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Classification and diagnosis of aggressive periodontitis
Author(s) -
Fine Daniel H.,
Patil Amey G.,
Loos Bruno G.
Publication year - 2018
Publication title -
journal of clinical periodontology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.456
H-Index - 151
eISSN - 1600-051X
pISSN - 0303-6979
DOI - 10.1111/jcpe.12942
Subject(s) - aggressive periodontitis , disease , medline , epidemiology , scopus , medicine , periodontitis , consistency (knowledge bases) , host (biology) , host factors , bioinformatics , genetics , biology , pathology , computer science , artificial intelligence , virus , biochemistry
Objective Since the initial description of aggressive periodontitis (AgP) in the early 1900s, classification of this disease has been in flux. The goal of this manuscript is to review the existing literature and to revisit definitions and diagnostic criteria for AgP. Study analysis An extensive literature search was performed that included databases from PubMed, Medline, Cochrane, Scopus and Web of Science. Of 4930 articles reviewed, 4737 were eliminated. Criteria for elimination included; age > 30 years old, abstracts, review articles, absence of controls, fewer than; a) 200 subjects for genetic studies, and b) 20 subjects for other studies. Studies satisfying the entrance criteria were included in tables developed for AgP (localized and generalized), in areas related to epidemiology, microbial, host and genetic analyses. The highest rank was given to studies that were; a) case controlled or cohort, b) assessed at more than one time‐point, c) assessed for more than one factor (microbial or host), and at multiple sites. Results Epidemiologic studies provided insight into ethnic and societal factors affecting AgP. DNA analysis of microbes showed some consistency but significant variability. Host factor analysis was less consistent. Many genetic studies were conducted but few had either sufficient power or looked at multiple genes in AgP. Conclusions Conflicting data resulted for several reasons; 1) the classification was too broad, 2) the disease (AgP) was not studied from its inception, at differing time points (temporal), and at different locations (topographic). New technologic advances coupled with a more delimiting definition of disease will allow for genetic, host and microbial factor analyses in an unbiased manner. As such we predict that progress can be made in identifying a robust group of genetic, host, and microbial risk‐markers associated with periodontal disease that can improve diagnostic capability in disease associated with juveniles, adolescents, and post‐adolescent individuals.