Mittendorf Dot

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Article Summary: The Mittendorf dot, an embryologic remnant of the hyaloid artery, is an exam finding of a posterior lens capsule circular opacity that is most commonly visually insignificant.

== Disease == 3,4

Mittendorf dot refers to a congenital vascular defect that manifests as a focal opacity classically located over the inferior nasal quadrant of the posterior lens capsule. It is a mild clinical variant of persistent fetal vasculature (PFV), a spectrum of conditions that arise when fetal hyaloid vasculature fails to involute. Although Mittendorf dot is typically small and round, it may present as a larger opacity that covers the entirety of the posterior lens capsule, though this is rare. A “brittle-star” formation may be observed if the Mittendorf dot anastomoses with other residual fetal vasculature. A Mittendorf dot is a relatively benign finding rarely causing visual impairment.

== Pathophysiology == 2,3,4

The hyaloid artery is a transient vessel that extends from the optic disc to the posterior pole of the lens during fetal development. A dense network of intraocular vessels branch from the hyaloid artery and proliferate during early embryogenesis in order to supply the developing ocular tissues and contribute to the primary vitreous. This hyaloid vasculature ultimately begins to involute at two to three months gestation, coinciding with the development of the retinal vasculature. Following involution, the perivascular sheath of the hyaloid artery typically remains forming Cloquet’s canal. This is seen in the image above. The underlying mechanism responsible for involution of this vascular system is theorized to involve apoptosis via a combination of macrophage activation and cessation of blood flow to the hyaloid artery and its branches. The cellular signaling that leads to macrophage activation has yet to be elucidated.

Mittendorf dot develops when the anterior terminus of the hyaloid artery fails to involute leaving behind an embryologic remnant at the posterior lens capsule. The proposed mechanisms causing persistent fetal vasculature involves improper gene expression of a number of molecules and growth factors including, but not limited to, vascular endothelial growth factor (VEGF), fibroblast growth factor (FGF), angiopoietin 2, Arf tumor suppressor gene, and collagen 18. This remains an active area of research.

== Physical examination == 1 A Mittendorf dot, due to the nature of its origin, may be diagnosed and characterized upon direct visualization during slit lamp examination.

== Signs == 5

Upon physical examination, a Mittendorf dot may be seen in the inferonasal quadrant on the posterior lens capsule.

== Prognosis == 1

The prognosis for Mittendorf dot is excellent as the embryologic remnant is not typically visually significant and does not progress. The Mittendorf dot should be monitored with ophthalmologic examinations including gonioscopy of the anterior chamber at regular intervals.

Additional Resources


Czepita, M., Szewczyk, A., & Twarużek, J. (2017). Mittendorf’s dot and posterior embryotoxon—incidental findings in a patient with a potentially occludable anterior chamber angle. Ophthalmology Journal, 2(4), 110-112.

Farber, N. C., MD, & Shrier, E. M., DO. (2015, February 05). How to treat persistent fetal vasculature. Retrieved April 02, 2021, from

Goldberg, M. F. (1997). Persistent fetal vasculature (PFV): an integrated interpretation of signs and symptoms associated with persistent hyperplastic primary vitreous (PHPV) LIV Edward Jackson Memorial Lecture. American journal of ophthalmology, 124(5), 587-626.

Saint-Geniez, M., & D'Amore, P. A. (2004). Development and pathology of the hyaloid, choroidal and retinal vasculature. The International journal of developmental biology.

Sheth, J. U., Sharma, A., & Chakraborty, S. (2013). Persistent hyaloid artery with an aberrant peripheral retinal attachment: A unique presentation. Oman journal of ophthalmology, 6(1), 58.

Image: Henry Vandyke Carter, Public domain, via Wikimedia Commons