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*
Department of Cytokine Biology, The Forsyth Institute, Boston, MA 02115;
Department of Biologic and Materials Sciences, University of Michigan, Ann Arbor, MI 48109; and
Orthopedic Biomechanics Laboratory, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA 02215.
Periapical bone resorption occurs following infection of the dental
pulp and is mediated mainly by IL-1
in the murine model. The
production and activity of IL-1 is modulated by a network of
regulatory cytokines, including those produced by Th1
(pro-inflammatory) and Th2 (anti-inflammatory) subset T cells. This
study was designed to assess the functional role of the Th2-type
cytokines IL-4 and IL-10 in infection-stimulated bone resorption in
vivo. The dental pulps of the first molars were exposed and infected
with a mixture of four common endodontic pathogens, and bone
destruction was determined by micro-computed tomography at sacrifice on
day 21. The results demonstrate that IL-10-/- mice had
significantly greater infection-stimulated bone resorption in vivo
compared with wild-type mice (p < 0.001), whereas
IL-4-/- exhibited no increased resorption.
IL-10-/- had markedly elevated IL-1 production within
periapical inflammatory tissues (>10-fold) compared with wild type
(p < 0.01), whereas IL-4-/-
exhibited decreased IL-1 production (p < 0.05).
IL-10 also suppressed IL-1 production by macrophages in a
dose-dependent fashion in vitro, whereas IL-4 had weak and variable
effects. We conclude that IL-10, but not IL-4, is an important
endogenous suppressor of infection-stimulated bone resorption in vivo,
likely acting via inhibition of IL-1
expression.
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