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Jost B. Jonas, MD; Sohan Singh Hayreh, MD, PhD, DSc, FRCS, FRCOphth; Yong Tao, MD, PhD

Arch Ophthalmol. 2009;127(10):1395-1396.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

In the Ocular Hypertension Treatment Study, central corneal thickness (CCT) has been recognized as a significant risk factor for progression of ocular hypertension to primary open-angle glaucoma.¹ Consequently, Herndon et al² demonstrated that CCT was inversely correlated with the amount of glaucomatous optic nerve damage at the time of referral of the patient. Several investigations confirmed that a thin cornea was a risk factor for development and progression of glaucoma.³ It has remained unclear whether a thin cornea was a clinical risk factor because the falsely low intraocular pressure measurements were not corrected for their dependence on CCT or whether a thin cornea was additionally a structural risk factor potentially due to an association with a thin lamina cribrosa. According to biomechanical considerations, a thin lamina cribrosa may be a risk factor for increased . . . [Full Text of this Article]

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