To investigate the association of Demodex with chalazia and to describe the associated histopathologic changes in the eyelid tissue.
In a retrospective histopathologic case–control study, 78 ectropion/entropion repair eyelid wedge resections were examined. Serial sections were obtained on formalin-fixed, paraffin-embedded tissues, stained with hematoxylin-eosin and studied by light microscopy. Thirty-eight patient specimens had evidence of chalazia and 40 did not. The main outcome measures included quantification of total eyelid hair follicles, meibomian glands, Demodex folliculorum and Demodex brevis; determining the presence of lipogranulomatous and non-lipogranulomatous inflammation, hair follicle and meibomian gland duct dilatation and hyperkeratinization, and meibomian gland acinar dilation, keratinization, and atrophy.
There was a significantly greater mean number of D. folliculorum in biopsies with chalazia, when compared with biopsies without chalazia (5.55 vs. 2.68, p = 0.044). The presence of D. folliculorum was strongly associated with hair follicle duct dilatation and hyperkeratinization and with perifollicular nongranulomatous inflammation (p = 0.00). Hair follicle duct dilatation, hyperkeratinization, and perifollicular inflammation were also independently associated with chalazia (p = 0.040 and 0.031, respectively). D. brevis was observed only in meibomian glands with chalazia (mean = 0.342), but this finding did not reach statistical significance; p= 0.068.
While the authors cannot establish causality between Demodex and chalazia, these findings suggest that D. folliculorum indirectly may be involved in the pathogenesis of chalazia via its effect on the anterior eyelid margin.