AIM: T lymphocytes play a central role during the pathogenesis of periodontitis,
and the imbalance between the pathogenic T-helper type 17 (Th17) and protective
T-regulatory (Treg) lymphocytes determines the tooth-supporting alveolar bone
resorption. Interleukin (IL)-35 is a novel anti-inflammatory cytokine with
therapeutic properties in diseases whose pathogenesis is associated with the
Th17/Treg imbalance; however, its role during periodontitis has not been
established yet. This study aimed to elucidate whether IL-35 inhibits the
alveolar bone resorption during periodontitis by modulating the Th17/Treg
MATERIALS AND METHODS: Mice with ligature-induced periodontitis were treated
with locally or systemically administrated IL-35. As controls,
periodontitis-affected mice without IL-35 treatment and non-ligated mice were
used. Alveolar bone resorption was measured by micro-computed tomography and
scanning electron microscopy. The Th17/Treg pattern of the immune response was
analysed by qPCR, ELISA, and flow cytometry.
RESULTS: IL-35 inhibited alveolar bone resorption in periodontitis mice.
Besides, IL-35 induced less detection of Th17 lymphocytes and production of
Th17-related cytokines, together with higher detection of Treg lymphocytes and
production of Treg-related cytokines in periodontitis-affected tissues.
CONCLUSION: IL-35 is beneficial in the regulation of periodontitis;
particularly, IL-35 inhibited alveolar bone resorption and this inhibition was
closely associated with modulation of the periodontal Th17/Treg imbalance.