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\n\n\n\nTissue fibrosis as a radiation-induced complication refers to the pathological accumulation of collagen and connective tissue within irradiated tissues, leading to progressive hardening, loss of elasticity and functional impairment.<\/p>\n\n\n\n
It represents the chronic end stage of radiation injury that was not treated at an early stage or that, by its nature, progresses towards fibrotic remodelling.<\/p>\n\n\n\n
It may affect any irradiated tissue, including the skin and subcutaneous tissue, muscles and fascia, the pulmonary parenchyma following thoracic radiotherapy, and the mucous membranes of the gastrointestinal and genitourinary systems.<\/p>\n\n\n\n
Patients may experience tissue hardening and stiffness, reduced range of motion, chronic pain and a sensation of tightness in the irradiated area.<\/p>\n\n\n\n
Fibrotic remodelling in irradiated tissue results from a chronic, clinically silent inflammatory process. Radiation causes persistent activation of fibroblasts and macrophages, which continue to produce collagen and transforming growth factor beta 1 (TGF-\u03b21) for years after treatment.<\/p>\n\n\n\n
The deposited collagen is abnormal: it is dense, rigid and disorganised, resembling scar tissue.<\/p>\n\n\n\n
This fibrotic tissue compresses the blood vessels supplying the affected area, further aggravating hypoxia and creating a self-perpetuating cycle in which hypoxia promotes fibrosis and fibrosis, in turn, worsens hypoxia.<\/p>\n\n\n\n
The resulting hardening may also compress local nerves, cause neuropathic pain, or lead to adhesions involving adjacent organs, with potentially serious functional consequences.<\/p>\n\n\n\n\n\n\n\n
Research into the effects of hyperbaric oxygen therapy on tissue fibrosis focuses on the molecular mechanisms that regulate the fibrotic process. Studies have shown that increased oxygenation inhibits the activity of transforming growth factor beta 1 (TGF-\u03b21), the principal regulator of fibrosis, and reduces the production of abnormal collagen by chronically activated fibroblasts.<\/p>\n\n\n\n
At the same time, induced neovascularisation improves oxygen delivery to fibrotic tissue, restoring the metabolic conditions required for cells to function more normally. The clinical outcomes reported, including improved tissue elasticity and reduced stiffness and pain, directly reflect these biological changes.<\/p>\n\n\n\n
In tissue fibrosis, hyperbaric oxygen therapy is used as an adjunctive intervention that addresses hypoxia, inflammation and fibrotic activity simultaneously. These three interconnected mechanisms cannot be managed as effectively through isolated pharmacological or physiotherapy interventions.<\/p>\n\n\n\n
Restoring tissue oxygenation allows fibroblasts to move away from a state of chronic pathological activation, thereby reducing the production of further abnormal collagen.<\/p>\n\n\n\n
Neovascularisation improves the nutritional supply to fibrotic tissue and creates the conditions required for gradual remodelling. It does not reverse fibrosis that has already developed, but it may slow or halt its progression and improve function.<\/p>\n\n\n\n
A typical treatment course consists of 30 to 40 sessions, following an individualized assessment carried out in collaboration with the oncologist and the physical and rehabilitation medicine specialist.<\/p>\n","protected":false},"excerpt":{"rendered":"
What Is Tissue Fibrosis? Tissue fibrosis as a radiation-induced complication refers to the pathological accumulation of collagen and connective tissue within irradiated tissues, leading to … <\/p>\n