• Share
  • Email
  • Embed
  • Like
  • Save
  • Private Content
Aggressive periodontitis

Aggressive periodontitis






Total Views
Views on SlideShare
Embed Views



0 Embeds 0

No embeds


Upload Details

Uploaded via as Microsoft PowerPoint

Usage Rights

© All Rights Reserved

Report content

Flagged as inappropriate Flag as inappropriate
Flag as inappropriate

Select your reason for flagging this presentation as inappropriate.

  • Full Name Full Name Comment goes here.
    Are you sure you want to
    Your message goes here
Post Comment
Edit your comment

    Aggressive periodontitis Aggressive periodontitis Presentation Transcript

    • What is PERIODONTITIS ???
    • ―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.‖
    • The age of onset The rapid rate of disease progression The nature and composition of associated microflora Alterations in the host response A familial aggregation of diseased individuals
    • “periodontitis that results in resorption of pdl in young children during or shortly following the eruption of the primary teeth‖ It may also affect permanent dentition Affected patients are usually diagnosed by age 4 Child may has affected leukocytes
    • -Minimal clincal signs of gingival inflammation -Only some of teeth are involved -Rate of tissue destruction is slower -Leukocytes defects involve polymorphonucear or mononuclear leukocytes, but not both. LOCALIZED PREPUBERTAL PERIODONTITIS GENERALIZED PREPUBERTAL PERIODONTITIS CLINICAL FEATURES ETIOLOGY
    •  Associated with abnormal cementum formation & defective pdl attachment results in decreased resistance of periodontal tissues to microbial infections & allow rapid tissue destruction. -Local mechanical debridement -Antibiotic therapy(penicillin or erythromycin –QD 250mg for 3 weeks) -improved oral hygiene ASSOCIATED FEATURES TREATMENT
    •  “uncommon form of periodontitis seen in children & adolescents‖ Characterised by rapid alveolar bone destruction with minimal signs of gingival inflammation
    • CHARACTERISED BY: loss of collagen fibers in pdl Replacement by loose connective tissue Extensive bone resorption Widened periodontal ligament space Gingiva is not involved
    • In 1928, Gottlieb termed the disease ―Deep cementopathia‖ disease of eruption & cementum initiated a foreign body response Host attempted to exfoliate the tooth Bone resorption Pocket formation
    • In 1938 Wannermacher described incisor- first molar involvement and called the disease ―parodontitis marginalis progressiva‖ Many author considered this to be a degenerative, non-inflammatory disease process & therefore gave it the name ―periodontosis‖
    • Age of onset is around puberty Localized involvement of 1st molar/incisor Interproximal attachment loss on atleast two permanent teeth, one of which is a 1st molar Involves no more than two teeth other than 1st molar & incisors Distolabial migration of maxillary incisors with concomitant diastema formation Increase mobility of first molars Sensitivity of denuded root surfaces to thermal & tactile stimuli. Deep,dull,radiating pain during mastication,probably caused by irritation of the supporting structures by mobile teeth & impacted food Periodontal abscess may form at this stage & regional lymph node enlargement may occur.
    • Classic diagnostic sign: Vertical loss of alveolar bone around 1st molars & incisors Beginning around puberty in an otherwise healthy teenagers ―Arc shaped loss of alveolar bone extending from distal surface of 2nd premolar to mesial surface of second molar‖
    • Colonization of Actinobacillus actinomycetemcomitans Impaired neutrophils chemotaxis lowers patient’s resistance to bacterial infection Intense immune responses
    • Patient education Oral hygiene instructions in plaque control & reinforcement Selective extraction & replacement scaling & root planing of teeth Surgical curretement of periodontal pocket Systemic administration of antibiotic (tetracycline—250mg—1 tab—6 hours for 3 weeks)
    • LJP affects both males and females Most frequently between puberty & 20 yrs of age Affects white females more & black males more
    • Affects individuals under the age of 30,but older patients may also be affected Involves entire dentition, frequently associated with down's syndrome and papillon-lefevre syndrome. Can also occur in individuals with no systemic disease
    • CHARACTERISED BY: Generalized interproximal attachment loss affecting atleast 3 permanent teeth other than 1st molars & incisors
    • Small amount of bacterial plaque with affected teeth Quantitatively—amount of plaque seems inconsistent with the amount of periodontal desruction Qualitatively- A.Actinomycetemcomitants,Bacteroides are detected in plaque
    • DESTRUCTIVE STAGE: severe acutely inflammed tissue Ulcerative fiery red bleeding may occur spontaneously or on stimulation pressure Suppuration maybe an important feature Attachment & bone are actively lost
    • OTHER CASES: Gingival tissues may appear pink Free of inflammation Absence of some degree of stippling Deep pockets demonstrated by probing Systemic manifestations: Weight loss Mental depression Malaise
    • Severe bone loss associated with minimal number of teeth, to advanced bone loss affecting the majority of teeth in dentition
    • Subgingival plaque from affected site Impaired neutrophils chemotaxis. Familial involvement.
    • Medical histories updated & reviewed Patient education Oral hygiene instructions in plaque control & reinforcement Periodic scaling & curettage Antibiotic therapy Surgical pocket elimination(periodontal flap procedure,osseous recontouring,root amputation) Extraction of all teeth & replacement with complete dentures Follow up
    • Blacks are at high risk than whites Males were more likely to have GAP then females
    • ―Periodontitis responsible for extensive bone destruction in a short period of time & may begin in puberty and 30-35 years of age‖
    • ACUTE PHASE • Highly inflammed gingiva • Bleeds easily & has mulberry like surface • Amount of plaque is variable QUIESCENT PHASE • Normal gingivaL appearance • Advanced bone loss • Deep periodontal pockets ACTIVE PHASE • Malaise • Weight loss • Depression
    • Immunocompromised host Defects in neutrophils & monocytes Bacterial flora e.g:Actinobacillus,Capnocytophaga Diabetes mellitus Down’s syndrome Neutropenia Crohn’s disease Agranulocytosis SYSTEMIC INVOLVEMENT
    • Scaling Open or closed curettage Antibiotic therapy Osseous grafts
    • MICROBIOLOGIC FACTORS: A.actinomycetemcomitans,Capnocytophaga sputigena IMMUNOLOGIC FACTORS: human leukocyte antigens,hyperresponsiveness of monocyte GENETIC FACTORS: familial pattern of alveolar bone,dominant mode of inheritance ENVIROMENTAL FACTORS: amount & duration of smoking
    • 9 mm probing depth 8 mm probing depth 2 mm probing depth 3mm probing depth 11mm probing depth 2mm probing depth
    • Clinically, localized juvenile periodontitis (LJP) patients rarely show calculus or plaque formation and often exhibit little or no gingivitis. However, deep probing, attachment loss, radiographic bone loss are found. Deep interproximal vertical bone loss on first molars and incisors are characteristic of LJP. Juvenile periodontits should be identified and treated early with antimicrobial therapy, scaling and root planing, and also surgery according to extent of destruction. 1. Generalized: affecting most of the dentition. 2. Localized: affecting only first molars and incisors.
    •  F  L  O  B R U S H I S N T S M I L E E E T H A N KY O U H