Background: The pathogenesis of early-onset periodontitis (EOP) can be expl
ained by various host risk factors. Previous studies have focused on a sing
le (among many possible) immunological risk factor and the association amon
g the factors has not been assessed. We comprehensively investigated the as
sociations among multiple host immunological risk factors in EOP patients t
o further elucidate their role in the pathogenesis of EOP.
Methods: Sixty-eight EOP patients (50 generalized EOP, 18 localized EOP), 5
1 EOP-suspected patients (S-EOP), 43 adult periodontitis (AP) patients, and
36 periodontally healthy subjects (HS) participated in this cross-sectiona
l study. We examined peripheral neutrophil functions, phenotypic and functi
onal characterization of peripheral lymphocytes (lymphocyte subsets, T-cell
proliferative activity), cytokine productivity (interleukin [IL]-1, IL-2,
tumor necrosis factor [TNF]-alpha, interferon [IFN]-gamma, IL-4 and IL-6),
serum immunoglobulin G (IgG) antibody titers against 12 periodontal bacteri
a, and HLA class II genotypes.
Results: G-EOP, S-EOP, and AP patient groups showed significantly lower per
centages of pan T cells and CD8-positive cells (P<0.02) compared with the H
S group. L-EOP patients showed depressed IL-4 and TNF-<alpha> productivity
compared with the HS group (P <0.02). The EOP group showed significantly el
evated antibody levels against Actinobacillus actinomycetemcomitans, Porphy
romonas gingivalis, Treponema denticola, and Fusobacterium nucleatum compar
ed with the HS group (P <0.05). The frequency with DQB1*0503 was significan
tly higher in the EOP patient group than the HS group (P = 0.045) due to th
e higher frequency in L-EOP patients than the HS group (P = 0.035). There w
ere wide interindividual variations in each of the tests among patient and
HS groups; however, EOP patients showed wider intradiagnostic group variati
ons in certain host defensive cell functions than the other groups. There w
ere some EOP patients who showed extremely low or high values in some tests
; the EOP patients could be further divided into subgroups according to the
ir host defensive and immunological profiles. However, there was heterogene
ity in some of the other host immunological tests even in the subgroups.
Conclusions: The association of host immunological risk factors in EOP pati
ents is widely varied and more complex than previously thought. These resul
ts indicate the difficulty of explaining the pathogenesis of EOP based on a
single host risk factor and also emphasize the importance of critical asse
ssment of not only EOP patient groups, but also individual patients.