AGGRESSIVE PERIODONTITIS

Presented by: Dr. Krishna Das 1st Yr PG Student Department of Periodontology and Oral Implantology

Aggressive Periodontitis
Aggressive periodontitis, by definition, causes rapid destruction of the periodontal attachment apparatus and the supporting alveolar bone.
Aggressive periodontitis may be further classified into: 1) Localized Aggressive Periodontitis 2) Generalized Aggressive Periodontitis

Aggressive Periodontitis
The following characteristics are common to patients with aggressive periodontitis:

Otherwise clinically healthy patient.

Rapid attachment loss and bone destruction.

Amount of microbial deposits inconsistent with disease severity.

Familial aggregation of diseased individual.

The following characteristics are common but not universal: Diseased sites infected with Actinobacillus actinomycetemcomitans (now Aggregatibacter actinomycetemcomitans, A.a.) Abnormalities in phagocyte function. Hyperresponsive macrophages, producing increased prostaglandin E2 (PGE2) and interleukin-1 (IL-1). In some cases, self-arresting disease progression.

Historical Background
In 1923, Gottlieb
In
called diffuse atrophy of the alveolar bone and deep cementopathia. 1938, Wannenmacher described incisor-first molar involvement and called the disease parodontitis marginalis progressiva. the concept of periodontosis as a degenerative entity was unsubstantiated and that the term should be eliminated from periodontal nomenclature. term juvenile periodontitis was introduced by Chaput and colleagues in 1967 and by Butler in 1969.

In 1966 the World Workshop in Periodontics concluded that

The

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."

In

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(LAP).

LOCALIZED AGGRESSIVE PERIODONTITIS

Clinical Features of Localized Aggressive Periodontitis

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 Onset of disease occurs between puberty & 20 years of age. Bone loss 3-4 times faster than in chronic periodontitis. Clinical inflammation may not be obvious. Robust serum antibody response to infecting agents.

 Minimal plaque that rarely mineralizes. However Maxillary incisors migrate in distolabial
direction diastema.

contains elevated levels of A.a. & Porphyromonas gingivalis (P.g.).

Increasing mobility of affected teeth. Sensitivity of denuded root surfaces. Periodontal abscess formation.

Regional lymph node enlargement may occur

Localized aggressive periodontitis in 17-year-old girl. Gingival inflammation, periodontal pockets, and pathologic migration.

Site Specific Destruction

Some reasons why disease activity affects certain teeth: #1:
A.a. colonize first permanent teeth to erupt. Evade host defenses

Following initial attack, host responds and produces antibodies which improve phagocytosis of bacteria and neutralize leucotoxic activity

Colonization of other sites may be prevented.

Additional reasons: #2: A.a. may lose its ability to produce leukotoxin. This may
slow or arrest the disease process.

#3: Antagonistic bacteria

Anti-A.a. bacteria may colonize sites & prevent A.a. from colonizing other sites in mouth. Localizes the infection & tissue destruction.

#4: Denuded root surfaces

The root surfaces of patient with LAP are often denuded (hypoplastic or aplastic cementum). Allows bacteria to penetrate the root and colonize the site.

Radiographic Evaluation
Vertical bone loss occurs ,usually bilateral, affecting first permanent molars & incisors. Arc-shaped bone loss extending from the distal surface of the 2nd premolar to the mesial surface of the 2st molar.

Clinical and cone beam CT view of advanced alveolar bone resorption around incisors and first molar in a 24-year-old male with aggressive periodontitis.

GENERALIZED AGGRESSIVE PERIODONTITIS

Clinical Features of Generalized Aggressive Periodontitis

Characterized by Generalized interproximal attachment loss affecting at least three permanent teeth other than first molars & incisors

Includes conditions formerly known as generalized juvenile and

rapidly progressive periodontitis

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

Poor serum antibody response to infecting agents.

Often plaque is minimal but contains high levels of: A.actinomycetemcomitans P..gingivalis Tannerella forsythia (previously B. forsythus)

Episodic nature to disease

-Periods of inactivity may last weeks, months, or years.

Episodic nature of disease produces two different tissue

responses

Destructive phase:

Tissue appears severely inflamed, ulcerated & fiery

red Bleeding with or without stimulation Suppuration Active attachment & bone loss

Non-destructive phase:

Tissues may appear pink with some stippling Lack of inflammation Probing will reveal deep pockets Bone & attachment levels relatively stable

Associated Systemic Complications

Some clients with GAP may exhibit: Weight loss Mental depression general malaise Systemic conditions may predispose patient 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

to

Advanced bone loss affecting the majority of teeth in the dentition.

Generalized aggressive periodontitis and poor crown-to-root ratio in 24year-old patient; overall prognosis poor. A, generalized periodontal attachment loss and pocket formation. B, Moderate to advanced bone destruction. The contrast between the well-formed crowns and the relatively short, tapered roots worsens the prognosis.

Prevalence of Aggressive Periodontitis

Prevalence estimates below 1% (U.S. & other countries). Prevalence for both types higher among African-Americans.

Gender differences unclear.

Distribution of disease by gender among race groups: Prevalence higher for African-American males compared to females. Reverse is true among whites.

Risk Factors
1) Microbiologic Factors
A.a. has been implicated as the primary pathogen associated with 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 People with the disease more likely to have highly toxic strains (African-Americans in particular)

2) Immunologic Factors
The human leukocyte antigens (HLAs), which regulate immune responses, have been evaluated as candidate markers for aggressive periodontitis( HLA A9 and B15 )

Functional defect in PMNs and monocytes or both: -Impaired chemotaxis -Impaired phagocytosis

Hyperresponsiveness of monocyte (LAP)

PGE2

increased connective tissue or bone loss

 Also, poorly functional inherited forms of monocyte FcRII , the

receptor for human immunoglobulin G2 (IgG2) antibodies, have been shown to be disproportionately present in patients with LAP. Autoimmunity has a role in GAP collagen, DNA and IgG.

host antibodies to

3) Genetic Factors All individuals are not equally susceptible to aggressive periodontitis. Familial pattern of alveolar bone loss

Data support the concept that a gene or genes of major effect exists
for aggressive periodontitis.

Data

also support a genetic basis for some of the immunologic defects seen in patients with aggressive periodontitis.

However,

it is unlikely that all patients affected with aggressive periodontitis have the same genetic defect.

As summarized by Tonetti and Mombelli,

it seems that specific genes may be different in various populations and/or ethnic groups and therefore true heterogeneity in disease susceptibility may be present. The role of specific genes remains to be elucidated

4) Environmental Factors
The amount and duration of smoking are important variables that can influence the extent of destruction seen in young adults. Patients with GAP who smoke have more affected teeth and more loss of clinical attachment than nonsmoking patients with GAP. However, smoking may not have the same impact on attachment levels in younger patients with LAP.

Systemic Conditions associated with Aggressive Periodontitis

Cyclic neutropenia Agammaglobulinemia

Ehlers Danlos Syndrome

Lazy leukocyte Syndrome Disease associated with deficient PMN leukocyte - Papillon Lefevre Syndrome - Downs Syndrome - Chediak Higashi Syndrome function:

Aggressive Periodontitis - Treatment

The prognosis for patients with aggressive periodontitis depends on:

whether the disease is generalized or localized, the degree of destruction present at the time of diagnosis, and the ability to control future progression.

Therapeutic Modalities
Early detection : preventing further destruction more
predictable than attempting to regenerate lost supporting tissues.

Conventional Periodontal therapy:

-Patient education: about disease, risk factors and patients role in success of treatment -oral hygiene improvement -scaling and root planning(SRP) -frequent recall maintenance (but response to conventional treatment is unpredictable)

Educate family members and examine siblings- familial

aggregation

Surgical Therapy:
1) Resective Therapy: decreases or eliminate pocket depth. Limitations: Further risk of increased mobility. careful evaluation of risk/benefit must be considered from case to case

2) Regenerative Therapy: bone grafts, barrier membrane and wound healing agents. In intrabony defect particularly vertical with multiple walls.
Limitations: -patients with severe bone loss -depends on anatomy of defect and tooth involved.

Antimicrobial Therapy: A.a. remains in pocket even after

conventional treatment systemic antibiotics. reinfection require use of

1) Systemic Antibiotics: -more favorable clinical response -increase in clinical attachment level -decrease probing pocket depth -decrease risk of additional attachment loss antibiotics used: amoxicillin tetracycline amoxicillin + metronidazole clindamycin doxycycline 2) Microbial testing: Advocated by some clinician for sensitivity and resistance to select antibiotics. But according to Carranza empirical use of antibiotic (amoxicillin and metronidazole) is more clinically sound and cost effective. 3) Local drug delivery: for localized infections. advantages: -small total dose -avoid systemic side effects - exposure to target microorganism to high concentration so more therapeutic level of medication is achieved

Full mouth disinfection:

Described by Quirynen et al Full mouth debridement (remove all plaque and calculus) completely in two appointments within 24 hours. Which also includes : -SRP -tongue brushed with CHX gel 1%(1 min) -full mouth rinse with CHX solution 0.2% (2min) -periodontal pocket irrigated with CHX solution 1%

Host Modulation: is a means of treating the host side of the

host-bacteria interaction. Several agents used: Sub-antimicrobial dose doxacycline(SDD) Flubriprofen Indomethacin Naproxen

PDL tissues(fibroblast, neutrophils..)

inflammation Downregulates

Matrix metalloproteinases(MMP8 & MMP9)

Degrades extracellular matrix material (collagen-I breakdown) SDD

Clinical signs of periodontitis

Also causes: Reduced cytokene level Stimulates osteoblastic activity New bone formation by upregulating collagen production

Restorative considerations:
Sever teeth should be extracted -outcome of treatment limited -their retention may cause additional bone loss Restoration of lost tooth: 1) Transplantation: have been attempted but with limited success. 2) Dental Implants: recent studies (eg. Mengel et al.) have shown successful implant rehabilitation for partially edentulous in patient with treated for GAP. But it was observed that the bone loss and attachment loss around implant patient in GAP > periodontally healthy patient.

Periodontal Maintenance: Frequent maintenance visit is one of

the most important factors in the control the disease and success of treatment. - no longer than 3 months after the surgical therapy - in case of active disease : 3-4 weeks

PARAMETERS Age Calculus Disease progression

GAP 20-35 yrs Scanty to moderate Rapid

LAP 11-19yrs moderate Rapid

Distribution
Antibody response

Generalized; no consistent pattern

Poor

1st molars and incisors

Strong

Racial predilection
Familial Tendency Gender distribution PMN/ Macrophage Defect

No
Yes ? Yes

More common in blacks

Yes ? Yes

Associated with systemic problems

Response to therapy

Some cases
Variable

Yes
Good