Achieving gingival immune homeostasis in periodontal disease
Researchers may have uncovered the mechanical processes underlying gingival tissue and extracellular matrix changes in patients with periodontal disease.
In a study published in Advanced Materials, the researchers developed a mechanically tunable hydrogel model involving both stiff and soft collagen-alginate hydrogels to analyze the mechano-immune crosstalk in the gingival extracellular matrix of materials replicating the rheological properties of healthy and inflamed gingival tissue.
After encapsulating human gingival fibroblasts in both hydrogels, the researchers discovered that the stiffness played a role in suppressing toll-like receptor-mediated inflammatory responses and that noncanonical nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kappa-B) pathway and epigenetic nuclear organization were responsible for regulating the fibroblasts’ inflammatory responses on the basis of stiffness. Further, when myeloid progenitors were co-cultured with human gingival fibroblasts in the stiff hydrogels, they differentiated into immunomodulatory dendritic cells. The researchers achieved increased stiffness and reduced inflammatory cytokine production through ex vivo cross-linking of human gingival tissue.
As a result of the findings, the researchers suggested that gingival stiffness could be critical in determining inflammatory responses and gingival fibroblast dysregulation in periodontal disease. They emphasized that restoring the mechanical integrity of the gingival tissue could represent a novel strategy to improve gingival immune homeostasis.
Read more: Advanced Materials
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