Glaucoma is an optic neuropathy in which the primary risk factor is increased intraocular pressure (IOP), attributed to increased resistance to trabecular outflow of aqueous humor (AH). This resistance is believed to result from trabecular degeneration secondary to chronic oxidative stress and cellular senescence but may also involve inflammatory mechanisms whose roles are little known. In fact, inflammatory processes play a major role in the pathophysiology of glaucoma to varying degrees, affecting all structures of the eye, including the ocular surface, the anterior and posterior segments, and even the visual pathways of the brain. These processes are thought to result from dysfunction of a regulatory, protective para-inflammation, becoming chronic and harmful in glaucoma. While the mechanisms of the retinal inflammation which accelerates the degeneration of retinal ganglion cells (RGCs) as well as the inflammation of the ocular surface aggravated by long-term use of preserved glaucoma eye drops have been described for several years, very little is known about the pathophysiology of trabecular inflammation in glaucoma. The objective of this literature review is to provide a synthesis of knowledge on the roles and mechanisms of inflammation in both the healthy and glaucomatous trabecular meshwork, as well as its role in the pathophysiology of glaucoma. Therefore, after a review of the mechanisms of cellular senescence and oxidative stress – sources of trabecular inflammation, we will approach the study of the expression and roles of the main inflammatory mediators within the trabecular meshwork. Finally, we will discuss current knowledge on the toxicity of glaucoma eye drops and their preservatives on the ocular surface and trabecular meshwork as well as their role in trabecular inflammation.