Aggressive periodontitis refers to the multifactorial,severe,&rapidly progressive form of periodontitis,which is primarily but not exclusively affects younger patients.

• Other Findings (not universal):

• • A.a. found in diseased sites
  • Host response abnormalities (phagocytosis, chemotaxis)
  • Hyperresponsive macrophages
  • Disease may be self-arresting

CLASSIFICATION

RISK FACTORS

Microbiologic factors

• a. produces a strong leukotoxin that kills neutrophils
• actinomycetumcomitans has been implicated as primary pathogen associated with LAP
• Different strains of 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

Immunologic factors

• HLAs(human leukocyte antigen),which regulate immune responses are candidate markers for aggressive periodontitis-HLA-A9,B-15
• Defective neutrophil function causing depressed neutrophil chemotaxis & phagocytosis
• Hyper-responsive macrophage phenotype, including elevated levels of PGE2 and IL-1b in response to bacterial endotoxins
• This hyperresponsive phenotype could lead to increased connctive tissue breakdown or boneloss

Genetic factors

• Familial clustering of neutrophil abnormalities seen in LAP suggesting defects may be inherited
• Also,Ab response to Aa is under genetic control and the ability to produce IgG2(protective Ab against Aa) may be race dependent

Environmental factors

• Patients with GAP who smoke have more affected teeth and more loss of clinical attatchment than non smokers

TREATMENT

• Depends on type and degree of destruction
• Usually,patients with GAP have a poorer prognosis becoz,disease is less likely to go spontaneously into remission compared with LAP
• Treatment must be pursued with a logical and regimented approach

CONVENTIONAL PERIODONTAL THERAPY

Includes

• Educating the patient about the disease
• Oral hygiene instructions and reinforcement.
• Scaling and root planing and control of local factors.

SURGICAL RESECTIVE THERPY

• To reduce or eliminate pocket depth
• In patients with severe horizontal bone loss it is contraindicated since it can result in increased tooth mobility

REGENERATIVE THERAPY

• Potential for regeneration appears to be good for patients with AP
• Using open flap surgical debridement, root surface conditioning (tetracyclinesolution) and an allogenic bone graft with sterile saline and tetracycline,reduced pocket depth with significant bone fill
• Recent advances-use of enamel matrix protien to aid in regeneration of cementum and new attatchment in periodontal defects

ANTIMICROBIAL THERAPY:

• Adjunctive therapy often required to eliminate a. from tissues
• Genco et al-Tetracycline (250 mg qid for 8 weeks)
• Lindhe treated patients with LAP with-Tetracycline (250 mg qid for 2 weeks,modified Widman flaps and periodic recall visits(1 visit monthly for 6 months,then 1 visit every 3 months)
• Tetracycline concentrate periodontal tissues & inhibit growth of Aa
• Has anticollagenase effect-inhibit tissue destruction
• Aid in bone regeneration
• Haffajee et al- Metronidazole combined with amoxicillin along with periodontal therapy
• Doxycycline 100mg /day also used
• Irrigation with CHX, home rinsing with CHX

HOST MODULATION

• Involves use of SDD(sub antimicrobial dose doxycycline) to prevent the destruction of periondontal attatchment by controlling the activation of MMPs ,primarly collagenase & gelatinase from both infiltrating cells and resident cells of periodontium.