Clinical signs
Clinical signs of this disorder are those indicative of pain, including blepharospasm, photophobia, and epiphora. An ophthalmic
examination usually reveals mild corneal edema in the area of the defect, and a lip or roll of corneal epithelium often surrounds
the stained area. Fluorescein staining is positive but may look dull or appear dull around the edges of the defect where the
stain dissects under the unattached epithelial lip. Many cases (58% to 64%) of SCCED have some degree of superficial corneal
neovascularization, and most SCCEDs are located in the axial or paraxial cornea.7
Signalment and history
SCCEDs occur most commonly in dogs, although they are reported in cats and horses.9 They are more common in middle-aged dogs of either sex. Although they were originally described in Boxers,10 SCCEDs have since been documented to occur in most dog breeds.9 Boxers are still thought to be overrepresented.
Although most of these ulcers occur secondarily to trauma, they may occur spontaneously and without apparent cause.9
Pathophysiology
Healing of an uncomplicated superficial corneal ulcer is rapid, and most heal in three to five days.9 The cornea undergoes healing via epithelial sliding to cover the ulcerated area and mitosis helps restore the abnormally
thin corneal epithelium to its normal thickness.6 If the epithelium does not cover the ulcer and adhere to the underlying stroma properly, it becomes indolent.
The pathophysiology of SCCEDs remains unclear. An early ultrastructural investigation of affected corneas suggested that a
defect in the epithelial basement membrane with associated basal-cell abnormalities at the ulcer site may prevent corneal
reepithelialization.1
Abnormal epithelial structure. More recent studies have used standard techniques such as immunohistochemistry and more sophisticated, quantitative microscopy
techniques to examine SCCEDs in dogs. In one study, 48 corneal samples from dogs with SCCEDs taken during therapeutic superficial
keratectomies demonstrated that the corneal tissue adjacent to the ulcerated area had epithelium that was not only poorly
attached to the underlying stroma but also had abnormal epithelial structure.11 The adhesion complexes between the epithelium and its basement membrane were often deficient or absent in the areas of and
surrounding the ulceration.11 Particularly interesting was the presence of an abnormal, acellular zone consisting of collagen fibrils and amorphous material
in the superficial corneal stroma of all the samples.11 In samples of normal cornea surrounding the ulcer in these affected dogs, no basement membrane abnormalities were present.11
Acellular barrier. The epithelial changes seen in the SCCED dogs were not seen in dogs that had experimentally induced chronic ulcers.12 The investigators suggested that the acellular zone in the superficial stroma plays an important role in the refractory
nature of these ulcers in that it presents a barrier to the reformation of the corneal adhesion complexes and to the formation
of normal basement membranes.12 They also concluded that this disease is not analogous to chronic superficial corneal erosions in people, which are thought
to be a form of corneal dystrophy.12,13
Substance P. Recent studies have also evaluated the role of substance P in dogs with indolent ulcers. Substance P is a neuropeptide that
is found in nearly all canine corneal nerves.7,14 Apparently, a dense abnormal plexus of substance P is present around the periphery of the erosion in dogs with SCCED.7 That suggests that substance P may play a possible, yet unknown, role in the pathophysiology of this disease.7
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