侵袭性牙周炎PPT课件

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Clinical Features
• Rapid progression; • Early age of onset; • Familial aggregation; • The amount of biofilm and calculus accumulation in aggressive
periodontitiΒιβλιοθήκη Baidu subjects is inconsistent with the severity and progression of the periodontal destruction.
A. actinomycetemcomitans JP2 clone: characterized by a 530-base-pair deletion in the leukotoxin operon, associated with increased leukotoxic activity;
AGGRESSIVE PERIODONTITIS
Stomatology Of Lanzhou University
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Content
Classification Etiology Clinical Features Diagnosis Treatments
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Classification
• Localized aggressive periodontitis(LAgP) • Generalized aggressive periodontitis(GAgP)
Genetic studies : AgP encompasses a large range of conditions clinically undistinguishable but possibly with different initiating factors.
Luigi Nibali*. Aggressive Periodontitis: microbes and host response, who to blame?[J]. Virulence 6:3, 223--
•Others:
To estimate probability density functions of clinical and immunologic datasets derived from periodontitis patients and construct artificial neural networks (ANNs) to correctly classify patients into AgP or CP class.
It is some neutrophil features that makes individuals more susceptible to periodontitis upon subgingival microbial colonization, for example: increased adhesion, reduced chemotaxis, increased superoxide, nitric oxide production and reduced phagocytosis.
Filifactor alocis; Centipeda genus; Mitsuokella sp; Selenomonas genus; Actinobacter baumannii; Treponema lecithinolyticum; Archaea.
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Host Response
• Innate immune response
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4
Etiology
• Microbiological Profile
A. actinomycetemcomitans: plays a strong role in disease initiation and is then replaced by other pathogenic bacteria, presumably obligate anaerobic, as the disease progresses;
Georgios Papantonopoulos. Artificial Neural Networks for the Diagnosis of Aggressive Periodontitis Trained
by Immunologic Parameters[J]. PLoS One. 2014; 9(3): e89757.
3
Etiology
•Host susceptibility
Familial aggregation:neutrophil abnormalities or dysfunctions;
Ethnic variations:IL-6 genetic variants and increased detection of A. actinomycetemcomitans(Aa);
Preclinical“physiological”inflammation: neutrophils and macrophages, fibroblasts, epithelial and dendritic cells;
• Adaptive immune response
A progressive shift from a predominantly T-cell lesion to a B-cell dominated lesion typical of periodontitis;
Chan-Myung, Cho. The clinical assessment of aggressive periodontitis patients[J]. J Periodontal Implant
Sci , 2011, 41(3): 143-148
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Diagnosis
•Clinical experiences
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