Researchers found that reduced gingival extracellular matrix stiffness in periodontal disease promotes a pro-inflammatory phenotype in gingival fibroblasts, driven in part by non-canonical nuclear factor kappa B signaling and epigenetic regulation, whereas restoring stiffness suppresses cytokine production and supports immune homeostasis. These findings suggest that targeting tissue mechanics—potentially through biomaterial-based approaches—may offer a novel adjunctive strategy to modulate inflammation and improve periodontal disease outcomes.

Source: Advanced Materials