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.
Techniques to treat contracted sockets continue to evolve; however, large multicenter trials as well as an updated classification scheme are needed to devise standardized treatment protocols.
The three muscle subdivisions are therefore physically joined together and appear to act as a single functional entity that should be collectively referred to as the muscle of Riolan.
Development of the orbit is a collective enterprise necessitating interactions between, as well as contributions from different cell populations both within and beyond the realm of the orbit. A basic understanding of the processes underlying orbital ontogenesis is a crucial first step toward establishing a genetic basis or an embryologic link with orbital disease.
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