logging in or signing up AGGRESSIVE PERIODONTITIS vyomika Download Post to : URL : Related Presentations : Share Add to Flag Embed Email Send to Blogs and Networks Add to Channel Uploaded from authorPOINT lite Insert YouTube videos in PowerPont slides with aS Desktop Copy embed code: Embed: Flash iPad Dynamic Copy Does not support media & animations Automatically changes to Flash or non-Flash embed WordPress Embed Customize Embed URL: Copy Thumbnail: Copy The presentation is successfully added In Your Favorites. Views: 2433 Category: Education License: All Rights Reserved Like it (1) Dislike it (0) Added: February 17, 2011 This Presentation is Public Favorites: 1 Presentation Description No description available. Comments Posting comment... Premium member Presentation Transcript Slide 1: CHAPTER 28 AGGRESSIVE PERIODONTITIS Affects systemically healthy individuals less than 30yrs. 2. Distinguished from chronic periodontitis by : 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 . Classified as : Localized Aggressive Periodontitis . Generalized Aggressive Periodontitis . Rapidly Aggressive Periodontitis . (a) and ( b) formerly known as Localized juvenile periodontitis (LJP) and generalized juvenile periodontitis (GJP) .Slide 2: LOCALIZED AGGRESSIVE PERIODONTITIS : HISTORICAL BACKGROUND : In 1923, Gottlieb reported a disease called Diffuse atrophy of the alveolar bone . Characterized by : A loss of collagen fibres in the periodontal ligaments . 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 and cementum initiated a foreign body response . Host attempt to exfoliate the tooth . Bone resorption . Pocket formation .Slide 3: In 1938, Wannenmacher described incisor- first molar involvement called parodontitis marginalis progressiva . A degenerative, non inflammatory disease process called PERIODONTOSIS . In 1966, World Workshop in Periodontics concluded that concept of periodontosis as a degenerative entity was unsubstantiated and the term should be eliminated from periodontal nomenclature . The term Juvenile Periodontitis was introduced by Chaput and colleagues in 1967 and by Butler in 1969 . 6. In 1971, Baer defined it as : “ A disease of the periodontium occuring 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 ) . 8. Most recently, LJP has been renamed LOCALIZED AGGRESSIVE PERIODONTITIS .Slide 4: LOCALIZED AGGRESSIVE PERIODONTITIS : CLINICAL CHARACTERISTICS : Age of onset is around puberty . Localized involvement of first molar/ incisor . Interproximal attachment loss on at least two permanent teeth, one of which is a first molar . Involves no more than two teeth other than first molars and incisors . Possible reasons for limitations of periodontal destruction are : Initial colonization of first permanent teeth to erupt ( first molars and incisors ) . Actinobacillus actinomycetemcomitans evades host defenses by different mechanisms : Production of polymorphonuclear leukocyte chemotaxis – inhibiting factors, endotoxin, collagenases, leukotoxin . Production of other factors that colonize the pocket and initiate the destruction of the periodontal tissues . After initial attack, adequate immune defenses are stimulated to produce opsonic antibodies. This enhance the clearance and phagocytosis of invading bacteria and neutrlize leukotoxic activity . Thus colonization of other sites may be prevented . A strong antibody response to infecting agents is one characteristic of Localized Aggressive Periodontitis.Slide 5: Antagonistic bacteria to A.actinomycetemcomitans colonize the periodontal tissues and inhibit its further colonization of periodontal sites in the mouth and localize A. actinomycetemcomitans infection and tissue destruction. c) A. actinomycetemcomitans loses leukotoxin producing ability which results in arrested or retarded progress of disease and colonization of new periodontal sites. d) A defect in cementum formation may be responsible for localization of the lesions. A striking feature of localized aggressive periodontitis is the lack of clinical inflammation despite the presence of periodontal pockets. 7. The amount of plaque in the affected teeth is minimal when compared with the amount of periodontal destruction . The rate of bone loss is about three to four times faster than chronic periodontitis . Distolabial migration of the maxillary incisors with concomitant diastema formation . Increase mobility of first molars . Sensivity of denuded root surfaces to thermal and tactile stimuli .Slide 6: Deep, dull, radiating pain during mastication because of irritation of supporting structures by mobile teeth and impacted food . Periodontal abscesses form at this stage and regional lymph node enlargement occurs . RADIOGRAPHIC FINDINGS : Classic diagnostic sign : Vertical loss of alveolar bone around first molars and incisors . Beginning around puberty in an otherwise healthy teenagers . “ Arc- shaped shaped loss of alveolar bone extending from distal surface of second premolar to mesial surface of second molar . “ PREVALENCE AND DISTRIBUTION BY AGE AND SEX : Localized Aggressive Periodontitis affects both males and females . Most frequently between puberty and 20yrs. of age . A predilection for females , particularly youngest age group, affects white females more and black males more .Slide 7: GENERALISED AGGRESSIVE PERIODONTITIS CLINICAL CHARACTERISTICS : Affects individuals under the age of 30, but older patients also may be affected. Generalized interproximal attachment loss affecting at least three permanent teeth other than first molars and incisors. The destruction appears to occur episodically with periods of advanced destruction followed by stages of quiescence of variable length (weeks to months or years). Often have small amounts of bacterial plaque associated with the affected teeth. Quantitatively the amount of plaque seems inconsistent with the amount of periodontal destruction. Qualitatively, P.Gingivalis, A. Actinomycetemcomitans, and Bacteriodes forsythus frequently are detected in the plaque.Slide 8: Two gingival tissue responses found : DESTRUCTIVE STAGE : A severe acutely acutely inflamed tissue proliferating, ulcerative and fiery red. Bleeding may occur spontaneously or with slight stimulation. Suppuration may be an important feature. Attachment and bone are actively lost. OTHER STAGE : The gingival tissues may appear pink, free of inflammation. Absence of some degree of stippling. Deep pockets demonstrated by probing. This stage has been considered by Page and Shroeder to coincide with periods of quiescence in which the bone level remains stationary .Slide 9: Systemic manifestations such as weight loss, mental depression, and general malaise are associated with generalised aggressive periodontitis. Cases of generalised aggressive periodontitis may be arrested spontaneously or after therapy. Whereas others may continue to progress to tooth loss despite intervention with conventional treatment. RADIOGRAPHIC FINDINGS : Severe bone loss associated with minimal number of teeth, to advanced bone loss affecting the majority of teeth in the dentition. PREVALENCE AND DISTRIBUTION BY AGE AND SEX : Blacks are at higher risk than whites for all forms of aggressive periodontits . Males were more likely to have generalized aggressive periodontitis than females . RISK FACTORS FOR AGGRESSIVE PERIODONTITIS : Microbiologic Factors . Immunologic Factors . Genetic Factors . Environmental Factors .Slide 10: MICROBIOLOGIC FACTORS : Several specific microorganisms are detected in localized aggressive periodontitis : ( A.actinomycetemcomitans, Capnocytophaga, Eikenella corrodens, Provetella intermedia, and Camphylobacter rectus ). A.actinomycetemcomitans has been implicated as primary pathogen associated with this disease . Summarized by Tonetti and Mombelli , this link is based on following evidence : A.Actinomycetemcomitans is found in high frequency in localised aggressive periodontitis. Sites with disease progression show elevated levels of A.actinomycetemcomitans . Elevated serum antibody titres to Actinomycetemcomitans, seen in localised aggressive periodontitis. Clinical studies show a correlation between reduction in subgingival load of A.Actinomycetemcomitans during treatment and a successful clinical response. A.Actinomycetemcomitans produces a number of virulence factors that may contribute to the disease process.Slide 11: ELECTRON MICROSCOPIC STUDY : In localized aggressive periodontitis there is bacterial invasion of connective tissue that reaches the bone surface. The invading flora is mainly composed of gram negative bacteria, including cocci, rods, filaments, and spirochetes. Immunocytochemistry and electron microscopy has identified several tissue invading microorganisms as A.actinomycetemcomitans, Capnocytohaga Sputigena, Mycoplasma spp., and spirochetes. IMMUNOLOGIC FACTORS : Some immune defects implicated in pathogenesis of aggressive periodontitis. The human leukocyte antigens (HLA), which regulate immune responses have been evaluated as candidate markers for aggressive periodontitis . HLA-A9 and B15 antigens are consistently associated with aggressive periodontitis. Patients with aggressive periodontitis display functional defects of polymorphonuclear leukocytes (PMNs), monocytes, or both.Slide 12: There is hyper responsiveness of monocytes from localised aggressive periodontitis which leads to increased conective tissue or bone loss due to excessive production of catabolic factors. According to Anusaksathien and Dolby, autoimmunity play an important role in generalized aggressive periodontitis. Possible immune mechanisms includes : An increase in type II major histocompatibility complex (MHC) molecules. HLA DR4 . Altered helper or suppressor T cell function. Polyclonal activation of B cells by microbial plaques and genetic predisposition. GENETIC FACTORS : Currently, specific genes responsible for aggressive periodontitis have not been identified. A major gene plays a role in segregation analyses and linkage analyses and families with genetic predisposition for localized aggressive periodontitis . Some immunologic defects associated with aggressive periodontitis may be inherited . Van Dyke et al reported a familial clustering of the neutrophil abnormalities seen in localized aggressive periodontitis may be inherited .Slide 13: According to : 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 . ” ENVIRONMENTAL FACTORS: The amount and duration of smoking are important variables that can influence the extent of destruction seen in young adults. Patients with generalized aggressive periodontitis who smoke have more affected teeth and more loss of clinical attachment than non smoking patients with generalized aggressive periodontitis. Smoking does not have same impact on attachment levels in younger patients with localized aggressive periodontitis. You do not have the permission to view this presentation. In order to view it, please contact the author of the presentation.