Abstract

The success rate of glaucoma filtration surgery is closely related to conjunctival inflammation, and the main mechanism of dry eye disease (DED) is inflammation. The aim of this study was to evaluate the effect of DED on bleb scar formation after rabbit glaucoma filtration surgery. Sixteen New Zealand white rabbits were randomly divided into control and DED groups. A DED model was induced by twice-daily topical administration of 0.1% benzalkonium chloride (BAC) drops for three weeks. Ocular examinations were performed to verify the DED model. Surgical effects were assessed, and histologic assessments were performed on the 28th postoperative day. Higher fluorescein staining scores, lower basal tear secretion levels and goblet cell counts, and increased interleukin 1β (IL-1β) levels were observed in the DED group. The DED eyes displayed significantly higher intraocular pressure (IOP)% on the 14th postoperative day; a smaller bleb area on days 14, 21 and 28; and a shorter bleb survival time. Moreover, proliferating cell nuclear antigen (PCNA) and alpha-smooth muscle actin (α-SMA) levels were significantly increased in the DED group. These results demonstrate that DED promotes filtering bleb scar formation and shortens bleb survival time; these effects may be mediated via IL-1β.

Highlights

  • Glaucoma is a major eye disease that results in blindness [1] whose first-line surgical treatment is filtration surgery

  • Long-term benzalkonium chloride (BAC)-containing antiglaucoma eye drop treatment is an important cause of dry eye disease (DED) in patients with glaucoma [6,21,22,23]; treatment with BAC was considered a better approach for establishing the rabbit DED model used in this study

  • We found that the levels of proliferating cell nuclear antigen (PCNA) and α-Smooth Muscle Actin (α-SMA) were significantly increased in the DED group, illustrating that fibroblast proliferation and transformation were increased in DED eyes compared with those in control eyes, resulting in shorter bleb survival times in the former group than in the latter group

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Summary

Introduction

Glaucoma is a major eye disease that results in blindness [1] whose first-line surgical treatment is filtration surgery. Due to increases in fibroblast activity, which impairs the formation of filtering blebs and reduces aqueous humor outflow, the failure rate of this surgery can reach 15–30% [2,3]. Conjunctival inflammation is an important contributor to the development of fibrosis. When corneal and conjunctival tissues are exposed to an inflammatory milieu, fibroblasts will undergo transformation into myofibroblasts, which leads to increases in proliferation and tissue remodeling [4]. In 2007, the Dry Eye Work Shop (DEWS) updated the definition of dry eye disease (DED).The new definition emphasized that DED must be accompanied by ocular surface inflammation [5]. Glaucoma patients are at risk for developing DED. Baudouin et al [6] reported that the prevalence rates of severe ocular surface disease in patients with severe and mild glaucoma were 63% and 41%, respectively. The reasons include that glaucoma typically affects elderly individuals, and intraocular pressure (IOP)-lowering drugs with preservatives are widely used in patients with glaucoma

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