- Sun exposure (UV rays) (M/C cause)
- Hot, dry & dusty conditions (#2 M/C cause)
Limbal stem cells:A healthy corneal surface is maintained by self-renewing, lineage-specific stem cells (SCs) that reside in the limbus, a narrow annular transition zone that circumscribes the cornea. This regenerative capacity is regulated by exquisite programs that govern stem cell quiescence, proliferation, migration, and differentiation. Failure to maintain a normal microenvironment as a result of extrinsic (eg, UV radiation) or intrinsic (eg, cytokines) signals can result in the development of ocular disorders.
UV rays cause the insufficiency of the limbal stem cells of the cornea. It causes activation of the tissue growth factors, which further lead to angiogenesis and cell proliferation. The limbal stem cells are damaged by the UV rays that cause conjunctivalization of the cornea, and the cornea is invaded by aggressive fibroblasts. UV radiation may cause mutations in the p53 tumor suppressor gene, resulting in the abnormal pterygial epithelium.
Recurrent pterygium:Reactivation of inflammatory process: Proliferative cytokines and growth factors (including VEGF) can increase after surgery if limbal stem cells remain activated, and fibroelastic tissue is also involved. Because of this, there is an acceleration of fibrovascular proliferation and an increase in metalloproteinase synthesis that destroys the Bowman membrane and the stromal collagen that may increase the progress of pterygium.
Histopathology:Microscopically, pterygium is considered to be composed of elastotic fibro-vascular tissue. Leaving the top, mostly, the pterygium is covered by conjunctival epithelium. Extensions of fibrous tissue are seen on the top of pterygium, and as the head encroaches on to the cornea, the Bowman’s layer gets involved and is fragmented. The fibrous connective tissue fills these cavities.
- Hyperplastic, centripetally directed growth of altered limbal epithelial cells
- Bowman’s layer dissolution
- Epithelial-mesenchymal transition
- Activated fibroblastic stroma with inflammation, neovascularization, and matrix remodeling, mediated through the concerted actions of cytokines, growth factors, and matrix metalloproteinases
- Irritation in the eye
- Foreign body sensation
- Cosmetic blemish
- Defective vision
Pterygium description:Triangular fold of conjunctiva encroaching the eye
- Cap: At the leading edge, distinguished by a halo-like avascular zone
- Head: Peripheral to the cap
- Body: Main part of pterygium communicating with bulbar conjunctiva
- Progressive type: Thick, fleshy, vascular, progressively encroaching towards the center of the cornea. “Fuck’s spots or Islets of Vogt”
- Atrophic type: Thin, attenuated, poor vascularity, stationary
- Regressive type:”Stocker’s line” (line of iron deposition)
- Pseudopterygium: Fold of bulbar conjunctiva attached to cornea
|Etiology||Degenerative process||Inflammatory process|
|Site||Always in palpebral aperture||Any site|
|Stages||Progressive, regressive, stationary||Always stationary|
|Probe test||Cannot be passed underneath||Can be passed under the neck|
Medical management:Medical care is given to relieve the patient from the inflammatory symptoms and reduce the persistent discomfort that persists.
- Lubrication with artificial tear drops or decongestants
- Topical NSAIDs
- Eye drop loteprednol
- Vasoconstrictive agents minimize redness and enhance the appearance and add antihistamines to the decongestant drops to help prevent the effect of histamine associated edema and itching.
Surgical management:Reasons for surgery are decreased vision due to visual axis encroachment, chronic pain, persistent inflammation, abnormal astigmatism, restrictive ocular motility, and cosmesis.