Traumatic cataract is a clinical condition in which the lens becomes rusty. Direct or indirect mechanical injury to the lens can produce cloudy changes called traumatic cataract. Patients are most often seen in children, young adult males and soldiers. What can cause iron deposition in the lens? Causes Common causes include penetrating eye injuries, tonographic cataracts, and electric shock injuries. Blunt contusion cataract: Mostly caused by boxing or ball or other objects hitting the eye, atrial aqueous conduction causes external forces to act on the inelastic lens and also produce rebound on the vitreous surface, so blunt contusion causes lens clouding in a variety of ways, namely Vossius annular clouding, rosette-like clouding, rounded nucleus cataract, punctate cataract and total cataract. In blunt contusion cataracts, trauma disrupts lens epithelial function, which leads to edema and degeneration of the superficial cortical lens fibers, eventually producing a confined and permanent thin area of vacuolation. As time progresses, new normal lens cells form and the injured epithelial layer is compressed and encapsulated, resulting in access to the deep cortex and eventual clouding. Penetrating injury cataract: The penetrating injury of the eye simultaneously ruptures the lens capsule membrane and the atrial water enters the lens, causing fiber edema, degeneration and clouding. If the perforation is very small it can close on its own, leaving the lens with a small confined clouding that will not develop again. However, after the lens capsule is broken, most people develop rapid cortical clouding, and large perforations can also cause secondary glaucoma due to excessive expansion of the lens cortex. Pathogenesis In basic studies of traumatic cataracts, it has been found that various contingencies, such as oxidizing substances, ultraviolet light, and toxic substances, can initiate apoptosis of lens epithelial cells, so it is believed that lens epithelial cell apoptosis is a common cytological basis for non-congenital cataracts in humans and animals. A rat model of blunt contusion cataract has been established in China, and it was found that the ultrastructure of lens epithelial cells in SD rats underwent obvious changes: the nuclear membrane was broken and invaginated, chromatin was condensed; the mitochondrial structure was disrupted and showed vacuolar-like changes, and the number was reduced; the endoplasmic reticulum was dilated, which was consistent with the morphological manifestation of apoptosis. This shows that the occurrence of blunt contusion cataract may be related to apoptosis of lens epithelial cells. One study found that the healing process of lens trauma after penetrating injury initiates the accumulation of extracellular matrix, whose main components include chondroitin sulfate, heparan sulfate, and collagen. The accumulation of extracellular matrix under the capsule membrane not only leads to folds in the lens capsule membrane, but also enhances the adhesion, proliferation, and migration of lens epithelial cells, which eventually leads to lens clouding. Matrix metalloproteinases (MMPs) and their migrating TIMPs play a considerable role in the aggregation and degradation of extracellular matrix, with MMPs promoting extracellular matrix aggregation and TIMPs promoting degradation. In a study of a rabbit penetrating cataract model, it was found that the activities of TIMP-1 and 2 in the injured eye were significantly increased on the first day after injury and gradually decreased thereafter, while the changes in the activities of MMPs-2 corresponded to this, i.e., they were inhibited on the first day after injury and gradually recovered thereafter. Therefore, it is hypothesized that the transient increase in the content of TIMP-1 and 2 in rabbit eyes changes the balance of MMPs/TIMPs, which may have the effect of antagonizing the degradation of extracellular matrix by MMPs and inhibiting the development of intraocular inflammation after injury, with the result that the process of extracellular matrix remodeling and cell proliferation repair after tissue injury is enhanced, thus promoting wound healing, but excessive extracellular matrix aggregation and cell excessive accumulation of extracellular matrix and excessive cell proliferation may lead to clouding of the lens.