Spray-dried microparticles of encapsulated gefitinib for slow-release localized treatment of periodontal disease.

Periodontal disease (PD) can be prevented by local or systemic application of epidermal growth factor receptor inhibitors (EGFRIs) that stabilize αvβ6 integrin levels in the periodontal tissue, leading to an increase in the expression of anti-inflammatory cytokines, such as transforming growth factor-β1. Systemic EGFRIs have side effects and, therefore, local treatment of PD applied into the periodontal pockets would be preferrable. Thus, we have developed slow-release three-layered microparticles of gefitinib, a commercially available EGFRI.

Gingival epithelial cell-derived microvesicles activate mineralization in gingival fibroblasts.

Soft tissue calcification occurs in many parts of the body, including the gingival tissue. Epithelial cell-derived MVs can control many functions in fibroblasts but their role in regulating mineralization has not been explored. We hypothesized that microvesicles (MVs) derived from gingival epithelial cells could regulate calcification of gingival fibroblast cultures in osteogenic environment.

Altered composition of the oral microbiome in integrin beta 6-deficient mouse.

In periodontal disease (PD), bacterial biofilms suppress β6 integrin expression transforming growth factor-β1 signaling, resulting in gingival inflammation and bone loss. β6 integrin-null ( ) mice develop spontaneous PD. The aim of this study was to unravel potential differences in oral microbiome in wild-type (WT) and FVB mice.

Leucocyte- and platelet-rich fibrin regulates expression of genes related to early wound healing in human gingival fibroblasts.

Background: Leucocyte- and platelet-rich fibrin (L-PRF) is a blood-derived biomaterial rich in leucocytes and platelets embedded in a high-density fibrin network that can be compressed into a membrane and used in surgical applications to stimulate tissue regeneration and wound healing, especially in oral cavity. This study aimed to determine the combined effects of the growth factors and cells present in L-PRF on fibroblasts that directly face the L-PRF membranes placed during surgical procedures.

Methods: The effect of L-PRF from six donors on the expression of 84 key wound healing genes in normal human gingival fibroblasts was tested by RT-qPCR.

Epidermal growth factor receptor signaling suppresses αvβ6 integrin and promotes periodontal inflammation and bone loss.

In periodontal disease (PD), bacterial biofilms cause gingival inflammation, leading to bone loss. In healthy individuals, αvβ6 integrin in junctional epithelium maintains anti-inflammatory transforming growth factor-β1 (TGF-β1) signaling, whereas its expression is lost in individuals with PD. Bacterial biofilms suppress β6 integrin expression in cultured gingival epithelial cells (GECs) by attenuating TGF-β1 signaling, leading to an enhanced pro-inflammatory response.