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J Dent Res. 2014 Sep;93(9):834-9. doi: 10.1177/0022034514544300. Epub 2014 Jul 23.

Restoring host-microbe homeostasis via selective chemoattraction of Tregs.

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Department of Biological Sciences, School of Dentistry of Bauru, São Paulo University (FOB/USP), Bauru, SP, Brazil
Bioengineering The McGowan Institute for Regenerative Medicine Department of Oral Biology The Center for Craniofacial Regeneration, University of Pittsburgh, Pittsburgh, PA, USA.
Departments of Chemical Engineering Bioengineering Immunology The McGowan Institute for Regenerative Medicine The Center for Craniofacial Regeneration, University of Pittsburgh, Pittsburgh, PA, USA.


The disruption of host-microbe homeostasis at the site of periodontal disease is considered a key factor for disease initiation and progress. While the downstream mechanisms responsible for the tissue damage per se are relatively well-known (involving various patterns of immune response operating toward periodontal tissue destruction), we are only beginning to understand the complexity of host-microbe interactions in the periodontal environment. Unfortunately, most of the research has been focused on the disruption of host-microbe homeostasis instead of focusing on the factors responsible for maintaining homeostasis. In this context, regulatory T-cells (Tregs) comprise a CD4+FOXp3 +T-cell subset with a unique ability to regulate other leukocyte functions to avoid excessive immune activation and its pathological consequences. Tregs act as critical determinants of host-microbe homeostasis, as well as determinants of a balanced host response after the disruption of host-microbe homeostasis by pathogens. In periodontitis, Tregs play a protective role, with their natural recruitment being responsible for conversion of active into inactive lesions. With controlled-release technology, it is now possible to achieve a selective chemoattraction of Tregs to periodontal tissues, attenuating experimental periodontitis evolution due to the local control of inflammatory immune response and the generation of a pro-reparative environment.


bone regeneration; chemokines; drug delivery systems; inflammation; periodontal disease(s)/periodontitis; regulatory T-Lymphocytes

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