Contrary to earlier belief—which ascribed basic secretion to the accessory lacrimal glands of Krause and Wolfring and reflex secretion to the main lacrimal gland—it is now thought that all lacrimal glands function as a unit in conjunction with the ocular surface and the brain. In addition, the cornea and conjunctiva can respond by secreting electrolytes, water, and mucins.
Although the meibomian glands are innervated, it is not known whether nerves mediate lipid secretion from these glands. Reflex tear secretion is neurally mediated and induced in response to physical irritation (ie, superficial corneal and conjunctival sensory stimulation by mechanical, thermal, or chemical means), psychogenic factors, and bright light. Induction of sensory nerves by a local neural reflex activates the parasympathetic and sympathetic nerves that innervate the tear glands and epithelia, causing secretion (Fig 7-4). Tear turnover rate has been demonstrated to be significantly lower in a symptomatic patient with dry eye (5%) than in an asymptomatic dry eye patient (12%).
A neural feedback mechanism for tear secretion has been widely accepted. The cornea and lacrimal gland are not directly connected; however, corneal damage profoundly affects the lacrimal gland, which, in turn, downregulates tear production. In the vicious circle theory of DES, this downregulation is due to the secretion of inflammatory cytokines that block neural signals for tear secretion (Fig 7-5). The feedback loop, initiated by inflammation on the surface of the eye, further suppresses or downgrades lacrimal gland function, creating a vicious circle that worsens DES (Fig 7-6).
Peptide and steroid hormones constitute another mechanism for stimulating tear secretion (in addition to nerves), as follows:
Peptide hormones, including α-melanocyte-stimulating hormone (α-MSH) and adrenocorticotropic hormone (ACTH), stimulate protein secretion from the main lacrimal gland.
Steroid hormones, specifically the androgens, stimulate secretion of sIgA from the main lacrimal gland and lipid from the meibomian glands.
Figure 7-4 Sensory and motor nerves connecting the components of the lacrimal functional unit. Sensation (afferent) from the ocular surface is provided by branches of the long ciliary nerve of the ophthalmic division of cranial nerve V (CN V1). Efferent fibers from both members of the autonomic nervous system stimulate lacrimal secretion at the main and accessory lacrimal glands.
(Modified with permission from Pflugfelder SC, Beuerman RW, Stern ME, eds. Dry Eye and Ocular Surface Disorders. New York: Marcel Dekker; 2004.)
Figure 7-5 Disruption of the neural feedback loop in dry eye syndrome (DES). The white lines represent the normal pathway of the lacrimal functional unit. The red lines demonstrate disruption of the pathway.
(Illustration by Cyndie C.H. Wooley.)
Eyelid movement is important in tear film renewal, distribution, turnover, and drainage. As the eyelids close in a complete blink, the superior and inferior fornices are compressed by the force of the preseptal muscles, and the eyelids move toward each other, with the upper eyelid moving over the longer distance and exerting force on the globe. This force clears the anterior surface of debris and any insoluble mucin and expresses secretions from meibomian glands. The lower eyelid moves horizontally in a nasal direction and pushes tear fluid and debris toward the superior and inferior puncta. When the eyelids are opened, the tear film is redistributed. The upper eyelid pulls the mucoaqueous phase of the tear film by capillary action. The lipid layer spreads as fast as the eyelids move, so that no area of the tear film is left uncovered by lipid.
See BCSC Section 7, Oculofacial Plastic and Orbital Surgery, which discusses the lacrimal system in depth, with numerous illustrations.
Stern ME, Gao J, Siemasko KF, Beuerman RW, Pflugfelder SC. The role of the lacrimal functional unit in the pathophysiology of dry eye. Exp Eye Res. 2004;78(3):409–416.
Figure 7-6 The vicious circle theory of DES. LASIK = laser in situ keratomileusis; MGD = meibomian gland dysfunction; MMP = matrix metalloproteinase.
(Modified with permission from Baudouin C, Aragona P, Messmer EM, et al. Role of hyperosmolarity in the pathogenesis and management of dry eye disease: proceedings of the OCEAN group meeting. Ocul Surf. 2013;11(4):Fig 1.)
Excerpted from BCSC 2020-2021 series: Section 2 - Fundamentals and Principles of Ophthalmology. For more information and to purchase the entire series, please visit https://www.aao.org/bcsc.