Purpose:To review the recent data about eyelid morphogenesis, and outline a timeline for eyelid development from the very early stages during embryonic life till final maturation of the eyelid late in fetal life.Methods:The authors extensively review major studies detailing human embryologic and fetal eyelid morphogenesis. These studies span almost a century and include some more recent cadaver studies. Numerous studies in the murine model have helped to better understand the molecular signals that govern eyelid embryogenesis. The authors summarize the current findings in molecular biology, and highlight the most significant studies in mice regarding the multiple and interacting signaling pathways involved in regulating normal eyelid morphogenesis.Results:Eyelid morphogenesis involves a succession of subtle yet strictly regulated morphogenetic episodes of tissue folding, proliferation, contraction, and even migration, which may occur simultaneously or in succession.Conclusions:Understanding the extraordinary process of building eyelid tissue in embryonic life, and deciphering its underlying signaling machinery has far reaching clinical implications beyond understanding the developmental abnormalities involving the eyelids, and may pave the way for achieving scar-reducing therapies in adult mammalian wounds, or control the spread of malignancies.

Purpose:To determine the impact of a single injection of various anti-inflammatory, antimitotic, and antiangiogenic agents on the cell count of myofibroblasts in an eviscerated socket.Methods:One eye from 15 skeletally mature New Zealand white rabbits was eviscerated, and the rabbits were divided into 5 groups. Each group of 3 rabbits received a 0.1 ml subconjunctival injection of a different agent. Group I received bevacizumab 25 mg/ml, group II received triamcinolone 40 mg/ml, group III received 5-fluorouracil 50 mg/ml, group IV received mitomycin-C 0.4 mg/ml, while group V was the control group and received no injections. The animals were euthanized 19 days after evisceration and conjunctival samples were submitted for histopathological examination. Monoclonal α-smooth muscle actin antibody was applied, and the mean of 5 readings of the number of myofibroblasts was recorded in each slide.Results:The mean count of myofibroblasts was highest for the control group and all groups achieved a statistically significant reduction in myofibroblast count compared with the control group. Sorting the means showed that Group IV (mitomycin-C) achieved the lowest mean value (p = 0.000006) followed by triamcinolone (p = 0.00048), while group I (bevacizumab) achieved the least reduction in myofibroblast count (p = 0.00148).Conclusion:Until newer antimyofibroblast medications and antibodies are commercially available, a single injection of mitomycin-C or triamcinolone during surgery achieves the highest mean reduction of myofibroblast count.

Purpose:To review the recent literature and describe the authors’ experience with congenital upper eyelid coloboma.Methods:In this review, we will summarize the embryologic and etiopathogenetic bases of congenital upper eyelid coloboma, and study the published clinical reports. We will also attempt to briefly shed some light on the rarer syndromic curiosities associated with upper eyelid coloboma.Results:Congenital upper eyelid colobomas are one of the few nontraumatic oculoplastic emergencies that may occasionally present in the first few days of life with a corneal ulcer and may even present with impending perforation. They can present with or without corneopalpebral adhesions, may be isolated findings or a part of a larger spectrum of congenital anomalies as in the case of Fraser syndrome or Goldenhar syndrome, or could be associated with other rare curiosities that could challenge the clinician with a huge diagnostic dilemma.Conclusions:Existing literature dealing with congenital colobomas of the upper eyelid is fraught with nosologic problems, confusing etiologies, and overlapping clinical features. We attempted to clarify the salient clinical features, outline the management principles, and until a time in the not-so-distant future where advances in molecular genetic testing would help redefine the etiology and the diverse clinical spectrum of genetic diseases associated with upper eyelid colobomas, we propose a simplified classification scheme based on the relation of the coloboma to the cornea, the presence or absence of systemic features, and all the syndromic and nonsyndromic associations of congenital coloboma of the upper eyelid known today.

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