MANAGEMENT OF AGGRESSIVE PERIODONTITIS

Aggressive Periodontitis

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In the year 1999 American Academy of Periodontology in an international workshop reached to a consensus on classification of periodontal disease. As per this workshop following terminologies were changed. A. ADULT PERIODONTITIS BE CALLED CHRONIC PERIODONTITIS. B. EARLY- ONSET FORMS OF PERIODONTITIS BE CALLED AGGRESSIVE PERIODONTITIS. C. SYSTEMIC DISEASE FORMS OF PERIODONTITIS. D. NECROTIZING FORMS OF PERIODONTITIS.

Aggressive Periodontitis

Definition: Comprises of a group of rare , often severe, rapidly progressive forms of periodontitis often characterized by an early age of clinical manifestation and a distinctive tendency for cases to aggregate in families.

Aggressive periodontitis have been defined based on the following Primary features:
Non-contributing medical history. Rapid attachment loss and bone destruction. Familial aggregation of cases.

SECONDARY FEATURES
Amounts of microbial deposits inconsistent with the severity of periodontal tissue destruction. Elevated proportions of Aa comitans & in some Far East populations, P. gingivalis. Phagocyte abnormalities. Hyper-responsive macrophage phenotype, including elevated production of PGE2 & IL-1β in response to bacterial endotoxins. Progression of attachment loss & bone loss may be selfarresting.

LOCALISED AgP
Circumpubertal onset. Localized first molar/incisor presentation with interproximal attachment loss on at least two permanent teeth, one of which is a first molar, & involvement no more than two teeth other than first molars & incisors. Robust serum antibody response to infecting agents.

GENERALISED AgP
Usually affecting persons < 30 years of age, but patients may be older. Generalized interproximal attachment loss affecting at least 3 permanent teeth other than first molars & incisors. Pronounced episodic nature of the destruction of attachment & alveolar bone. Poor serum antibody response to infecting agents.

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. The role of the bacterium is specially relevant in localized juvenile periodontitis and acute progressive periodontitis.

Rapidly progressive adult periodontitis in a 28-year-old female, clinical view.

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

CLINICAL PHOTOGRAPH

RADIOGRAPHIC PICTURE
SEVERE BONE LOSS

PREPUBERTAL PERIODONTITIS

13 YEAR BOY

PRINCIPLE OF THERAPEUTIC INTERVENTION Treatment should be initiated after completion of a carefully diagnosis by a specifically trained periodontist.

Successful treatment is depended on
Early diagnosis. Directing therapy towards elimination or suppression of the infecting micro-organism. Providing an environment considered to longterm maintaince.

THERAPEUTIC GOALS
To alter or eliminate the microbial etiology and contributing risk factors for periodontitis. Arrest/slowdown the progression of disease. Preserving the dentition in comfort, function, and appropriate esthetics and to prevent the recurrence of disease.

GENERAL PRINICIPLES IN TREATING AgP
These case are often associated with alteration in host defenses, the therapy should begin by exploring factors that may contribute to changes in the defence system.

The lack of a strong association between plaque accumulation & disease severity in the AgP & the alteration noted above often means that these patients are less responsive to conventional periodontal therapy. Surgery may not be advisable in AgP, until the infection is under control.

TREATMENT CONSIDERATION
Initial therapy. Antibmicrobial therapy. Antimicrobial therapy & non-surgical management Antimicrobial therapy & surgical management Surgical procedures. Grafting procedures. Tooth transplantation. Other dental consideration.

DECISION PATHWAY

INITIAL THERAPY
1) Instruction, reinforcement, and evaluation of the patient’s plaque control should be performed. 2) Supra- and subgingival scaling and root planing.

INITIAL THERAPY
3) Local factors contributing to aggressive periodontitis should be eliminated or controlled. A. Removal or reshaping of restorative overhangs and over-contoured crowns. B. Correction of ill-fitting prosthetic appliances. C. Restoration of carious lesions.

INITIAL THERAPY
D. Odontoplasty. E. Tooth movement. F. Restoration of open contacts which have resulted in food impaction. G. Treatment of occlusal trauma. H. Extraction of hopeless teeth.

Localized Agg. Periodontitis
Depending on the preference of the Practitioner & the patient Two approaches are proposed.
(Wilson/Kornman)

1. Treatment with the aid of microbial information 2. Treatment with out the aid of microbial information

Treatment with the aid of Microbial information

Treatment with out the aid of microbial information
The clinician can assume that micro-org present will be sensitive to a member of the Tetracycline family of antibiotics. Surgery is carried out in conjunction with the antibiotic regimen. STP is accompanied by DNA Probes or microbiologic monitoring if clinical / radiographic signs of the disease recur.

Antibiotic Therapy
Mainly Tetracycline & its derivatives are used. Systemic Ab’tics should only be administered as an adjunct to mechanical debridement.

STAGED APPROACH

(Lindhe)

Mechanical therapy + Meticulous oral hygiene Clinically re-assessed after 4-6 wks Decision made to gain to deep lesions(surgery) & Ab’tic selection depending on culture sensitivity tests

Microbiology testing may be repeated at 1-3 months after completion of therapy Combination therapy is appropriate. Ab’tics should not be administered systemically before completion of thorough mechanical debridement. Recommended to start drug administration immediately following a mechanical instrumentation.

Antimicrobial Therapy + Non-surgical Therapy
A combination pf SRP with systemic tetracycline therapy has been shown to be effective treatment for control of localized Agg. Periodontitis.

Antimicrobial Therapy + Surgical Therapy Baer & Socransky (1979) 1st reported the combination of flap surgery & systemic antibiotic therapy. Effective means of treating localized Agg. Periodontitis.

Surgical Management
Recommended to gain access to the subgingival microflora & to remove granulation tissue and infected connective tissue.

Grafting Procedures
Autogenous bone chips
(Oshrain & Kaslick-1981)

Osseous coagulum (Burnett & Stewark- 1969) Frozen autogenous hip marrow
(Demarco & Scaletter-1970)

FDBA + Tetracycline (Yukna & Sepe-1982) GTR may be useful in the treatment of local defects associated with localized Agg. Periodontitis.

Tooth Transplantation
1st Advocated by Baer & Gamble ( 1966) Criteria for successful transplantation are as The 3rd molar crown should be slightly smaller than the tooth it is replacing. Root development of the 3rd molar should be incomplete. The transplanted tooth should be kept out of occlusion for 3-4 wks posttransplantation.

Other Dental Consideration
Root canal treatment Root amputation Hemisection

Current Approach
In almost all cases ,tetracycline(250mg qid,at least 1 wk) should be given. If surgery is indicted, then Ab’tic should be started approximately 1 hr before surgery. Doxycycline – 100 mg/day Chlorhexidine rinses used to augment plaque control.

In Refractory LAP cases, Tetracycline-resistant Actinobacillus species suspected.

Combination therapy preferred. Amoxicilin-375 mg & Metronidazole-250 mg TID for 7 days.

Generalized Agg. Periodontitis
Other micro-organism also present. Microbial analysis is recommended before therapy & at each re-evaluation. GOAL :- Elimination of the suspected pathogen which requires systemic Ab’tics adjunct to mechanical therapy

Surgery is not advisable until there are clinical & microbial signs of periodontal stability is achieved. Monitor & observe 1. Pt’s overall physical status as weight loss, mental depression & malaise. 2. For flare-ups of proliferative gingival inflammation. Currently monitoring every 3 wks or less is suggested while the disease is in active state.

OUTCOME ASSESSMENT
Significant reduction of clinical signs of gingival inflammation. Reduction of probing depths. Stabilization or gain of clinical attachment. Radiographic evidence of resolution of osseous lesions. Progress toward occlusal stability. Progress toward the reduction of clinically detectable plaque to a

Areas where the periodontal condition does not resolve may occur and be characterized by the presence of:
Persistent gingival inflammation. Persistent or increasing probing depths. Progressive loss of clinical attachment. Persistent clinically detectable plaque levels

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