaque is minimal but contains high levels of:– A.a.– P.g.– F.n. & C.r.– Spirochetes

Severe generalized aggressive periodontitis

in 22-year old black male patient

Destructive phase:– Tissue appears severely inflamed, ulcerated & fiery red– Bleeding with or without stimulation– Suppuration– Active attachment & bone loss

Non-destructive phase:– Tissues appear pink with some stippling– Lack of inflammation– Probing will reveal deep pockets– Bone & attachment levels relatively stable

patient has advanced generalized aggressive periodontitis with deep pockets throughout the mouth.

Associated Systemic Complications

Some clients with GAP may exhibit:– Weight loss– Mental depression, general malaise

Systemic conditions may predispose client to GAP, these include:– Chronic neutrophil defects, leukocyte adherence

deficiency

Functional defects of PMNs, monocytes or both impaired chemotaxis & phagocytosis

Radiographic Evaluation

Severe bone loss affecting minimal number of teeth OR

Majority of teeth affected by advanced bone loss

TREATMENT CONSIDERATIONS

Initial therapy.

Antibmicrobial therapy. Antimicrobial therapy & non-surgical

management Antimicrobial therapy & surgical management

Surgical procedures.

Grafting procedures.

Tooth transplantation.

Other dental consideration

TREATMENT

Depends on type and degree of destruction Management of LAP: Extraction of involved teeth (depends on severity of tissue

loss) Periodontal therapy:

– Plaque control instruction– Debridement with or without flap surgery– Irrigation with CHX, home rinsing with CHX– Bone grafts, root resections, hemisections

Frequent maintenance visits– 1/month for 6 months, then every 3 months

Antibiotic therapy:– Adjunctive therapy often required to eliminate A.a. from

tissues– Tetracycline (250 mg qid for 2 weeks)– Metronidazole combined with amoxicillin– Doxycycline

Management of GAP: Careful monitoring of younger clients with GAP b/c

rate of disease progression is often faster Maintenance every 3 weeks or less is

recommended if disease in active phase Periodontal therapy:

– Debridement in combination with antibiotic therapy, strict plaque control, CHX irrigation & rinsing

– Periodontal surgery

Antibiotic therapy:– Highly recommended that microbial diagnostic

& susceptibility testing be done– Combination therapies include:

Metronidazole/amoxicillin Amoxicillin/doxycycline Clindamycin

– Local therapies in the form of gels, chips or fibers

??Risk factors for AGP

A.a. found in large numbers in LAP A.a. produces a strong leukotoxin kills neutrophils Different strains of A.a. produce different levels of leukotoxin

– Highly toxic strains produce greater numbers of leukotoxin Depressed neutrophil chemotaxis & phacytosis common for both forms Neutrophil dysfunction has genetic basis BUT, not all people with this dysfunction have aggressive perio AND not all people with the dysfunction have aggressive perio

PREVALENCE

Localized aggressive periodontitis affects both males and females and is seen most frequently in the period between puberty and 20 years of age.

Some studies have suggested a predilection for female patients, particularly in the youngest age groups.

Blacks are at higher risk for LAP. And black male teenagers are 2.9 times more likely to have the disease than black

female adolescents.

In a study of untreated periodontal disease conducted in Sri Lanka by Loe et al, 8% of the population had rapid progression of periodontal disease, characterized by a yearly loss of attachment of 0.1 to 1.0 mm.

Blacks are at much higher risk than whites for all forms of aggressive periodontitis, and male teenagers were more

likely to have GAP than female adolescents.

THANK YOU…