Mechanism of Action
When LTP was first attempted in the 1970s, the belief was that the application of thermal energy to the trabecular meshwork (TM) would create holes, thereby bypassing the primary site of resistance to aqueous outflow and reducing IOP. Subsequent electron microscopy studies showed that this hypothesized mechanism of action was incorrect. Although the actual mechanism of LTP remains unclear, several theories have been put forward. In ALT, thermal damage to the treated trabecular meshwork causes shrinkage of collagen fibers, stretching and widening adjacent areas of the uveoscleral TM. This may play a role in improving aqueous outflow facility; however, other lasers are as effective despite causing little or no damage to the collagen fibers. In all forms of LTP, possible mechanisms of action include the following:
Table 13-1 Locations and Mechanisms of Action for Intraocular Pressure Reduction
stimulation of cell division
release of cytokines from treated trabecular meshwork cells resulting in alterations of the extracellular matrix of the TM or biomechanical changes in the Schlemm canal endothelial cells
recruitment of monocytes and macrophages in the TM
increased phagocytic activity of cells in the TM
*Note: This term is based on the historical use of argon laser technology; most green lasers currently used in ophthalmology are diode-pumped solid-state (eg, frequency-doubled Nd:YAG or Nd:YLF) lasers.
Alvarado JA, Alvarado RG, Yeh RF, Franse-Carman L, Marcellino GR, Brownstein MJ. A new insight into the cellular regulation of aqueous outflow: how trabecular meshwork endothelial cells drive a mechanism that regulates the permeability of Schlemm’s canal endothelial cells. Br J Ophthalmol. 2005;89(11):1500–1505.
Excerpted from BCSC 2020-2021 series: Section 10 - Glaucoma. For more information and to purchase the entire series, please visit https://www.aao.org/bcsc.