Pterygia are triangular hyperplastic lesions of the conjunctiva composed of fibrovascular tissue that grow into superficial layers of the cornea at the level of the interpalpebral fissure, usually located on the eye’s nasal side (Duke-Elder, 1965). Early studies by Cameron (1965) suggest that environmental factors, such as dust and arid air, and/or high levels of ultraviolet light exposure contribute to the development of pterygia. However, the occurrence of pterygia in patients who do not fit this demographic profile force us to question whether these triggers are the only ones responsible for the appearance of pterygia. For example, could Demodex overpopulation stimulate pterygium formation?
The ubiquitous skin mite Demodex has been implicated as an instigator of anterior blepharitis. Generally considered a harmless saprophyte of the skin, growing opinion suggests that Demodex can be pathogenic. Some have speculated that Demodex overpopulation (demodicidosis) is responsible for various skin diseases such as rosacea, perioral dermatitis, and blepharitis (Turgut Erdemir et al, 2016; Dolenc-Voljc et al, 2005; Nicholls et al, 2017). In fact, meta-analysis found the association between Demodex and acne vulgaris and blepharitis to be statistically significant (Zhao, Hu et al, 2012; Zhao, Wu et al, 2012). Abundant Demodex populations may exacerbate coexisting lid-margin disease.
Two distinct species of Demodex mites have been identified in humans: Demodex folliculorum and Demodex brevis. In the eyelids, Demodex folliculorum can be found in the lash follicle, whereas Demodex brevis burrows deep into sebaceous and meibomian glands. It has been proposed that these mites feed on follicular and glandular epithelial cells, leading to direct damage of the lid margin.
Demodex overpopulation is associated with trichiasis and eyelash disorganization, madarosis (Kumar et al, 2012), meibomian gland dysfunction, conjunctival inflammation, and corneal pathology (Kheirkhah et al, 2007).
A recent study by Tarkowski et al (2017) suggests that Demodex mites may contribute to the development of pterygium. The authors argue that the potential antigenicity of mite-derived materials, such as molt or eggs, may irritate the conjunctiva mechanically, stimulating and accelerating inflammatory processes related to pterygium formation. Similarly, fragments of Demodex’s chitin cuticle, acting as a foreign body, may cause a host inflammatory response. Furthermore, separate research points to ocular demodicidosis as a risk factor for pterygium recurrence, especially conjunctival, after pterygium removal (Huang et al, 2013). It is considered that underlying these associations is the existence of chronic, low-grade inflammation mediated by T helper-cell lymphocytes and elevated interleukin-17 (IL-17) cytokine levels.
T helper cells are a type of T cell that play an important role in the immune system, particularly in the adaptive immune system. These T cells release cytokines, specifically IL-17, a pro-inflammatory cytokine; cytokines are a broad category of small proteins that are involved in cell signaling. IL-17 increases chemokine production—a class of cytokines with functions that include attracting white blood cells to sites of infection—in various tissues.
Infestation of Demodex mites induces a change of tear cytokine levels, especially IL-17, that can cause inflammation of the lid margin and ocular surface (Kim et al, 2011). Also, interestingly, IL-17 is expressed in the basal layer of epithelial cells, in the perivascular tissue, and in the vascular endothelial cells of pterygia (Jabarin et al, 2016).
Can the control of Demodex, with resultant interleukin blockade, have a potential role in managing pterygia? We look to future studies to tease out answers to this question.
Until then, it seems prudent for appropriate lid margin hygiene in an effort to maintain lid margin, conjunctival, and corneal homeostasis. CLS
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