Early-onset periodontitis.
The group of periodontal diseases known as the early-onset periodontal diseases are defined by the age of onset of periodontal destruction, distribution of lesions, association of disease with specific microbial infections, and identification of characteristic alterations, in the host response. Significant progress has recently been made in our understanding of the etiology of juvenile and rapidly progressive periodontitis. Considerable evidence points to a familial pattern of disease; both localized and generalized forms of disease may be observed in the same family. The exact mode of inheritance remains unclear, and disease may be the result of a complex interplay between genetically determined alterations of the host response and a specific bacterial challenge. Both neutrophil function and immunoglobulin response are altered and appear to be characteristic of an immunologic hyperresponsiveness. Bacterial colonization by Actinobacillus actinomycetemcomitans (serotype b) and/or Porphyromonas gingivalis appears to be the primary initiator of disease. Evidence suggests that lesion distribution may be a function of the nature of the infecting agent and the characteristics of the immune response.
Novak
M J
MJ
University of Texas Health Science Center, San Antonio, USA.
Novak
K F
KF
D000293:Adolescent; D000328:Adult; D016976:Aggregatibacter actinomycetemcomitans / Q000472:pathogenicity; D010520:Aggressive Periodontitis / Q000209:etiology* / Q000235:genetics / Q000276:immunology / Q000382:microbiology; D000907:Antibodies, Bacterial / Q000097:blood; D002634:Chemotaxis, Leukocyte; D002648:Child; D002675:Child, Preschool; D004198:Disease Susceptibility / Q000276:immunology; D020022:Genetic Predisposition to Disease; D006801:Humans; D009504:Neutrophils / Q000276:immunology; D010518:Periodontitis / Q000209:etiology* / Q000235:genetics / Q000276:immunology / Q000382:microbiology; D016966:Porphyromonas gingivalis / Q000472:pathogenicity; D012307:Risk Factors
D000907:Antibodies, Bacterial