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*
Department of Periodontics, School of Dental Medicine, State University of New York, Stony Brook, NY 11794;
Baylor Institute for Immunology Research, Dallas, TX 75204; and Baylor College of Dentistry, Dallas, TX 75246
Previous studies have analyzed the lymphoid and myeloid foci within
the gingival mucosa in health and chronic periodontitis (CP); however,
the principal APCs responsible for the formation and organizational
structure of these foci in CP have not been defined. We show that in
human CP tissues, CD1a+ immature Langerhans cells
predominantly infiltrate the gingival epithelium, whereas
CD83+ mature dendritic cells (DCs) specifically infiltrate
the CD4+ lymphoid-rich lamina propria. In vivo evidence
shows that exacerbation of CP results in increased levels of
proinflammatory cytokines that mediate DC activation/maturation, but
also of counterregulatory cytokines that may prevent a Th-polarized
response. Consistently, in vitro-generated monocyte-derived DCs pulsed
with Porphyromonas gingivalis strain 381 or its LPS
undergo maturation, up-regulate accessory molecules, and release
proinflammatory (IL-1
, PGE2) and Th (IL-10, IL-12)
cytokines. Interestingly, the IL-10:IL-12 ratio elicited from P.
gingivalis-pulsed DCs was 3-fold higher than that from
Escherichia coli-pulsed DCs. This may account for the
significantly (p < 0.05) lower proliferation of
autologous CD4+ T cells and reduced release of IFN-
elicited by P. gingivalis-pulsed DCs. Taken
together, these findings suggest a previously unreported mechanism for
the pathophysiology of CP, involving the activation and in situ
maturation of DCs by the oral pathogen P. gingivalis,
leading to release of counterregulatory cytokines and the formation of
T cell-DC foci.
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