Purchase this article with an account.
R.C. Tripathi, B.J. Tripathi, R.M. Davis; Pathophysiology of Corneal Mucous Plaques . Invest. Ophthalmol. Vis. Sci. 2006;47(13):1968.
Download citation file:
© ARVO (1962-2015); The Authors (2016-present)
To investigate the pathophysiology of corneal mucous plaques (CMPs) in a variety of ocular surface disorders.
A total of 32 patients (age range, 27 to 75 years) with CMPs were included in the study. The majority of patients had keratoconjunctivitis sicca; 15 also had filamentary keratitis and 14 had staphylococcus blepharitis with or without systemic collagen and autoimmune disorders. 3 patients were post–Lasik or post–penetrating keratoplasty. Under topical anesthesia, biopsy of the CMPs was performed in selected patients and the tissue was processed immediately for light and electron microscopy.
CMPs varied in size (a few µm to a few mm) and in shape forming multiple small islands to irregular patterns and, in some patients, involved more than half the corneal surface. Usually, CMPs were semi–translucent, white to gray, and slightly elevated from the corneal surface and co–existed with mucous filaments. Some plaques were opaque, thickened and elevated well above the tear film and had a dry surface. Histologically, CMPs consisted of a mixture of mucous blobs and filaments, proteinaceous and lipoidal material, and degenerating epithelial cells, whereas filaments had a mucous string substrate covered with epithelial cells. Many CMPs enmeshed calcareous granules, bacteria, dust particles and other foreign bodies. Variable amounts of mucus adhered to the superficial squamous cells as well as to the underlying cells through both transcellular defects and the widened intercellular spaces of adjoining surface cells.
Despite variations in the clinical presentation of CMPs, the plaques shared a common pathology. Disruption of the integrity of the corneal epithelium and innervation (trophic keratitis), systemic collagen and autoimmune disorders, surgical procedures of penetrating keratoplasty or Lasik, infective agents, and epithelial desiccation are predisposing factors. CMPs form when high–viscosity mucus, proteinaceous and other components adhere to exposed receptor sites in the superficial and deeper squamous cells of the cornea through intercellular spaces or abnormal transcellular defects in the surface cells. Use of mucolytic agents, such as acetylcysteine, tear substitutes, soft contact lenses, and debridment, as well as therapy of co–existing systemic disorders, are key to management.
This PDF is available to Subscribers Only