What is traumatic cataract?

Eyes are the key objects of protection, but even so, many people still have problems with their eyes. People often suffer from decreased vision and amblyopia due to lack of attention to eye rest or long-term use of electronic products. Others may suffer from trauma, such as accidental knocking or bruising, which causes rupture of the inner membrane, redness and swelling of the lens, and traumatic cataracts after the lens flows out. Patients with traumatic cataracts will be invaded by viruses and even cause cell infections, and even recurrent attacks of the disease, which are very harmful. Severe cases may also cause glaucoma. In order to prevent the continued worsening of traumatic cataracts, which will affect the patient's body, you should pay attention to improving the lens through reasonable treatment methods, speed up the body's recovery, and prevent the disease from getting worse, which will cause some adverse harm to the body.

What is traumatic cataract?

Clinically, traumatic cataracts are those caused by penetrating injuries, blunt trauma, radiation injury, and electric shock to the eye that damage the lens capsule (equivalent to the grape skin) and cortex (equivalent to the grape flesh), resulting in reduced transparency or complete turbidity, forming cataracts of varying degrees.

Penetrating and blunt trauma of the eyeball are often caused by rupture of the lens capsule, which causes aqueous humor to penetrate into the lens, causing the protein to denature and become turbid. The cortex may float in the anterior chamber (one of the intraocular cavities) in a flocculent state. Alternatively, a strong external force may be transmitted to the lens through the fluid (aqueous humor) in the eye. Although no rupture can be seen in the capsule, its permeability changes, causing the lens to become turbid. Generally speaking, perforated traumatic cataracts develop within a few hours. Cataracts caused by blunt trauma develop more slowly.

In addition, infrared rays, microwaves, ionizing radiation and electric shock can cause damage to lens epithelial cells; lens proteins (enzymes) electrolyze, hydrolyze and thermally denature; tissues undergo ionization, producing superoxide free radicals, which damage the epithelial cells in the germinal zone of the lens to produce DNA (deoxyribonucleic acid), leading to lens opacity and the formation of infrared linear, microwave, ionizing radiation and or electric shock cataracts. All of the above fall into the category of traumatic cataracts.

Pathogenesis

In basic research on traumatic cataracts, it was found that various emergency factors, such as oxidative substances, ultraviolet rays, and toxic substances, can initiate apoptosis of lens epithelial cells. Therefore, it is believed that apoptosis of lens epithelial cells is a common cytological basis of non-congenital cataracts in humans and animals. A blunt trauma cataract rat model has been established in China, and it was found that the ultrastructure of the lens epithelial cells of the experimental eyes of SD rats underwent significant changes: the nuclear membrane was damaged and invaginated, and the chromatin was condensed; the mitochondrial structure was destroyed, showing vacuolar changes, and the number was reduced; the endoplasmic reticulum expanded, which was consistent with the morphological manifestations of cell apoptosis. It can be seen that the occurrence of blunt trauma cataract may be related to the apoptosis of lens epithelial cells.

Studies have found that the accumulation of extracellular matrix is ​​initiated during the healing process of lens trauma after penetrating injury, and its main components include chondroitin sulfate, heparin sulfate and collagen. The accumulation of subcapsular extracellular matrix not only causes wrinkles in the lens capsule, but also enhances the adhesion, proliferation and migration of lens epithelial cells, ultimately leading to lens opacity. Matrix metalloproteinases (MMPs) and their counterparts TIMPs play a very important role in the aggregation and degradation of extracellular matrix. MMPs promote the aggregation of extracellular matrix, while TIMPs promote its degradation.

In the study of the rabbit penetrating cataract model, it was found that the activities of TIMP-1 and 2 in the injured eye increased significantly on the first day after injury and then gradually decreased, while the changes in MMPs-2 activity corresponded to this, that is, it was inhibited on the first day after injury and then gradually recovered. Therefore, it is speculated that the transient increase in the content of TIMP-1 and 2 in the rabbit eye changes the balance of MMPs/TIMPs, which may antagonize the degradation of the extracellular matrix by MMPs and inhibit the development of intraocular inflammation after injury. As a result, the extracellular matrix remodeling and cell proliferation and repair process after tissue damage are enhanced, thereby promoting wound healing. However, excessive aggregation of the extracellular matrix and excessive cell proliferation may lead to lens opacity.