fibroosis

Fibroosis is a pathological process in which normal tissue is progressively replaced by fibrous connective tissue. It involves proliferation of fibroblasts and excessive deposition of collagen and other extracellular matrix components, leading to scarring and architectural distortion of the affected organ. The term is sometimes used interchangeably with fibrosis, though some sources treat fibroosis as a broader or distinct stage of fibrotic change.

Causes typically include chronic injury or inflammation from toxins, infections, ischemia, autoimmune disease, or metabolic disturbances. Ongoing injury stimulates fibroblasts to become myofibroblasts and to produce collagen, while remodeling enzymes alter the matrix. This response can become self-perpetuating, particularly when the underlying insult persists.

Common sites of fibroosis include the liver, lungs, skin, heart, kidneys, and brain. In the liver it contributes to fibrotic liver disease and cirrhosis; in the lungs it underlies several interstitial lung diseases and idiopathic pulmonary fibrosis; in the heart it can cause stiffening and diastolic dysfunction. The clinical impact depends on the extent and location of scarring.

Diagnosis relies on clinical context, imaging, and histology when available. Biopsy or surgical specimens show increased collagen deposition and fibrous septa with loss of normal tissue architecture. Radiologic features vary by organ, with reticulation or honeycombing on chest imaging and nodular or bandlike fibrosis on other sites.

Management focuses on treating the underlying cause and slowing progression with supportive care. Some organs may benefit from antifibrotic medicines in specific diseases; severe cases may require transplantation. Prognosis is highly variable and depends on the organ involved and the extent of fibrootic change.