This presentation explored the role of hyperbaric oxygen therapy (HBOT) in the management of delayed radiation injury, with a particular focus on osteoradionecrosis and soft tissue radionecrosis. It began by revisiting the traditional understanding of radiation damage and then expanded on this to highlight the more complex cellular and biochemical processes involved. The talk emphasised that radiation injury is not purely a vascular problem, but a dynamic and progressive condition affecting cellular function, collagen integrity, and the body’s ability to repair itself. A key theme was the central role of oxygen in healing, demonstrating how adequate oxygen availability is essential for energy production, collagen synthesis, angiogenesis, host defence, and overall tissue repair. Building on this, the concept of the hyperoxic–hypoxic paradox was introduced, illustrating how intermittent exposure to high oxygen levels during HBOT can stimulate hypoxia-inducible pathways, leading to the release of growth factors such as VEGF, activation of repair mechanisms, and the formation of new blood vessels. This reframes HBOT not simply as a means of correcting hypoxia, but as a powerful biological stimulus for regeneration. Clinical application was discussed with reference to established protocols, including the Marx protocol for osteoradionecrosis, and supported by long-term outcome data demonstrating sustained healing benefits over several years. Real-world patient responses were incorporated to highlight functional improvements in quality of life, including pain reduction, improved oral intake, and restoration of tissue integrity. Overall, the presentation positioned HBOT as a scientifically grounded, evidence-based therapy that addresses both the underlying pathophysiology and the downstream consequences of radiation injury, offering meaningful and durable clinical outcomes when applied appropriately.