Gliosis

Gliosis, or reactive gliosis, is a non-specific response of glial cells in the brain and spinal cord to injury or disease. It is dominated by astrocytes, with microglia and, to a lesser extent, oligodendrocyte lineage cells participating. The process is marked by astrocyte hypertrophy and proliferation and increased expression of intermediate filament proteins such as GFAP, leading to an expansion of glial processes that can envelop and stabilize damaged tissue.

Causes and mechanism include ischemic or traumatic injury, infection, inflammation, neurodegenerative or demyelinating conditions, and other CNS insults. Activated microglia release cytokines and growth factors that promote astrocytic reactivity. Astrocytes upregulate GFAP and vimentin, migrate toward the lesion, and secrete extracellular matrix components, including chondroitin sulfate proteoglycans. Over time, a dense network of glial processes can form a glial scar that demarcates damaged from healthy tissue.

Function and outcomes are dual. On one hand, gliosis helps contain injury, re-establish the blood-brain barrier, limit inflammation, and create a supportive environment for tissue repair. On the other hand, the glial scar can impede axonal regeneration and remyelination, contributing to persistent functional deficits in chronic lesions.

Diagnosis and histology rely on immunohistochemical markers such as GFAP. Microscopic features include increased astrocyte size, elongated processes, and altered tissue architecture around the lesion. Gliosis is a reactive, non-neoplastic process and should be distinguished from glial tumors such as gliomas.