侵袭性牙周炎
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the periodontal destruction.
Chan-Myung, Cho. The clinical assessment of aggressive periodontitis patients[J]. J Periodontal Implant Sci , 2011, 41(3): 143-148
undistinguishable but possibly with different initiating factors.
Luigi Nibali*. Aggressive Periodontitis: microbes and host response, who to blame?[J]. Virulence 6:3, 223-228
Clinical Features
• Rapid progression; • Early age of onset;
• Familial aggregation;
• The amount of biofilm and calculus accumulation in aggressive
periodontitis subjects is inconsistent with the severity and progression of
Diagnosis
•Clinical experiences •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.
Treatments
• The treatment concept for aggressive periodontitis is largely similar to that for chronic periodontitis • Systemic antibiotics as an adjuvant to scaling and root planing • Azithromycin has been shown to be a valid alternative to the regimen of amoxicillin plus metronidazole
• Adaptive immune response
A progressive shift from a predominantly T-cell lesion to a B-cell dominated lesion typical of periodontitis;
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.
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; A. actinomycetemcomitans JP2 clone: characterized by a 530-base-pair deletion in the leukotoxin operon, associated with increased leukotoxic activity; Filifactor alocis; Centipeda genus; Mitsuokella sp; Selenomonas genus; Actinobacter baumannii; Treponema lecithinolyticum; Archaea.
Host Response
• Innate immune response
Preclinical“physiological”inflammation: epithelial and dendritic cells; neutrophils and macrophages, fibroblasts,
• A strict maintenance
Teughels W. Treatment of aggressive periodontitis.[J]. Periodontol 2000. 2014 Jun;65(1):107-33.
THANK YOU FOR WATCHING
• Localized aggressive periodontitis(LAgP) • Generalized aggressive periodontitis(GAgP)
Etiology
•Host susceptibility
Familial aggregation：neutrophil abnormalities or dysfunctions;
AGGRESSIVE PERIODONTITIS
Stomatology Of Lanzhou University Wenge Shi
Content
Classification Etiology Clinical Features
Diagnosis
Treatments
Classification
Georgios Papantonopoulos. Artificial Neural Networks for the Diagnosis of Aggressive Periodontitis Trained by Immunologic Parameters[J]. PLoS One. 2014; 9(3): e89757.
源自文库
Ethnic variations：IL-6 genetic variants and increased detection of A.
actinomycetemcomitans(Aa);
Genetic studies : AgP encompasses a large range of conditions clinically
Chan-Myung, Cho. The clinical assessment of aggressive periodontitis patients[J]. J Periodontal Implant Sci , 2011, 41(3): 143-148
undistinguishable but possibly with different initiating factors.
Luigi Nibali*. Aggressive Periodontitis: microbes and host response, who to blame?[J]. Virulence 6:3, 223-228
Clinical Features
• Rapid progression; • Early age of onset;
• Familial aggregation;
• The amount of biofilm and calculus accumulation in aggressive
periodontitis subjects is inconsistent with the severity and progression of
Diagnosis
•Clinical experiences •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.
Treatments
• The treatment concept for aggressive periodontitis is largely similar to that for chronic periodontitis • Systemic antibiotics as an adjuvant to scaling and root planing • Azithromycin has been shown to be a valid alternative to the regimen of amoxicillin plus metronidazole
• Adaptive immune response
A progressive shift from a predominantly T-cell lesion to a B-cell dominated lesion typical of periodontitis;
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.
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; A. actinomycetemcomitans JP2 clone: characterized by a 530-base-pair deletion in the leukotoxin operon, associated with increased leukotoxic activity; Filifactor alocis; Centipeda genus; Mitsuokella sp; Selenomonas genus; Actinobacter baumannii; Treponema lecithinolyticum; Archaea.
Host Response
• Innate immune response
Preclinical“physiological”inflammation: epithelial and dendritic cells; neutrophils and macrophages, fibroblasts,
• A strict maintenance
Teughels W. Treatment of aggressive periodontitis.[J]. Periodontol 2000. 2014 Jun;65(1):107-33.
THANK YOU FOR WATCHING
• Localized aggressive periodontitis(LAgP) • Generalized aggressive periodontitis(GAgP)
Etiology
•Host susceptibility
Familial aggregation：neutrophil abnormalities or dysfunctions;
AGGRESSIVE PERIODONTITIS
Stomatology Of Lanzhou University Wenge Shi
Content
Classification Etiology Clinical Features
Diagnosis
Treatments
Classification
Georgios Papantonopoulos. Artificial Neural Networks for the Diagnosis of Aggressive Periodontitis Trained by Immunologic Parameters[J]. PLoS One. 2014; 9(3): e89757.
源自文库
Ethnic variations：IL-6 genetic variants and increased detection of A.
actinomycetemcomitans(Aa);
Genetic studies : AgP encompasses a large range of conditions clinically