Shuyu Yang, Xi Yang
BACKGROUND: ROS are pivotal in maintaining periodontal tissue health due to their dual role in physiological and pathological states. At physiological levels, ROS are essential for host defense, effectively eliminating pathogenic bacteria during inflammation and sustaining the homeostasis of the periodontal microenvironment. However, excessive ROS production disrupts the balance between oxidative activity and antioxidant defenses, leading to oxidative stress (OS). This imbalance exacerbates inflammation, damages cellular components, and drives periodontal tissue destruction. Recognizing the dual role of ROS underscores the importance of studying their regulatory mechanisms, which is crucial for advancing understanding and therapeutic strategies in periodontitis management. OBJECTIVE: This review summarizes the latest research advancements on the molecular mechanisms linking ROS to the progression of periodontitis and explores related therapeutic strategies. RESULTS: This review focuses on the pivotal role and specific mechanisms of periodontal tissue destruction by excess ROS, which mediate signaling pathways such as nuclear factor kappa B (NF-κB) and mitogen-activated protein kinase (MAPK), as well as the activation of OS response-associated proteins, including thioredoxin-interacting protein (TXNIP) and mitochondrial antiviral signaling protein (MAVS). Additionally, we provide a concise summary of emerging therapeutic strategies for periodontitis, including the use of antioxidants, photodynamic therapy (PDT), and nanomaterials. Gaining a more profound comprehension of these mechanisms may pave the way for the formulation of enhanced therapeutic strategies for periodontitis. CONCLUSION: Understanding the interplay between ROS and periodontal tissue destruction is essential for advancing periodontitis research. Targeting the NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome with antioxidant and ROS-modulating therapies presents a promising strategy to mitigate both inflammation and OS, thereby reducing periodontal degradation.