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Recurrence rates with current treatment approaches, such as surgical evacuation with burr hole craniostomy or craniotomy, are high. These treatments often do not address the underlying inflammatory process, which is a key driver in cSDH development and progression. cSDHs develop when trauma to the inner dural border cell layer leads to an inflammatory response promoting neoangiogenesis, the ingrowth of new fragile vessels that are highly prone to leakage. Subsequent rebleeding, exudation, and incomplete resorption exacerbate the inflammatory response, leading to a self-perpetuating process. This review provides an overview of the inflammatory mechanisms involved in cSDHs, highlighting key biomarkers and cellular pathways, as well as associated translational clinical implications. 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