In 1995 Brewitt defined dry eye as an ocular surface disorder that results in instability of the tear film during transients due to impairment of the natural function and protective mechanisms of the external eye. sjögren (1933) referred to the triad of dry eyes, dry mouth and arthralgia collectively as Sjögren syndrome. The disease occurs over 40 years of age and is more common in women.
I. Classification
1.Simple dry eye (SDE): the blood circulation does not contain autoantibodies.
2, autoimmune dry eye, but not Sjögren syndrome.
3, dry eye combined with Sjögren syndrome.
II. Epidemiology
Germany: >40 years old, prevalence 23%.
Sweden: 55-72 years of age, prevalence 15%.
Japan: patient screening, 17%.
Copenhagen: 30-60 years, 11%.
United States: >65 years, 15% symptomatic, 2.2% Schirmer test positive
Australia: >40 years, 10.8 %, 16.3 %, 8.6 %, 1.5 % and 7.4 %
Canada: 28.7% (13517), male:female 1:46, 50.1% with contact lenses
China: about 2.7%. Liu, Ying et al: In outpatients of ophthalmology, the prevalence was 32.1%, male:female 1:4.
Three, tear production and regulation
1.Neural regulation.
2, hormonal regulation.
Androgens: regulate the secretion of oil from the lid gland to the tear film and control the degenerative and inflammatory response of the lacrimal gland. Luteinizing hormone, follicle stimulating hormone, lactogen, thyroid stimulating hormone, progesterone, estrogen.
Fourth, the composition and role of the tear film
From the inside out: mucus layer, aqueous layer and lipid layer.
It has been recently proved that: the lower layer of the outer lipid layer is water-mucus gel layer.
1.Mucus layer
Secreted by conjunctival cupped cells, it forms a layer of polysaccharide quilt on the corneal surface, providing hydrophilicity on the ocular surface and enabling uniform distribution of tears, about 30μm thick.
2.Aqueous layer
Secreted by the lacrimal and paracrine glands under hormonal and neurological regulation.
Provides nutrition and oxygen to the cornea and removes epithelial debris, toxic substances and foreign bodies.
Contains many growth factors: EGF, TGF-α, HGF.
3.Lipid layer
secreted by the lid gland, prevents tear evaporation, enhances tear film stability, refractive action.
Office syndrome: related to the thinning of the lipid layer.
V. Overall function of the ocular surface.
1, normal flora and natural barriers.
2, lysozyme and other antibacterial, lysis substances.
3, rapid tear film renewal.
Six, the etiology of dry eye
I, poor tear film formation
1, aqueous layer changes.
①, reduced secretion: disease, trauma.
②, evaporation too fast: lack of lipid layer.
2, lack of lipid layer: lid gland dysfunction disease, androgen related.
3, lack of mucus layer: cupular cell damage, Vit A deficiency disease, preservatives.
II. Excessive evaporation of tear film and abnormal cell distribution
1, poor formation and distribution of the lipid layer.
2, lid entropion, lid margin abnormalities, hyperthyroidism, corneal disease, etc.
III, systemic diseases
1.Collagenous diseases: rheumatoid arthritis, scleroderma, lupus erythematosus, Sjögren’s syndrome
2.Other diseases: allergic diseases, chronic conjunctivitis, skin mucosa syndrome, Stevens-Johnson syndrome, etc.
IV.Systemic medication
Thiazides, antidepressants, beta-blockers, anticholinergics, phenylsulfonamides, antiparkinsonians, antihistamines and antihypertensives, etc.
V. Dry eye and ocular surface inflammatory diseases
1, Sjögren syndrome: exocrine gland inflammatory dip, CD4-positive T, lymphocytes in contact with epithelial cells, resulting in tear gland destruction.
2, Dry eye with allergy: cupular cell destruction.
3, dry eye with conjunctivitis: destruction of cupular cells, long-term application of antimicrobials and hormones.
4.Dry eye and blepharitis: destruction of the lid and sebaceous glands, change in tear composition, and excessive evaporation.
5, dry eye and eye medication: preservatives lead to toxic effects.