In this study, meibography revealed frequent meibomian gland losses in patients with phlyctenular keratitis, while the morphology of meibomian glands in healthy controls was normal. Moreover meiboscore of lids with phlyctenular keratitis was higher than that of non-inflamed lids in patients with unilateral phlyctenular keratitis. Previous studies have reported a relationship between phlyctenular keratitis and inflammation of the eyelids and meibomian glands [
3‐
10]. Koh et al. demonstrated meibomian gland loss in an eye with unilateral marginal staphylococcal keratitis and eyelid inflammation [
16]. Meibomian gland inflammation may induce ocular surface inflammatory disease [
7]. Morphology of meibomian gland may be influenced by meibomian gland inflammation because inflammatory cells could obstruct meibomian gland. Thus patients with phlyctenular keratitis may accompany with meibomian gland losses. Moreover there are other possibilities. Since abnormalities of meibomian glands have been found in allergic conjunctivitis and in contact lens wearers [
13], meibomian gland loss in phlyctenular keratitis might be caused by the mechanical friction between the ocular surface and eyelid, by inflammation of the cornea and conjunctiva, and bacterial exposure. Another possibility is that meibomitis with meibomian gland loss occurs before the appearance of phlyctenular keratitis, and imbalances in the bacterial flora of meibomian glands, including
P. acnes, induce a corneal DTH reaction to a microbial protein, causing phlyctenular keratitis. However some limitations exist in our study. First, since we did not check bacterial culture of eye lids and meibomian gland in all patients, little is known about relationship between bacteria species and morphology of meibomian gland. Along with
P. acnes,
Staphylococcus aureus which can produce toxins and proteases might be related to pathology of meibomian gland. Second, patients group included three adults (>20 years). Thus ages could influence to meibomian gland pathology. We need to increase number of patients and investigate relationship between ages of patients with phlyctenular keratitis and morphology of meibomian gland. Third, we did not check meibography after treatment for phlyctenular keratitis using antibiotics and steroids. It is important to know if morphology of meibomian gland normalizes after disappearance of inflammation in cornea and meibomian gland. Thus further investigation revealing the relationship between meibomian gland loss and phlyctenular keratitis is required.
The diagnosis of phlyctenular keratitis is made based on clinical manifestations, such as corneal nodules, their vascularization, and meibomitis, along with a positive bacterial culture of the eyelid or meibum. Adding to these conventional examinations, noncontact meibography is useful for visualization of the condition of the meibomian glands. Our data demonstrate a high frequency of meibomian gland loss in phlyctenular patients.