![]() |
| Pathophysiology, genomic architecture, clinical progression, and therapeutic management of canine ocular melanosis Image Credit: Scientific Frontline |
In the discipline of veterinary ophthalmology, few conditions present as complex a challenge as Canine Ocular Melanosis (OM). Predominantly affecting the Cairn Terrier, yet not exclusive to this breed. This hereditary disorder is characterized by a relentless, progressive infiltration of pigmented cells within the ocular tissues, leading to severe morbidity through the development of intractable secondary glaucoma. Historically and colloquially referred to as "pigmentary glaucoma," this terminology has largely been abandoned in the academic literature in favor of "ocular melanosis" to more accurately reflect the underlying pathological process: a primary proliferation and migration of melanocytes, rather than a passive dispersion of pigment granules as seen in human pigmentary glaucoma. The disease represents a significant welfare concern due to the chronic pain associated with ocular hypertension and the eventual, often bilateral, loss of vision. Furthermore, its entrenched status within the Cairn Terrier gene pool, driven by an autosomal dominant mode of inheritance and a late age of onset, poses a profound dilemma for breeders and geneticists alike.


