| Anterior segment mesenchymal dysgenesis | |
|---|---|
| Other names | Anterior segment dysgenesis |
 | |
| Anterior segment mesenchymal dysgenesis is inherited in anautosomal dominant manner. | |
| Specialty | Medical genetics  |
Anterior segment mesenchymal dysgenesis, or simplyanterior segment dysgenesis, is a failure of the normal development of the tissues of theanterior segment of the eye. It leads to anomalies in the structure of the mature anterior segment, associated with an increased risk ofglaucoma andcorneal opacity.
Peters' (frequently misspelled asPeter's)anomaly is a specific type ofmesenchymal anterior segment dysgenesis, in which there is central corneal leukoma, adhesions of theiris andcornea and abnormalities of the posteriorcorneal stroma,Descemet's membrane,corneal endothelium,lens andanterior chamber.[1]
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Several gene mutations have been identified underlying these anomalies, with the majority of anterior segment dysgenesis genes encodingtranscriptional regulators. In this review, the role of the anterior segment dysgenesis genesPITX2 andFOXC1 is considered in relation to the embryology of the anterior segment, the biochemical function of these proteins, and their role in development and diseaseaetiology. The emerging view is that these genes act in concert to specify a population of mesenchymal progenitor cells, mainly ofneural crest origin, as they migrate anteriorly around the embryonicoptic cup. These same genes then regulatemesenchymal cell differentiation to give rise to distinct anterior segment tissues. Development appears critically sensitive togene dosage, and variation in the normal level oftranscription factor activity causes a range of anterior segment anomalies. Interplay betweenPITX2 andFOXC1 in the development of different anterior segment tissues may partly explain the phenotypic variability and the genetic heterogeneity characteristic of anterior segment dysgenesis. In the most recent research, thePAX6 gene has been implicated in Peters' Anomaly.[2]
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There is no standard treatment approval, yet numerous surgical techniques have been tried during the latest years, including: penetrating keratoplasty,[3] cataract aspiration or lensectomy,[4][5] optical iridectomy,[6] selective endothelial removal,[7] trabeculectomy and implant of glaucoma draining devices.[8] However, postoperative outcomes are not very promising due to severe amblyopia and other ocular complications, including glaucoma or retinal detachment.[citation needed]
This congenital anomaly was first described by German ophthalmologist Albert Peters (1862–1938).[9]