localized juvenile periodontitis and pre-pubertal periodontitis

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juvenile periodontitis & Pre-pubertal periodontitis:

juvenile periodontitis & Pre-pubertal periodontitis Presented by: Rajesh k shah Intern (4 th batch)

Juvenile periodontitis:

Juvenile periodontitis Defn : it is defined as “ a disease of the periodontium occuring in an otherwise healthy adolescents, which is characterized by a rapid loss of alveolar bone around more than one tooth of the permanent dentition” (Baer) The term has been largely replaced by a new term “AGGRESSIVE PERIODONTITIS” Depending upon its distribution, it may be 1) localized juvenile periodontitis 2) generalized juvenile periodontitis


A) LOCALIZED JUVENILE PERIODONTITIS (LJP) The term localized juvenile periodontitis was used in the past, and currently, it is known as “localized aggressive periodontitis “ (LAP) Defn: it is defined as “ a disease occurring in an otherwise healthy individuals under the age of 30 years with destructive periodontitis localized to the first permanent molars and molars and incisors, not involving more than 2 teeth.” (Genco et al )

Clinical features::

Clinical features: Age of onset: around puberty (11 to 14 years) to 20 years of age with predilection for females (a/c to some studies) distribution of lesions: LAP is characterized by localized first molar/ incisor involvement with interproximal attachment loss on at least 2 permanent teeth , one of which is a first molar, and involving no more than 2 teeth other than first molars and incisors.

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3) The most striking feature is lack of clinical inflammation, despite the presence of deep periodontal pocket. Small amount of plaque is seen, which seems inconsistent with the amount of periodontal destruction. The thin film of plaque rarely mineralizes to calculus. Most common initial symptoms are mobility, migration of the incisors and first molars. Classically, a distolabial migration of the maxillary incisors with diastema formation occurs.


Pathogenesis : Although there is a minimal quantity of associated plaque in LAP, it often contains elevated level of following 2 microorganisms. These two types of bacteria are considered to be pathogenic in LJP: 1) Actinobacillus actinomycetemcomitans 2) porphyromonas gingivalis Of which Actinobacillus actinomycetemcomitans is more commonly associated with the initiation and progression

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Virulence factors produced by A. actinomycetemcomitans : a) leukotoxin – destroys PMNs and macrophages b) endotoxin – activates host cells to secrete inflammatory mediators (PGs, IL-1, TNF) c) Bacteriocin – may inhibit the growth of beneficial species. d) Immunosuppressive factors- may inhibit IgG and IgM production e) collagenase - causes degradation of collagen f) Chemotactic inhibition factors- may inhibit neutrophil chemotaxis

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Possible reasons for the limitation of periodontal destruction to only certain teeth (1 st molar / incisor) may be: 1) The 1 st molar and incisors are the first permanent teeth to erupt and the reasons behind only these teeth being involved may be a) after initial colonization by A.a. into these specific teeth, until other teeth are erupted , the host-body immune response is already sensitized to the microorganism and its toxins; hence preventing any further colonization to other sites.

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b) Due to progressive development of A.a. - antagonist bacteria, thereby decreasing the no. of colonization sites. c) Due to progressive loss of leukotoxin -producing ability of A.a . – for unknown reasons. 2) Due to specificity of certain tooth for susceptibility to invasion by A.a . - due to anatomical factors like defective cementum ( hypoplastic or aplastic cementum ).

Histopathological/microscopic features:

Histopathological/microscopic features Similar to those seen in pocket formation like- Ulcerated pocket epithelium accumulation of various inflammatory cells in the connective tissue (mainly leukocytes, plasma cells and small no. of lymphocytes and macrphages ). Under E.M.- bacterial invasion of connective tissue that reaches the bone surface Flora involves A. actinomycetemcomitans , Capnocytophaga sputigena , and others.

Radiographic findings:

Radiographic findings 1) Vertical/ angular bone loss around the first molars and incisors in an otherwise healthy teenagers is a classical diagnostic sign of LAP. 2) “arc-shaped” loss of alveolar bone extending from the distal surface of 2 nd premolar to the mesial surface of the 2 nd molar 3) Bilateral symmetrical patterns of bone loss (“mirror-image” pattern).


B) GENERALIZED JUVENILE PERIODONTITIS The term “generalized juvenile periodontitis” is replaced by a new term “ GENERALIZED AGGRESSIVE PERIODONTITIS (GAP)” . Beside generalized juvenile periodontitis, GAP also includes “rapidly progressive periodontitis”. It is the disease of periodontium, which is characterized by generalized interproximal attachment loss affecting at least 3 permanent teeth other than first molars and incisors.

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The disease process appears to progress in episodes which includes 2 stages a) periods of advanced destruction b) periods of quiescence (weeks to months or years). These 2 stages alternate with each other during the progression of disease. Also, unlike LAP, a poor antibody response to the pathogens is seen in GAP.


CLINICAL FEATURES Age and sex distribution: usually affected between puberty and 30 years of age (however, older individuals may also be affected). males and females almost equally affected. Distribution of lesion: no specific pattern is observed; all or most of the teeth are affected. Relation with local factors: like LAP/LJP, even though plaque may be present, the amount of plaque is inconsistent with the amount of periodontal destruction.

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Also, qualitatively, plaque may be associated Actinobacillus actinomycetemcomitans , Porphyromonas gingivalis , and Bacteroides forsythus . 2 types of gingival responses can be seen- One => corresponding to the stage of advanced destruction, following features may be seen: a) severe, acutely inflamed gingival tissue, often proliferating, ulcerated and fiery red. b) bleeding- spontaneous or with slight stimulation. c) presence of suppuration d) loss of clinical attachment and active bone loss

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In other cases, a) gingival tissues may appear pink, free of inflammation with occasionally presnce of stippling. b) presence of deep pockets. This features indicate the stage of quiescence, when the bone level remains stationary. 5) Some of the patients may have systemic manifestations like loss of weight, malaise, and depression.


RADIOGRAPHIC PRESENTATION Radiographically, there is no specific pattern of bone loss involvement. The appearance under radiograph may range from severe bone loss associated with mnimal no. of teeth, to advanced bone loss affecting the majority of the teeth in the dentition.


RISK FACTORS FOR AGGRESSIVE PERIODONTITIS Microbiologic factors Immunologic factors Genetic factors Environmental factors MICROBIOLOGIC FACTORS: Although a different types of microorganisms have been detected in patients with LAP (including prevotella intermedia, capocytophaga sp. , campylobacter rectus),

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Actinobacillus actinomycetemcomitans has been implicated as the primary pathogen associated with the disease because of the following reasons: 1) 90% of lesions show the presence of A.a. 2) affected sites show eleveted level of A.a. 3) affected patients with clinical symptoms show elevated serum antibody titres to A.a. 4) during treatment and positive clinical outcome, level of subgingival A.a. decreases. 5) A.a. can produce a number of virulence factors that may contribute to disease. However, other studies show since A.a. is found in a periodontially healthy subjects, it may be considered as a normal flora of oral cavity and hence, it may not be a significant risk factor associated with periodontal disease.


B) IMMUNOLOGIC FACTORS Certain immune defects (either due to bacterial ininfection or of genetic origin) are implicated in the disease process. These may be 1) functional defects in leukocytes (like neutrophils and monocytes ) leading to either impaired chemotaxis to the site of infection or impaired phagocytosis and killing of microorganisms. 2) hyperresponsiveness of monocytes in response to bacterial lipopolysachharide (LPS) leading to increased destruction of connectiive tissues and bone. 3) autoimmune response to self-antigens like collagen, DNA and IgG .


C) GENETIC FACTORS Some of the above mentioned immunologic defects associated with aggressive periodontitis may have genetic origin (like familial clustering of neutrophil abnormalities). Also it has been suggested that a major gene plays a role in this disease , which could be transmitted through an autosomal dominant mode of inheritence. D) ENVIRONMENTAL FACTORS Smoking is one of the factors that can influence the extent of destruction . also greater no. of teeth involvement is seen in smokers than in non-smokers.

Treatment plan:

Treatment plan Standard periodontal therapy: includes scaling, root planing and curettage; flap surgery with/without bone grafts, root amputation, hemisection , occlusal adjustment and strict plaque control prognosis- unpredictable, requiring multiple maintenance visits Antibiotic therapy: as an adjunct to standard periodontal therapy 3) Extraction of the affected tooth /teeth


CURRENT APPROACH TO THERAPY Local mechanical therapy + tetracycline 250 mg qid X 7 days (minm.) If surgery indicated, antibiotic taken 1 hr. prior to surgery. Also, chlorhexidine mouthwash should be prescribed Alternatives to tetracycline, doxycycline 100 mg/day or in refractory cases, amoxicillin + metronidazole can be used.

Pre-pubertal periodontitis:

Pre-pubertal periodontitis It is the periodontal disease affecting children before the age of their puberty. Etiology: Familial in origin. Females more affected than males which suggests the defect is based on X-linked inheritance . However the defect may be an acquired one, the reason being decreased chemotaxis of imflammatory cells , due to bacterial infection.

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a) GENERALIZED PREPUBERTAL PERIODONTITIS: clinical features 1) age of onset- about 4 yrs. 2) usually low plaque level 3) all primary teeth are affected; the permanent dentition may or may not be affected. 4) extremely acute inflammation is present, with proliferation of the gingiva with the entire width of attached gingiva appearing fiery-red in addition to gingival hyperplasia, cleft formation, and recession 5) rapid alveolar bone loss 6) defect in neutrophil or monocyte functions; neutrophils may remain absent from the gingival tissue. 7) markedly raised peripheral WBC count 8) system involvement like recurrent bacterial infection ( Otitis media and skin and upper respiratory tract infection are frequently seen) 9) periodontitis is refractory to antibiotic therapy


b) LOCALIZED PREPUBERTAL PERIODONTITIS features: 1) age of onset- about 4 yrs. 2) usually low plaque level 3) only some teeth are involved, and the pattern of involvement not ascertained 4) gingival tissues may exhibit little or no inflammation. 5) destruction is not as rapid as in generalized form. 6) functional defects (like defects in chemotaxis and/or phagocytosis ) in either neutrophils or in monocytes but never both 7) recurrent otitis media not a frequent finding and usually there is no history of frequent infections 8) the disease is amenable to treatment by curettage and antibiotic therapy

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DIAGNOSIS Analysis of the pocket flora assessment of blood leukocyte chemotaxis and serum antibodies measurement of serum and urinary biochemical markers for hypophosphatasia TREATMENT Curretage , antibiotic therapy , and improved oral hygiene arrest the progression of prepubertal periodontitis Tetracycline being the drug of choice (as it attains a higher concentration in gingival fluid than in plasma)


References: reddy, shantipriya: essentials of clinical periodontology and periodontics. 2 nd e/d. 2008. jaypee. tandon, shobha: textbook of pedodontics.1 st e/d 2003.paras various dental web-sites

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