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The Paediatric Cataract: an Overview of the Embryology and Pathophysiology

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The Paediatric Cataract: an Overview of the Embryology and Pathophysiology TRAINEES The paediatric cataract: an overview of the embryology and pathophysiology In the first of the two articles on paediatric cataracts,Samuel Aryee reviews the aetiology of this condition. ataracts arise from opacification Treating the childhood cataract involves epithelium. This is particularly interesting of the natural transparent lens, early diagnosis and prompt management as other vital ocular structures such as which can cause partial or in order to prevent irreversible sequalae. the retina, ciliary body, iris and optic Ctotal blindness. Although the Complications of the unresolved paediatric nerves are derived from neuroepithelium mechanism underlying the pathological cataract include strabismus, amblyopia [6,7] (Figure 1). processes of cataract formation is still and blindness [4,5]. The mortality Pax6 is a crucial gene in eye development, being actively researched, the vast rate is also found to be higher in blind and its main role is to initiate evagination of majority of cataracts can be treated very children. However, this is hard to quantify the optic grooves or sulci. The optic grooves effectively. Paediatric cataracts occur numerically due to a lack of reliable later turn into optic vesicles, which make much less commonly than cataracts in the surveillance. This is especially the case in contact with surface ectoderm and induce adult and elderly population, yet pose a developing countries where underlying the necessary developmental changes in significant challenge for the child, family, systemic complications and lower socio- this germ layer. The lens placode forms ophthalmologist and wider society. The economic standing further impede the from thickening of the surface ectoderm paediatric cataract is a significant cause of management of more complex needs adjacent to the optic vesicles. Optic cups blindness in childhood, and it is estimated amongst blind children [3]. These potential further develop from the optic vesicles and that approximately 200,000 children complications further stress the importance interact with the retina while the iris and worldwide are blind due to cataracts [1]. of early management of paediatric cataracts ciliary body develop from the central optic Epidemiological studies also suggest a in order to reduce disability and the cup (Figure 2). prevalence of between 1.2 and six cases likelihood of childhood ‘blind-years’. The lens vesicle is developed from per 10,000 infants worldwide [2], with continued thickening of the ectoderm and their occurrence being either congenital Embryology and pathophysiology eventual separation from this layer. This or developmental. Cataracts are deemed stage of lens development is complete by congenital if they present within the first Normal lens development week eight (Carnegie Stage 22) and the lens year of life while developmental cataracts It is important to consider the complexity of occur after infancy or following trauma. the development of the human eye in order at this point measures ~400µm. Further It is difficult to determine the absolute to better understand the pathophysiology growth takes place as epithelial cells in timing of onset, and there is also a small of paediatric cataracts. Ocular development the lens germinative zone anterior to the degree of overlap between congenital in utero begins roughly in the third week equator undergo mitosis. Daughter cells and developmental cataracts. The of gestation, lasting till the 10th week. migrate to the transitional zone posterior variability in prevalence is largely down to Closure of the neural tube is essential for to the equator where they differentiate and socioeconomic factors in different parts the optic vesicles to bud properly, and elongate into secondary lens fibre cells. of the world and the presence of other failure of this can also result in improper The new crescent-shaped fibre cells are predisposing conditions such as intrauterine eye development. In particular, induction deposited in concentric shells over older infection, malnourishment and metabolic of lens growth occurs around four weeks cells while synthesising large amounts disease which are more common in the gestation. The lens is derived from surface of crystallin proteins in the bow region of developing world [3]. ectoderm, along with the eyelid and corneal the lens [6-9]. Figure 2: Gestational development of the lens and optic vesicle. Figure 1: Schematic representation of typical lens development [8]. a. Week five gestation: development of lens placode and optic vesicle. b. Week six to seven gestation: thickening of lens placode, optic vesicle enlargement and initiation of lens vesicle [9]. Eye News | FEBRUARY/MARCH 2020 | VOL 26 NO 5 | www.eyenews.uk.com TRAINEES This is an extremely complex and delicate formation; however, their inhibition prevents most common inheritance pattern [11]. process on cellular and molecular levels, as lens suppression by NCCs. Smad3-mediated While other modes of inheritance such these different germ layers must interact TGF-β and Wnt molecular signalling as autosomal recessive or x-linked are correctly to ensure that the visual axis and co-operate to restrict lens potential to a possibility, it may also be associated ocular architecture are maintained, allowing the ectoderm overlying the retina, thus systemic syndromes [8,11]. It is important to the eye to grow appropriately during playing a critical role in the formation of a note it is not uncommon that genetic causes childhood. Lens potential must also be functional eye [10]. of congenital cataracts can present with actively suppressed in non-lens ectoderm in other ocular anomalies such as aniridia, order to restrict lens growth in germ layers Congenital and juvenile coloboma and posterior lenticonus among not destined to become lens tissue. Neural cataract development others [8,12] (Table 1). crest cells (NCCs) inhibit lens development The pathogenesis of cataract formation in Several genetic components that except in the vicinity of the retina, ensuring childhood is not completely understood. influence congenital caractogenesis have the alignment of the lens and central However, there are a range of causes been identified. Some of the key players retinal components. Transforming growth thought to be associated with congenital implicated in genetic causes of congenital factor-β (TGF-β) is involved in this process, and developmental cataracts. cataracts include crystallin, lens specific by activating both Smad3 and canonical Wnt Idiopathic congenital cataracts account connexin, major intrinsic protein (MIP), signalling in the non-lens ectoderm. In the for 50% of cases, and 30% are monogenetic paired-like homeodomain transcription lens territory, both pathways prevent lens with autosomal dominance being the factor 3 (PITX3), cytoskeletal structural proteins and heat shock transcription factor Table 1: Causes of congenital or developmental cataract in childhood. 4 (HSF4). Crystallin, in particular, a highly Aetiology Example(s) essential protein component of the lens, has been demonstrated to be affected in Idiopathic About 50% nearly 50% of congenital cataracts with Genetic [8] Genes encoding Crystallin (CRYA, CRYB, CRYG) recognised mutations [8]. It is thought that Genes encoding membrane proteins (GJA3, GJA8, MIP, LIM2) some mutations in genes encoding different Genes encoding cytoskeletal proteins (BFSP1, BFSP2) types of crystallin can lead to improper aggregation and clearance of these proteins, Genes encoding transcription factors (HSF4, PITX3, MAF, PAX6, FOXE3) which result in lens opacification seen in Hereditary Autosomal dominant congenital cataracts. Missense mutations X-linked resulting in amino acid substitutions are the Autosomal recessive mainly dominantly inherited [11] and cause aberrant protein synthesis and lens opacity. Chromosomal Trisomy 21 (Down’s) Unilateral congenital cataracts tend to Trisomy 18 (Edward) be sporadic and can present as a result of Trisomy 13 (Patau) TORCH pathogens (toxoplasma, rubella Systemic Renal – Lowes syndrome, Alport syndrome virus, cytomegalovirus, and herpes simplex virus (HSV) I and II). In these cases, it is Skeletal – Weill-Marchesani syndrome, Bardet-Biedl syndrome, Stickler thought that viral or parasitic infections syndrome during embryogenesis can influence CNS – Norrie’s disease, Zellweger syndrome, Meckel Gruber syndrome the development of the crystalline lens. Muscular – myotonic dystrophy Maternal HSV infection is thought to affect Mandibulofacial – Hallermann- Streiff syndrome, Nance – Horan foetal ectodermal tissue from which the syndrome lens is derived from, likely due to maternal IgG and IgM crossing the placenta and Ocular anomalies [13] Microphthalmia causing a degree of embryological lens Aniridia disruption [15,16]. However, not all cases Retinopathy of prematurity present with cataracts at birth, suggesting Anterior segment dysgenesis syndrome potential re-infective causes or triggers that re-activate the latent virus. Infectious [14] Maternal intrauterine infections e.g. rubella Developmental or juvenile cataracts HSVI & II tend to present within the first or even CMV second decade of life. However, they are Herpes Simplex more likely to be associated with inherited metabolic diseases such as galactosaemia. Toxoplasma Even so, there is still a degree of overlap Metabolic [17] Galactosaemia between congenital and developmental Galactokinase deficiency onset [17]. Galactosaemia is a rare disorder that leads to a build up of galactose due to Hypocalcaemia
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