**9. Conclusion**

[78] found a mean 6.9-micron CCT decrease after 6 weeks of travoprost treatment. Sen et al. [79] reported 1.9 ± 2.4% and 2.8 ± 1.8% CCT decreases over 24 months with latanoprost and bimatoprost, respectively. Hatanaka et al. [80] also reported that topical PGAs were associat‐ ed with a CCT reduction over at least 8 weeks (the bimatoprost 0.03% group decreased from 544.41 ± 35.4 to 540.35 ± 35.9 µm; the travoprost 0.004% group decreased from 538.47 ± 32.0 to 532.25 ± 30.4 µm; the latanoprost 0.005% group decreased from 548.57 ± 32.4 to 543.88 ± 35.6 µm). Zhong et al. [81] reported CCT reductions in the latanoprost, travoprost, and bi‐ matoprost groups of 14.95 ± 5.04, 15.73 ± 3.25, and 17.00 ± 6.23 mm, respectively, and no sig‐ nificant difference was seen in the CCT reductions between patients with 6 months or

shorter treatment and patients with 6 months or longer treatment in the three groups.

might also result in changes in the ECM [87].

240 Glaucoma - Basic and Clinical Aspects

chanical properties, at least in rabbits.

The reason for the effect of the PGAs on the CCT is unknown, but it is widely accepted that PGAs seem to induce ECM remodeling due to a FP-receptor-mediated increased synthesis of matrix metalloproteinases (MMPs) [82]. The MMPs are a family of enzymes that degrade several com‐ ponents of the ECM, thus decreasing the levels of collagen types I, II, III, and IV. Published evi‐ dence suggests that the PGA-related activation of the MMPs activity takes place in the ciliary body, the trabecular meshwork [83], the conjunctiva, the sclera, and the zonular fibers-ciliary muscle complex [84]. Further, naturally occurring prostaglandins seem to play a relevant role in physiologic corneal conditions, i.e., repair after corneal injuries, and in pathologic corneal con‐ ditions, i.e., corneal ectasia. In fact, PGA treatment may be related to keratoconus progression [85]. Thus, there is enough evidence to suggest that topical PGAs might induce changes in the ECM of the corneal stroma via up-regulation of MMPs that may slightly change the CCT and perhaps the corneal viscoelastic properties. In fact, CH seems to be significantly lower in PGAtreated eyes [86]. PGAs also seem to increase the keratocyte density in the corneal stroma, which

Previous reports have suggested that chronic topical PGA treatment is associated with a slight decrease in the CCT [86,88] and an increase in the CH. We studied the response of CCT to increased IOP in rabbit eyes treated with travoprost for 1 month and in an untreated control group, and found that the decrease in CCT induced by a sudden increase in IOP was greater in the PGA-treated eyes than in the control eyes [88]. The changes in corneal thick‐ ness induced by IOP increases are believed to be a strain response and thus are probably a biomechanical response of the corneal tissue to the IOP changes. Then the differences in the CCT behavior between groups also suggest that PGAs induce changes in the corneal biome‐

Topical dorzolamide induces a 14.4% increase in CCT in patients with corneal guttata [89]. Patients with severe corneal guttata or a highly compromised endothelial function may have

Dorzolamide is a potent cytosolic carbonic anhydrase inhibitor (CAI) isoenzyme II, and the cor‐ neal endothelium contains carbonic anhydrase (CA) II and the cytosolic CA I, which plays a ma‐ jor role in keeping the cornea relatively dehydrated. Dorzolamide has a high affinity for CA II and low affinity for CA I, and thus, it has the potential to interfere with the pump function of the corneal endothelium, which could theoretically lead to corneal edema. Changes in CCT have been used as an indirect indicator of the endothelial function. Some investigations have report‐

a higher risk of corneal decompensation after prolonged topical use of dorzolamide.

There is growing interest in the possible effect of some corneal parameters in glaucoma. There is sufficient evidence to suggest that CCT evaluation predicts the risk of conversion from OHT to glaucoma. The influence of the CCT on the GAT IOP is clear, so true IOP is higher than GAT IOP in patients with thinner corneas and true IOP is lower than GAT IOP in patients with thicker corneas. In addition, some data suggest that CCT may be an inde‐ pendent risk factor for glaucoma development, although there is no clear evidence to sup‐ port this hypothesis.

Of special interest is the fact that GAT is affected by laser excimer refractive surgery, a pop‐ ular procedure that changes some corneal properties that affect accurate IOP measurement. New tonometers with a lower relationship to the corneal thickness and viscoelastic proper‐ ties need to be developed.

Finally, widely used topical antiglaucomatous medications can alter the corneal viscoelastic properties and thus affect the GAT readings. This also needs to be investigated further.
