Journal of Dental Research, Vol 65, 394-399, Copyright © 1986 by International & American Associations for Dental Research Online Journals
Host factors in juvenile periodontitis
R. B. Cogen, J. M. Roseman, W. Al-Joburi, W. C. Louv, R. T. Acton, B. O. Barger, R. C. Go and R. A. Rasmussen
This study was undertaken to determine whether defects in leukocyte
function or in genes at the MHC play a role in the etiology of either
localized (LJP) or generalized (GJP) juvenile periodontitis. Thirteen LJP
and five GJP patients (ranging in age from 13 to 22 years) and their
matched controls were compared with respect to selected leukocyte functions
and HLA phenotypic frequencies. The results of these studies indicated that
there were significant decreases in the phagocytic and chemotactic
abilities of polymorphonuclear leukocytes (PMN) in both LJP and GJP. All JP
patients displayed intrinsic cell defects in chemotaxis compared with
controls; in addition, some patients displayed multiple defects, including
those which were serum-associated. Also, there appeared to be a significant
association between JP and HLA-DR2 and HLA-A33 phenotypes. Fifty percent of
the JP patients were HLA-DR2-positive, whereas only six percent of the
matched controls were positive. Thirty-six percent of JP patients were
HLA-A33-positive, whereas none of the controls was positive. The
association seen with DR2 may be due to sampling, since there were no
significant differences between the JP cases and a larger unmatched control
sample which was not evaluated for periodontal disease. We conclude from
these data that increased susceptibility of some patients to a very
aggressive and destructive form of periodontal disease (JP) is based on
defects in PMN responsiveness. Further investigations are necessary to
determine whether these defects are under genetic control.
