Carvacrol as a Potential Modulator of TGF-β Expression in Periodontitis: A Narrative Review

Abstract

Periodontitis is a chronic inflammatory disease driven by polymicrobial infection and an imbalance between subgingival microbiota and the host inflammatory response, leading to progressive destruction of the periodontal ligament and alveolar bone. Carvacrol, a phenolic monoterpene found in oregano and thyme, demonstrates antimicrobial and anti-inflammatory properties relevant to periodontal pathogens. Transforming growth factor-beta (TGF-β) plays a dual, context-dependent role in periodontal tissue, supporting early anti-inflammatory responses and matrix repair but promoting fibrosis and periodontal ligament stem cell senescence when its activity is sustained. Carvacrol and TGF-β have largely been studied independently, and direct evidence linking the two in periodontitis remains limited. This review summarises current knowledge on carvacrol’s chemical properties, molecular mechanisms of anti-inflammatory action, effects on periodontal-related cytokines including TGF-β, and available preclinical evidence. Carvacrol suppresses inflammation by inhibiting NF-κB and MAPK/ERK signalling, reducing IL-1β, TNF-α, and IL-6, and increasing IL-10. Its effects on TGF-β are context-dependent, increasing expression in an autoimmune CNS model but decreasing it in a murine asthma model; the only study demonstrating direct TGF-β1 modulation was conducted in renal epithelial cells rather than periodontal tissue. Preclinical evidence supports carvacrol’s antimicrobial and anti-inflammatory effects in periodontal disease, but its influence on TGF-β signalling in periodontal tissue remains unexplored. Further studies using periodontal cell and animal models are needed to clarify this relationship.