title: Gingival crevicular fluid inflammatory mediators and bacteriology of gingivitis in nonhuman primates related to susceptibility to periodontitis.
abstract: The hypothesis to be tested was that the microbiota and resulting local host inflammatory response characteristics in oral conditions of high levels of chronic gingival inflammation increases susceptibility to progressing periodontitis. This study used cynomolgus monkeys, Macaca fascicularis (nonhuman primates), with high and low levels of long-standing gingival inflammation to define the profiles of gingival crevicular fluid mediators, cytokines and immunoglobulins; describe the subgingival microbiota; and evaluate their susceptibility to ligature-induced periodontitis. Sixteen nonhuman primates were stratified into two groups (HI, LO) based upon Bleeding Index as a measure of the natural level of inflammation (HI = 1.26 +/- 0.45; LO = 0.22 +/- 0.16). The host mediator levels, subgingival microbiota, and clinical characteristics of the LO and HI groups were compared after 30 days of oral hygiene, during a 30 day experimental gingivitis (7, 14, and 30 days), and during periodontitis (30, 60, and 90 days). The results demonstrated that nonhuman primates with high levels of long-standing gingival inflammation when compared to those nonhuman primates with low inflammation show: 1) different inflammatory mediator profiles in gingival crevicular fluid (particularly for immunoglobulin A (IgA) and IgG levels), 2) a different quantitative and qualitative subgingival microbiota; and 3) a similar progression of periodontitis. Thus, while variations in host inflammatory responses to local factors exist in the nonhuman primates, an extensive subgingival challenge (such as ligation) may negate these individual differences.
authors.affiliation: Department of Periodontics, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Dr., San Antonio, TX 78284, USA.
authors.forename: J L
authors.initials: JL
authors.lastname: Ebersole
authors.forename: D
authors.initials: D
authors.lastname: Cappelli
authors.forename: S C
authors.initials: SC
authors.lastname: Holt
authors.forename: R E
authors.initials: RE
authors.lastname: Singer
authors.forename: T
authors.initials: T
authors.lastname: Filloon
mesh_terms: D000818:Animals; D001421:Bacteria, Anaerobic / Q000302:isolation & purification; D002908:Chronic Disease; D016207:Cytokines / Q000032:analysis; D003773:Dental Plaque / Q000382:microbiology; D003774:Dental Plaque Index; D004195:Disease Models, Animal; D018450:Disease Progression; D004198:Disease Susceptibility; D005883:Gingival Crevicular Fluid / Q000276:immunology*; D005891:Gingivitis / Q000276:immunology* / Q000382:microbiology*; D007136:Immunoglobulins / Q000032:analysis; D018836:Inflammation Mediators / Q000032:analysis*; D008252:Macaca fascicularis / Q000276:immunology* / Q000382:microbiology; D015999:Multivariate Analysis; D010512:Periodontal Index; D010518:Periodontitis / Q000276:immunology* / Q000382:microbiology
chemical_list: D016207:Cytokines; D007136:Immunoglobulins; D018836:Inflammation Mediators