The lens capsule is in fact a transparent and elastic basement membrane that completely surrounds the lens. It is initially derived from the secretory product of the surface ectodermal cells that form the lens vesicle during embryonic development, and afterwards it is secreted by the lens epithelial cells. It is believed to be the thickest basement membrane of the body. Under light microscopy, the capsule is homogenously positive in PAS staining; under electron microscopy, it appears to consist of up to 40 parallel layers of collagen fiber lamellae. These collagen lamellae are mainly composed of type IV collagen. Other components include type I and type III collagen, laminin, fibronectin, and sulfated glycosaminoglycan [11]. The lens capsule varies in thickness in different parts, being thickest near the equator (21–23 μm) and thinnest at the posterior pole (2–3 μm). Therefore, rupture of the lens capsule is most likely to occur at the posterior pole during cataract surgery [12]. Besides, the thickness of the anterior lens capsule increases with age, but its elasticity decreases conversely. Hence, the anterior capsule is relatively thin and elastic during childhood, posing a greater challenge to continuous curvilinear capsulorhexis (CCC) [12].

Beneath the capsule at or near the equator is the actively germinative lens epithelium. This portion of capsule is thicker than at the anterior and posterior poles, and it is also connected with the zonules. Ultrastructure studies reveal that the part of the capsule where the zonules insert has a two-layer structure. The outer layer is an extremely thin zonular layer, while the inner layer is the real lens capsule [13]. The zonular layer is where the zonules attach to the lens capsule. The collagen bundles of the zonules intertwine with the collagen fiber lamellae of the capsule, forming close attachments. The “frontier” of the zonule insertion is situated 6–7 mm from the center of the anterior capsule, and thus a capsulorhexis diameter larger than 6 mm may lead to zonule injury and lens instability, and an outward radial tear may occur at the site of capsulorhexis [13].

The lens epithelium, located directly beneath the capsule at the anterior and equator of the lens, is a single-layer cuboidal epithelium. It is differentiated from cells that formed the lens vesicle during embryonic development. The cells beneath the equatorial capsule are cuboidal and rich in mitochondria, with active proliferation and smaller volumes than cells located below the anterior capsule. This region is referred to as the germinal zone [14]. Since the embryo was 25 mm in length, the lens epithelial cells have been proliferating and differentiating into secondary lens fiber cells, which elongate and further differentiate into lens fibers. In this manner the lens maintains a lifelong growth. The total number of lens epithelial cells in a mature human lens is about 500,000, but it varies substantially among individuals. The mean cell density in male adults is 5000 cells/mm² and in female adults 5800 cells/mm², which tends to increase from the center outward to the peripheral region [15]. It is generally believed that both the average density and proliferative capacity of the lens epithelial cells decrease with age, but some insist that there is no significant correlation between age and changes in density of the lens epithelial cells [16]. After cataract surgery, migration, proliferation, and epithelial–mesenchymal transition (EMT) of the residual lens epithelial cells contribute to the pathogenesis of posterior capsular opacification (PCO) [17–19].

The lens fibers, derived from the lens cells, appear as long stripes and are hexagonal in cross section. The primary lens fibers of embryonic nucleus are less than 250 μm long, but their length in adults is up to 10 mm. During the formation of the lens fibers, the lens cells derived from the lens epithelium transform into long stripes with elongation of cell nuclei. The basal projections of these cells stretch along the posterior capsule toward the posterior pole, while the apical projections stretch along the anterior capsule toward the anterior pole. Subsequently, the cell nuclei migrate anteriorly with an increase in cytoskeletal structures, e.g., microtubules, microfilaments, and intermediate filaments. As the transforming lens cells extend anteriorly and posteriorly, cellular nuclei are degraded, the basal part of the cell is separated from the posterior capsule, and all organelles migrate toward the anterior or posterior ends and gradually disappear. Finally, lens cells transform into lens fibers, which keep being pushed toward the center of the lens by new cells. The rate of differentiation of lens cells into lens fibers, as well as the rate of proliferation of lens epithelial cells, decreases with age, indicating a potential interaction between them. Both processes constantly repeat, so older fibers are continuously pushed by new fibers toward the center of the lens.

The lens fibers are unable to contract. However, the entire lens has to change its curvature during accommodation. Therefore, the cortical fibers located in the mid-peripheral portion of the lens are joined tightly with one another via “ball-and-socket” junctions, which can hold the lens against the traction force from the zonules during accommodation, leading to a change in the curvature of the lens.

Primary lens fibers, derived from the posterior cells of the lens vesicle during embryonic development, reach the center of the lens and form the embryonic nucleus, while secondary fibers formed during fetal life become the fetal nucleus. Junctions at the ends of lens fibers at the anterior and posterior of the lens are known as lens sutures. The suture anterior to the fetal nucleus is an upright Y and the posterior one is an inverted Y. As the lens grows and the fibers elongate, more complex lens sutures are formed, such as stellate-shaped sutures. In addition to the embryonic and fetal nuclei, the adult lens also has some other layers with different densities. These include, from inner to outer layers, the infantile nucleus consisting of lens fibers formed 1 month before birth until puberty, the adult nucleus consisting of fibers formed after puberty until adulthood, as well as the lens cortex consisting of superficial lens fibers after adulthood. As the lens epithelium continues to differentiate into lens fiber cells, the thickness of the lens cortex increases with age, while the thickness of the nucleus remains constant or even decreases. The density of the lens nucleus increases with age, adding a yellow or brown tint to the nucleus, and radial or gravel-like relief textures appear on the surface of the adult nucleus. With time, the rigidity of the nucleus progressively increases, the elasticity decreases, and its accommodative power reduces, resulting in presbyopia.

The zonules, also referred to as the suspensory ligaments of the lens, arise from the pars plana of the ciliary body near ora serrata. The zonules insert at the lens capsule around the equator, cross-linking with the capsular tissue in the outer zonular layer to maintain a firm attachment. The major role of the zonules is to hold the lens in its anatomic position and enable the lens to change its shape by transmitting the tension from the ciliary body onto the lens capsule during accommodation. In newborns, the fibers of zonules are relatively dense, but the amount of fibers decreases gradually with increasing age [20]. It is shown that the zonules are composed of a myriad of fibril bundles, with the pre- and post-equatorial bundles being thicker than the equatorial bundles [21]. Each fibril bundle, about 0.35–1.0 μm in diameter, consists of multiple microfilaments, which are 8–12 nm in diameter. Unlike the lens capsule that is made up of collagen, these microfilaments are mainly composed of fibrillin [20, 21]. Fibrillin is widely found in blood vessels and various types of connective tissue. It has been reported that fibrillin gene mutations can cause weakening of zonular fibers and subsequent subluxation or complete dislocation of the lens in Marfan’s syndrome [20, 21]. Some researchers further divide the zonular fibers into major fibers and accessory fibers. Fibers running from the ciliary body to the lens are major fibers, while those short fibers running perpendicularly to the major fibers in order to support and strengthen the principal fibers are accessory fibers. Once damaged, the zonular fibers cannot be regenerated [22].