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Aggressive Periodontitis
Aggressive Periodontitis
Aggressive Periodontitis
Aggressive Periodontitis
Aggressive Periodontitis
Aggressive Periodontitis
Aggressive Periodontitis
Aggressive Periodontitis
Aggressive Periodontitis
Aggressive Periodontitis
Aggressive Periodontitis
Aggressive Periodontitis
Aggressive Periodontitis
Aggressive Periodontitis
Aggressive Periodontitis
Aggressive Periodontitis
Aggressive Periodontitis
Aggressive Periodontitis
Aggressive Periodontitis
Aggressive Periodontitis
Aggressive Periodontitis
Aggressive Periodontitis
Aggressive Periodontitis
Aggressive Periodontitis
Aggressive Periodontitis
Aggressive Periodontitis
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Aggressive Periodontitis

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The presentation describe the loclized and generlized aggressive periodontitis. In addition to the risk factors and the treatment plans.

The presentation describe the loclized and generlized aggressive periodontitis. In addition to the risk factors and the treatment plans.

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  • 1. Prof Dr. Eman Abd El-Sattar Tella
  • 2. Aggressive periodontitis generally affects svstemicallyhealthy individuals less than 30 years old althoughpatients may be older.Aggressive periodontitis may be distinguished fromchronic periodontitis by the age of onset, the rapid rateof disease progression, the nature and composition ofthe subgingival microflora, alterations in the hostsimmune response and a familial aggregation ofdiseased individuals.
  • 3. LOCALIZED AGGRESSIVE PERIODONTITISClinical CharacteristicsLocalized aggressive periodontitis (LAP) has an age of onset around puberty.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".
  • 4. A striking feature of LAP is the lack of clinicalinflammation despite the presence of deepperiodontal pockets. Furthermore, the amount ofplaque on the affected teeth is minimal andinconsistent with the amount of periodontaldestruction present. The plaque that is presentforms a thin biofilm on the teeth and rarelymineralizes to form calculus. Although the quantityof plaque may be limited, it often contains elevatedlevels of A actinomvcetemcomitans and in somepatients, Porphvromonas gingivalis.
  • 5. - Localized aggressive periodontitis progresses rapidly. The rate of bone loss is about three to four times faster than in chronic periodontitis.- Other clinical features of LAP may include: * Distolabial migration of maxillary incisors with diastema formation. * Increasing mobility of first molars. * Sensitivity of denuded root surfaces to thermal and tactile stimuli. * Deep dull radiating pain during mastication because of irritation of the supporting structures by mobile teeth and impacted food. * Periodontal abscesses. * Regional lymph node enlargement.
  • 6. Radiographic Findings: Vertical loss of alveolar bone around the first molars and incisors, beginning around puberty in healthy teenagers, is a classic diagnostic sign of LAP. Radiographic findings may include an "arc-shaped loss of alveolar bone extending from distal surface of second premolar to mesial surface of second molar“.
  • 7. GENERALIZED AGGRESSIVE PERIODONTITISClinical CharacteristicsGeneralized aggressive periodontitis (GAP) usually affects individuals under the age of 30 but older patients also may be affected.Clinically, GAP is characterized by "generalized interproxirnal attachment loss affecting at least three permanent teeth other than first molars and incisors".- As seen in LAP, patients with GAP have small amounts of bacterial plague associated withthe affected teeth. Quantitatively, the amount of plaque seems inconsistent with the amount of periodontal destruction. Qualitatively, Porphvromonas giriaivalis. A. actinomycetem- comitans and Bactehodes forsvthus frequently are detected in the plaque that is present. In contrast to LAP, individuals affected with GAP produce a poor antibody response to the pathogens present.
  • 8. The destruction occurs episodically with periods of advanced destruction followed by stages of quiescence of variable length (weeks to months or years). Radiographs show bone loss that has progressed since the previous evaluation.In cases of GAP, the gingival tissue response is a severe acutely inflamed tissue, often proliferating ulcerated and fiery red. Bleeding may occur spontaneously or with slight stimulation. Suppuration may be an important feature. This tissue response occurs in the destructive stage in which attachment and bone are actively lost.
  • 9. In other cases, the gingival tissues may appear pink, freeof inflammation. However, deep pockets can bedemonstrated by probing. This tissue response coincidewith periods of quiescence in which the bone levelremains stationary. In other cases, the gingival tissues may appear pink,free of inflammation. However, deep pockets can bedemonstrated by probing. This tissue response coincidewith periods of quiescence in which the bone levelremains stationary. Some patients with GAP may have systemicmanifestations such as weight loss, mental depressionand general malaise. They should receive medicalevaluations to rule out possible systemic involvement.
  • 10. The radiographic picture in GAP range fromsevere bone loss associated with minimal numberof teeth to advanced bone loss affecting themajority of teeth in the dentition. Sites in GAP patients demonstrated osseousdestruction of 25 to 60 % during a 9-week period.Despite this extreme loss, other sites in the samepatient showed no bone loss.
  • 11. RISK FACTORS FOR AGGRESSIVE PERIODONTITISMicrobioloqic Factors- Although several specific microorganisms are detected in patients with LAP (A actinomycetemcomitans (A. a.), Capnocytophaga sp. Eikenella corrodens, Prevotella intermedia and Campyiobacter rectus), A. a. is implicated as the primary pathogen associated with this disease is based on the following evidence:
  • 12. 1- High frequency of A. a. (approximately 90%) in lesions characteristic of LAP.2- Elevated levels of A. a. were showed in sites with evidence of disease progression.3- Elevated serum antibody titers to A. actinomvcetemcomitans is showed in many patients with LAP.4- A correlation between reduction in the subgingival load of A. a. during treatment and a» successful clinical response.5- A. a. produces a number of virulence factors that may contribute to the disease process.
  • 13. Immunoloqic Factors: Some immune defects are implicated in the pathogenesisof aggressive periodontitis. The human leukocyte antigens (HLA), which regulateimmune responses, were evaluated as markers foraggressive periodontitis. HLA-A9 and B15 antigens areconsistently associated with aggressive periodontitis. Patients with aggressive periodontitis display functionaldefects of PMNs which can impair either the chemotacticattraction of PMN to the site of infection or their ability tophagocytose and kill microorganisms.
  • 14. Genetic Factors- All individuals are not equally susceptible to aggressive periodontitis. A familial pattern of alveolar bone loss have implicated genetic factors in aggressive periodontitis.- Genetic predisposition for LAP suggest that a major gene plays a role in this disease, which is transmitted through an autosomal dominant mode of inheritance.Environmental Factors- The amount and duration of smoking can influence the extent of destruction seen in young adults.
  • 15. TREATMENT OF AGGRESSIVE PERIODONTITISLocalized Aggressive Periodontitis- Standard periodontal therapy: Such therapy has included scaling and root planing, flap surgery with and without bone grafts, root amputations, hemisections, occlusal adjustment and strict plaque control. However, response was unpredictable. Frequent maintenance visits appear to be most important. Lack of response of aggressive periodontitis to local therapy alone is the result of the presence of A. actinomycetemcomitans in the tissues where it remains after therapy to reinfect the pocket. Systemic use of antibiotics eliminates bacteria from the tissues.
  • 16. Current Approach to Therapy. Patients who arediagnosed as having an early form of aggressiveperiodontitis may respond to standard periodontaltherapy. In almost all cases, systemic tetracycline (250mg of tetracycline 4 times daily for at least 1 week)should be given in conjunction with local mechanicaltherapy. If surgery is indicated, systemic tetracyclineshould be taken approximately 1 hour before surgery.Doxycycline 100 mg/day may also be used.Chlorhexidine rinses should also be prescribed andcontinued for several weeks to aid healing and augmentplaque control.In refractory localized aggressive periodontitis cases,tetracycline- esistant Actinobacilfus species have beensuspected. After performing antibiotic susceptibilitytests, the clinician may consider a combination ofamoxicillin and metronidazole.

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