The Pathogenesis of Pterygium: Current Concepts and Their Therapeutic Implications

Authors: Chui, Jeanie; Di Girolamo, Nick; Wakefield, Denis; Coroneo, Minas T.

Source: The Ocular Surface, Volume 6, Number 1, January 2008 , pp. 24-43(20)

Publisher: Ethis Communications

Key:
Free Content - Free Content
New Content - New Content
Subscribed Content - Subscribed Content
Free Trial Content - Free Trial Content

Abstract:

Pterygium is a disease of the ocular surface that is associated with chronic UV exposure and is characterized by proliferation, inflammatory infiltrates, fibrosis, angiogenesis and extracellular matrix breakdown. Although pterygium is not fully understood, significant progress has been made toward understanding the mechanisms involved in its pathogenesis. In this review, we provide an update on the signaling pathways activated by UV light that result in induction of mediators responsible for the growth of pterygium. We also review the recent genetic studies on hereditary factors and provide a brief overview of the role of epithelial mesenchymal transition, bone marrow progenitor cells, and neuronal signals that may also contribute to the pathogenesis of pterygium. Therapeutic options for pterygium are discussed based on the mechanisms that perpetuate its growth.

Keywords: CORNEAL NERVES; EPITHELIAL MESENCHYMAL TRANSITION; GENETICS; OXIDATIVE STRESS; PATHOGENESIS; PTERYGIUM; STEM CELLS; UV LIGHT

Document Type: Research article

The full text electronic article is available for purchase. You will be able to download the full text electronic article after payment.

$68.00 plus tax      Refund Policy

 

OR

Back to top

Key:
Free Content - Free Content
New Content - New Content
Subscribed Content - Subscribed Content
Free Trial Content - Free Trial Content
Share this item with others: These icons link to social bookmarking sites where readers can share and discover new web pages.
Page Help Click here for Page Help
Shopping cart
Tools
Sign in






Need to register?
Sign up here
Text size: A | A | A | A