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Learned and unlearned concepts in periodontal diagnostics: a 50‐year perspective

Identifieur interne : 001689 ( Main/Exploration ); précédent : 001688; suivant : 001690

Learned and unlearned concepts in periodontal diagnostics: a 50‐year perspective

Auteurs : Gary C. Armitage

Source :

RBID : ISTEX:58C3E80258C7F9459BB3123C17D5A7C296627969

Descripteurs français

English descriptors

Abstract

In the past 50 years, conceptual changes in the field of periodontal diagnostics have paralleled those associated with a better scientific understanding of the full spectrum of processes that affect periodontal health and disease. Fifty years ago, concepts regarding the diagnosis of periodontal diseases followed the classical pathology paradigm. It was believed that the two basic forms of destructive periodontal disease were chronic inflammatory periodontitis and ‘periodontosis’– a degenerative condition. In the subsequent 25 years it was shown that periodontosis was an infection. By 1987, major new concepts regarding the diagnosis and pathogenesis of periodontitis included: (i) all cases of untreated gingivitis do not inevitably progress to periodontitis; (ii) progression of untreated periodontitis is often episodic; (iii) some sites with untreated periodontitis do not progress; (iv) a rather small population of specific bacteria (‘periodontal pathogens’) appear to be the main etiologic agents of chronic inflammatory periodontitis; and (v) tissue damage in periodontitis is primarily caused by inflammatory and immunologic host responses to infecting agents. The concepts that were in place by 1987 are still largely intact in 2012. However, in the decades to come, it is likely that new information on the human microbiome will change our current concepts concerning the prevention, diagnosis and treatment of periodontal diseases.

Url:
DOI: 10.1111/prd.12006


Affiliations:


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Le document en format XML

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<term>Aggressive periodontitis</term>
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<term>American society</term>
<term>Anaerobic rods</term>
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<term>Campylobacter rectus</term>
<term>Chronic periodontitis</term>
<term>Clin</term>
<term>Clin microbiol</term>
<term>Clin periodontol</term>
<term>Clinical parameters</term>
<term>Colonizer</term>
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<term>Cytomegalovirus</term>
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<term>Homeostasis</term>
<term>Host responses</term>
<term>Human cytomegalovirus</term>
<term>Human microbiome</term>
<term>Human saliva</term>
<term>Immun</term>
<term>Immunol</term>
<term>Juvenile periodontitis</term>
<term>Listgarten</term>
<term>Local irritants</term>
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<term>Microbial</term>
<term>Microbial etiology</term>
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<term>Microbiome</term>
<term>Microbiota</term>
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<term>Natural history</term>
<term>Negative effects</term>
<term>Oral microbiol immunol</term>
<term>Oral microbiome</term>
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<term>Periodontal status</term>
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<term>Porphyromonas gingivalis</term>
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<term>Primary dentition</term>
<term>Proc natl acad</term>
<term>Putative</term>
<term>Pyorrhea alveolaris</term>
<term>Ranney</term>
<term>Relman</term>
<term>Risk assessment</term>
<term>Salivary</term>
<term>Salivary diagnostics</term>
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<term>Socransky criteria</term>
<term>Subgingival</term>
<term>Subgingival microbiota</term>
<term>Subgingival plaque</term>
<term>Subtraction radiography</term>
<term>Supragingival</term>
<term>Taichman</term>
<term>Treponema denticola</term>
<term>Untreated</term>
<term>Untreated gingivitis</term>
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<term>Actinobacillus actinomycetemcomitans</term>
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<term>Adult periodontitis</term>
<term>Aggressive periodontitis</term>
<term>Alveolar bone</term>
<term>American academy</term>
<term>American society</term>
<term>Anaerobic rods</term>
<term>Antibiotic</term>
<term>Armitage</term>
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<term>Bacteroides forsythus</term>
<term>Bacteroides gingivalis</term>
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<term>Campylobacter rectus</term>
<term>Chronic periodontitis</term>
<term>Clin</term>
<term>Clin microbiol</term>
<term>Clin periodontol</term>
<term>Clinical parameters</term>
<term>Colonizer</term>
<term>Current concepts</term>
<term>Cytomegalovirus</term>
<term>Dent</term>
<term>Dent assoc</term>
<term>Dental plaque</term>
<term>Diagnostics</term>
<term>Early colonizers</term>
<term>Environ microbiol</term>
<term>Etiologic</term>
<term>Etiology</term>
<term>Experimental gingivitis</term>
<term>Genco</term>
<term>Gingival</term>
<term>Gingival crevicular</term>
<term>Gingivalis</term>
<term>Gingivitis</term>
<term>Haffajee</term>
<term>Homeostasis</term>
<term>Host responses</term>
<term>Human cytomegalovirus</term>
<term>Human microbiome</term>
<term>Human saliva</term>
<term>Immun</term>
<term>Immunol</term>
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<term>Listgarten</term>
<term>Local irritants</term>
<term>Mergenhagen</term>
<term>Microbial</term>
<term>Microbial etiology</term>
<term>Microbial testing</term>
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<term>Microbiology</term>
<term>Microbiome</term>
<term>Microbiota</term>
<term>Microorganism</term>
<term>Natural history</term>
<term>Negative effects</term>
<term>Oral microbiol immunol</term>
<term>Oral microbiome</term>
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<term>Pathogenesis</term>
<term>Periodontal</term>
<term>Periodontal diagnostics</term>
<term>Periodontal disease</term>
<term>Periodontal disease activity</term>
<term>Periodontal diseases</term>
<term>Periodontal health</term>
<term>Periodontal infections</term>
<term>Periodontal pathogens</term>
<term>Periodontal pockets</term>
<term>Periodontal risk assessment</term>
<term>Periodontal status</term>
<term>Periodontal therapy</term>
<term>Periodontal tissues</term>
<term>Periodontally</term>
<term>Periodontics</term>
<term>Periodontitis</term>
<term>Periodontol</term>
<term>Periodontology</term>
<term>Periodontosis</term>
<term>Plaque</term>
<term>Porphyromonas</term>
<term>Porphyromonas gingivalis</term>
<term>Predominant cultivable microbiota</term>
<term>Primary dentition</term>
<term>Proc natl acad</term>
<term>Putative</term>
<term>Pyorrhea alveolaris</term>
<term>Ranney</term>
<term>Relman</term>
<term>Risk assessment</term>
<term>Salivary</term>
<term>Salivary diagnostics</term>
<term>Socransky</term>
<term>Socransky criteria</term>
<term>Subgingival</term>
<term>Subgingival microbiota</term>
<term>Subgingival plaque</term>
<term>Subtraction radiography</term>
<term>Supragingival</term>
<term>Taichman</term>
<term>Treponema denticola</term>
<term>Untreated</term>
<term>Untreated gingivitis</term>
<term>Untreated periodontitis</term>
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<div type="abstract" xml:lang="en">In the past 50 years, conceptual changes in the field of periodontal diagnostics have paralleled those associated with a better scientific understanding of the full spectrum of processes that affect periodontal health and disease. Fifty years ago, concepts regarding the diagnosis of periodontal diseases followed the classical pathology paradigm. It was believed that the two basic forms of destructive periodontal disease were chronic inflammatory periodontitis and ‘periodontosis’– a degenerative condition. In the subsequent 25 years it was shown that periodontosis was an infection. By 1987, major new concepts regarding the diagnosis and pathogenesis of periodontitis included: (i) all cases of untreated gingivitis do not inevitably progress to periodontitis; (ii) progression of untreated periodontitis is often episodic; (iii) some sites with untreated periodontitis do not progress; (iv) a rather small population of specific bacteria (‘periodontal pathogens’) appear to be the main etiologic agents of chronic inflammatory periodontitis; and (v) tissue damage in periodontitis is primarily caused by inflammatory and immunologic host responses to infecting agents. The concepts that were in place by 1987 are still largely intact in 2012. However, in the decades to come, it is likely that new information on the human microbiome will change our current concepts concerning the prevention, diagnosis and treatment of periodontal diseases.</div>
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