• This in vivo study used a laser scanning confocal microsope (LSCM) to examine the conjunctival and limbal morphology of vernal keratoconjunctivitis (VKC) patients. Believed to be the first in vivo LSCM study of conjunctival and limbal morphology in VKC patients, the authors conclude that their data provide in vivo morphological confirmation for the findings of previous research and were helpful in planning treatment for VKC patients with dry eye.

    They enrolled in the study 26 patients diagnosed with VKC with an average age of 13.8 ± 6.7 years and 26 age-matched healthy controls. The authors classified each VKC patient into one of the three VKC forms based on the results of a conventional slit-lamp microscopic exam. They used the Heidelberg Retina Tomograph II Rostock Cornea Module (Heidelberg Engineering GmbH, Dossenheim, Germany) to examine the bulbar and tarsal conjunctiva and superior and inferior limbus of all study subjects.

    They found infiltration of a larger number of Langerhans cells and inflammatory cells in both bulbar conjunctiva and tarsal conjunctiva of VKC patients compared with normal subjects. The density of Langerhans cells in tarsal conjunctiva was significantly higher in patients with the tarsal form or mixed form of VKC than in those with the bulbar form (P = 0.048). In VKC patients, normal Vogt palisades were visible in 15 eyes (57.7 percent) at the superior limbus and 23 eyes (88.5 percent) at the inferior limbus. Abnormal Vogt palisades were characterized by the atrophy or absence of stromal papillae and disappearance of bright basal cells, accompanied by infiltration of more Langerhans cells. At the superior limbal area, bulbar VKC subjects had the highest rate of abnormal Vogt palisades, followed by those with the mixed form, with both significantly higher than the tarsal form (P = 0.005).

    The authors conclude that damage to Vogt palisades may be due to severe inflammation at the superior limbal area. They note that abnormal Vogt palisades were found at the inferior limbus in three subjects, all of whom developed corneal neovascularization. They say this indicates that longstanding chronic immunological inflammation could thoroughly destroy Vogt palisades, cause limbal stem cell deficiency and lead to corneal angiogenesis. They also note that meibomian glands in tarsal conjunctiva were surrounded by infiltrated Langerhans cells. They say that immunological inflammation initiated by Langerhans cells probably damaged the structure and function of the meibomian gland and consequently caused meibomian gland dysfunction and overevaporation dry eye.