Primary glaucoma is a painful, progressive, and blinding disease reported in many canine breeds, characterized by intraocular pressure (IOP) elevation in the absence of antecedent intraocular disease. Clinical observations of dogs with primary glaucoma suggest that many affected eyes develop concurrent intraocular inflammation in addition to elevated IOP. In this work, we summarize the current knowledge that relates inflammation to primary glaucoma in dogs, reviewing studies focused on genetics, physiology, histopathology, bioanalysis of ocular fluids, therapeutics, and clinical outcomes of glaucomatous patients. Through disruption of the blood-aqueous and blood-retinal barriers, pigment dispersion, and biochemical changes to the aqueous humor and tear film, the pathogenesis of canine primary glaucoma appears to involve inflammatory changes to various extents and with various consequences from the front to the back of the eye. Among others, inflammation further impacts IOP by reducing aqueous humor outflow at the level of the iridocorneal angle and accelerates vision loss by promoting neuronal degeneration. As such, the vicious cycle of ocular inflammation and IOP elevation might warrant the use of anti-inflammatory medications as a core component of the treatment regime for dogs with primary glaucoma, either therapeutically (i.e., actively glaucomatous eye) or prophylactically in the yet unaffected contralateral eye.
Keywords: anti-inflammatory medications; glaucoma; goniodysgenesis; intraocular pressure; ocular inflammation; pigment dispersion; trabecular meshwork; uveitis.