The Dry Eye Workshop 2004, at the Puerto Rico TFOS (Tear Film and Ocular Surface Society) conference, defined dry eye (also termed sicca syndrome or keratoconjunctivitis sicca) as a multi-factorial disorder of tears and the ocular surface, associated with
Table 2.3. Summary of dry eye disease
Multifactorial disorder of tears and the ocular surface
Associated with symptoms of discomfort and/or visual disturbance
Pathological features include increased epithelial stratification and proliferative index and abnormal differentiation with maintenance of a basal phenotype
Reduced expression of secretory and membrane-bound mucins by the superficial ocular-surface epithelial cells
Worsened severity as aqueous tear secretion decreases and as the ability to reflex tears in response to sensory stimulation is lost
The normally constant absorption of tear-fluid components into the blood vessels of the surrounding cavernous body could come to halt if these tear components are not absorbed, and thus could initiate dry eye symptoms of discomfort and/or visual disturbance (Table 2.3). Much is known about the pathogenesis of the keratoconjunctivitis sicca that occurs in dry eye disease (Table 2.3). The pathological features of this condition include increased epithelial stratification and proliferative index and abnormal differentiation with maintenance of a basal phenotype (Table 2.3) . Furthermore, the expression of secretory and membrane-bound mucins by the superficial ocular surface epithelial cells is reduced (Table 2.3) [3, 6, 26]. An exact mechanism for the development of these pathological changes has not yet been elucidated. The severity of keratoconjunctivitis sicca worsens as aqueous tear secretion decreases and as the ability to reflex tear in response to sensory stimulation is lost. The disease results in a vicious cycle.
Clinical reports have suggested that tear production and outflow of tears from the ocular surface are linked [16, 17]. As described in Chap. 1, the human nasolacrimal ducts have absorptive functions. Based on this, hypothetically it could be suggested that the normally constant absorption of tear-fluid components into the blood vessels of the surrounding cavernous body, which are connected to the blood vessels of the ocular surface, could provide a signal for tear-fluid production, which ceases when these tear components are not absorbed .
If this hypothesis is true, the question remains: Why do not all possible forms of efferent tear-duct diseases that are related to tear-outflow disturbances lead to dry eye? And why do punctum plugs and other methods that interrupt the connection between the ocular surface and the nasolacrimal ducts sometimes show very good results in the therapy of dry eye? These questions can be answered as follows:
1. Currently, little is known about whether diseases of the drainage system coincide with changes in tear-fluid production, although patients with diseases of the nasolacrimal ducts suffer from tear overflow. On the other hand, it has been reported that patients with acquired obstruction of the efferent tear ducts rarely have symptoms of epiphora [5, 7], and lack of significant epiphora has also been reported in patients with congenital absence of lacrimal puncta . Moreover, as already mentioned, there are patients who suffer from functional dacryostenosis, i.e., patients with epiphora in spite of patent lacrimal passages on syringing.
2. Both dry eye and diseases of the efferent tear ducts occur with high frequency in women of middle to advanced age .
3. Considering the results after insertion of punc-tum plugs and other blocking methods, one can ascertain that patients, in the long run, require tear substitutes. Punctum plugs could initially function by totally preventing absorption of tear-fluid components, thus creating an "empty" tear-fluid system, which may be a strong stimulation signal for tear-fluid production. This stimulation signal decreases with passing of time. Ocular surface sensation and tear production also decrease after temporary punctual occlusion in normal subjects . These effects are more pronounced in subjects with both upper and lower puncta occluded; however, in normal subjects, there appears to be an autoregulatory mechanism that returns tear production and tear clearance to preocclu-sion levels 14-17 days after punctual occlusion, a mechanism that seems to be lacking in dry-eye patients .
The apparently contradictory findings raised above under point 1 above can be explained as follows: Cases of acquired obstruction of the lacrimal drainage system or congenital absence of lacrimal puncta result from fibrous obstruction secondary to chronic
Fig. 2.8. The normally constant absorption of tear-fluid com- signal for tear-fluid production (2; left) that comes to a halt if the ponents into the blood vessels of the surrounding cavernous nasolacrimal system has been occluded by punctum plugs body of the nasolacrimal ducts and their transport to the lacri- (right) mal gland by blood vessel connections (1) could be a feedback
Fig. 2.8. The normally constant absorption of tear-fluid com- signal for tear-fluid production (2; left) that comes to a halt if the ponents into the blood vessels of the surrounding cavernous nasolacrimal system has been occluded by punctum plugs body of the nasolacrimal ducts and their transport to the lacri- (right) mal gland by blood vessel connections (1) could be a feedback inflammation, with total obstruction of the whole lacrimal sac and nasolacrimal duct [4, 13, 14]. This scenario is comparable to the insertion of punctum plugs, as absorption of tear-fluid components is totally prevented and the production of tear fluid is downregulated by the lacrimal gland, leading to symptoms of epiphora (Fig. 2.8). In the second case (patients with epiphora in spite of patent lacrimal passages on syringing), a non-functioning segment in the lacrimal passage results from advanced structural changes with loss of specialized blood vessels of the cavernous body, with changes in the helical organization of connective tissue, and with epithelial metaplasia caused by chronic dacryocystitis (see section 2.2) . In this latter case, obstruction is not yet complete, but no tear transport takes place in the nonfunctioning segment. In this scenario, there is absorption of tear-fluid components in the area lying in front of the non-functioning segment , leading to normal tear-fluid production; however, as tear fluid is not drained, or is only minimally drained, a tear overflow results.
Disturbances in one part of the "lacrimal functional unit" (see Chap. 1, section 1.2.4) can have effects on all participant structures. As greater knowledge is gained about the regulation of the lacrimal gland/ocular surface/efferent tear duct integrated unit, new paradigms may emerge regarding which patients with dry-eye disease may benefit from punctual occlusion and which patients may suffer consequences.
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