CCN2: a potential contributor to gingival overgrowth.

Background: Fibrotic responses in the gingiva are characterized by their hyperproliferative nature instead of scar tissue formation. Clinically, these conditions appear as "gingival overgrowth" (GO), which can be of drug-induced or genetic origin. Despite surgical removal, GO can recur.

A modest proposal: targeting αv integrin-mediated activation of latent TGFbeta as a novel therapeutic approach to treat scleroderma fibrosis.

Introduction: The potent profibrotic cytokine transforming growth factor-β (TGF-β) has been associated with the onset and progression of the fibrosis seen in the autoimmune connective tissue disease scleroderma (systemic sclerosis, SSc).

Area Covered: This review explores the data supporting the notion that TGF-β contributes to SSc fibrosis and examines why initiating clinical trials in SSc aimed at targeting integrin-mediated latent TGF-β activation is timely.

Expert Opinion: Targeting TGF-β directly has not been proven to be clinically effective in this disease.

Hiding in Plain Sight: Human Gingival Fibroblasts as an Essential, Yet Overlooked, Tool in Regenerative Medicine.

Adult human gingival fibroblasts (HGFs), the most abundant cells in the oral cavity, are essential for maintaining oral homeostasis. Compared with other tissues, adult oral mucosal wounds heal regeneratively, without scarring. Relative to fibroblasts from other locations, HGFs are relatively refractory to myofibroblast differentiation, immunomodulatory, highly regenerative, readily obtained via minimally invasive procedures, easily and rapidly expanded in vitro, and highly responsive to growth factors and cytokines.