A triangular-shaped pterygium on the corneal surface is a clinical manifestation of a pterygium. It is a triangular shaped pterygium with vascularized tissue that resembles the wings of an insect, hence the name pterygium. The pterygium is usually found on the nasal side, but less frequently on the temporal side. When it extends into the cornea, it may invade the anterior elastic layer and superficial stroma. Pterygium is a common and frequent disease in ophthalmology. It is thought to be a chronic inflammatory lesion of the local bulbar conjunctival fibrovascular tissue caused by external irritation, triangular in shape, invading the cornea, and involving one or both eyes. It is called pterygium because of its resemblance to an insect’s wing, and in Chinese medicine, it is called “pterygium pancreaticum”. It is one of the most common clinical ophthalmic diseases and the oldest eye disease. It can not only cause eye irritation and cosmetic defects, but can also affect visual acuity to varying degrees. It mostly occurs in outdoor workers. It may be related to long-term irritation by wind, sand, smoke, sunlight and ultraviolet light. There are still many controversial factors in its pathogenesis, and it is generally believed that it may be the result of a combination of endogenous (genetic factors) and exogenous (environmental factors) factors. Among the exogenous factors, ultraviolet light from sunlight is the most important environmental factor. In addition, sand, dust and dryness are also important environmental factors affecting the pathogenesis. The specific pathogenesis is still not fully explained. There are several theories regarding the pathogenesis of pterygium. In early studies, a large number of lymphocytic and plasma cell infiltrates and mast cell reactions were found in pterygium tissue, leading to the suggestion that there is an immunological mechanism involved in the pathogenesis of pterygium. The presence of IgG, IgE, and small amounts of IgA and IgM in pterygium tissue and the presence of granular immunoglobulin and C3 deposits in the basement membrane were also found, leading to the suggestion that the pathogenesis of pterygium is associated with type I and type III metaplasia. However, mast cells are only present in the subepithelial stroma of the pterygium, especially near the degenerated elastic fibers, and are not detected in the epithelium and corneal rim; therefore, it is not possible to determine whether the immune response is a primary or secondary alteration in the pathogenesis of pterygium. Coroneo synthesized the results of recent studies and proposed a two-stage hypothesis for the development of pterygium. This hypothesis artificially divides the pathogenesis of pterygium into two stages: in the first stage, the stem cells at the corneal limbus are destroyed and the corneoconjunctival barrier becomes dysfunctional; in the second stage, active cell proliferation, inflammation, vascularization, and connective tissue remodeling occur, and the cornea “conjunctivates”, leading to the development of pterygium. This hypothesis is contrary to the previous concept of pterygium as a degenerative disease. According to the “two-stage” theory, corneal limbal stem cell dysfunction is the basis for pterygium pathogenesis. As mentioned earlier, when light from the temporal side is projected behind the nasal corneal limbus, the intensity of the light is amplified by a factor of 20, where the epithelial basal cells are “struck” from behind, resulting in dysfunction and a reduction in stem cell numbers. The intact corneal rim is the barrier that prevents conjunctival to corneal growth, and once this barrier is disrupted, actively proliferating conjunctival fibroblasts (or transformed corneal rim stem cells) can easily grow toward the cornea. For stage 2, a growing body of research supports the idea that pterygium is a proliferative disease and that degeneration is a secondary or minor change. The main evidence for this includes: 1. Disturbed expression of certain growth factors that regulate proliferation in pterygium tissue, such as transforming growth factor-β (TGF-β) and basic fibroblast growth factor (bFGF); 2. Transformation of pterygium fibroblasts: studies have shown that cultured pterygium fibroblasts are actively proliferating and can be proliferated by (TGF-β); 3. Pterygium epithelial cells Active proliferation: their epithelial layer cells are of variable thickness and hyperkeratinized, suggesting increased expression of proliferative active epidermal growth factor receptor (EFGR) family and keratin proteins (e.g. K3, K8, K16, etc.); 4. Increased p53 protein expression in pterygium epithelial cells, loss of heterozygosity and microsatellite instability changes occurring, which are generally detected mostly in tumor cells and pre-cancerous lesion cells The expression of bcl-2, a gene that inhibits apoptosis in pterygium epithelial and subepithelial fibroblasts, is increased, suggesting that the occurrence of pterygium may be related to a decrease in normal apoptosis; 6. Some anti-proliferative drugs and treatments may reduce to some extent the the recurrence rate of pterygium after surgery, such as intraoperative and postoperative local application of antimetabolites and β-radiation radiotherapy. In addition, recent studies have found disturbances in the activity of tissue metalloproteinases and their inhibitors in the epithelium of pterygium, suggesting that the occurrence of pterygium is associated with inflammation, tissue remodeling phenotype, and vascularization.
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