Photobiomodulation mitigates DAMP signaling to improve odontoblast survival

Photobiomodulation (PBM) activation of latent TGF-β1 has been noted to promote odontoblast differentiation and dentin repair under sterile conditions. However, its efficacy under pathophysiological damage stimuli remains undefined that motivated this study.

Murine odontoblasts (MDPC-23) were subjected to five DAMP stressors namely, TNF-α (inflammation), LPS (bacterial infection), CoCl₂ (hypoxia), serum deprivation (nutrient stress), and extreme pH 4 or 12 (acid / alkaline stress). Four PBM wavelengths, namely, 447 nm (blue), 532 nm (green), 658 nm (red), and 810 nm (near-infrared) at 0.03, 3, or 30 J/cm² were employed along with pathway inhibitors targeting ROS (N-acetylcysteine), ATP (sodium azide), NF-κB (BAY 11-7082), BCL-2, and Caspase-3. Cell viability (Alamar Blue) and mitochondrial membrane potential (JC-1) were assessed.

All four PBM wavelengths significantly (n = 4, p < 0.05) enhanced odontoblast viability at 3 J/cm². Among the stressors, TNF-α, hypoxia, nutrient deprivation, and alkaline pH significantly (n = 4, p < 0.05) reduced viability and rescued most consistently (n = 4, p < 0.05) by red (658 nm) and green (532 nm). LPS and acidic pH were not rescued by PBM treatments. Mechanistic analysis noted PBM-mediated survival response was significantly (n = 4, p < 0.05) abrogated by NF-κB inhibition, but not ROS, BCL-2, or caspase-3 suggesting selective integration of the signaling pathways. The two effective wavelengths exerted divergent effects on mitochondrial membrane potential suggesting they have discrete upstream signaling mechanisms.

PBM treatments evoked context-dependent, wavelength-specific odontoblast survival that could guide precision clinical protocols for pulp-dentin regeneration.