The nerve fibers can be stimulated by neurotransmitters in the body, and can lead the glands to secrete proteins that protect the eye. Although the size of a normal lacrimal gland can vary from individual to individual, the glands are usually symmetrical and similar in size.
The lacrimal gland is approximately 2 centimeters a little under an inch long. The tear film produced by your lacrimal glands consists of a clear fluid that keeps the surface of the eye moist and prevents it from drying out.
When you feel strong emotions, or your eyes become dry or irritated, your lacrimal glands produce extra tear film, or tears, to try to address the issue. There are three types of tears:. Basal tears — Always present to keep the eyes moist and protected and to help you see clearly.
Reflex tears — Produced to help clear the eyes in reaction to an irritant, such as wind, debris, smoke or fumes. On average, you produce around 15 to 30 gallons of tears a year, and each of those tears consists of three layers:.
An outer lipid layer produced by the meibomian glands more on these below to prevent the tear film from evaporating. A middle aqueous layer produced by the lacrimal glands that helps hydrate the eye, repel bacteria, protect the cornea and bring important electrolytes to the surface of the eye. This watery layer also helps smooth the surface of the eye and allows it to refract light so you can see clearly.
An inner mucin layer that helps the tear film spread evenly across the surface of the eye. This layer is produced by conjunctival goblet cells , specialized epithelial cells that secrete mucus onto the surface of the eyes. Tear film contains immune system antibodies, enzymes, and antifungal and antibacterial agents that fight germs and protect the eyes from invading pathogens. These antibacterial molecules allow the lacrimal gland to kill many kinds of organisms on the surface of the eye and react to irritants such as pollution and pollen.
Lacrimal glands also secrete growth factors to keep the corneas healthy, able to self-repair if injured, and able to receive oxygen from the air. Overall, the lacrimal glands secrete a complex fluid rich in antibodies, antimicrobial agents, lubricating fluid, and growth factors that:. While you only have two lacrimal glands — one over each eye — you have 25 to 40 meibomian glands in your upper eyelid and 20 to 30 in your lower eyelid.
These oils also sit along the edges of the eyelids, forming a barrier to keep your tears in your eyes. Dry eye syndrome is a common condition that can cause you to experience feelings of eye dryness, burning, itching and soreness. Dry eye can occur if the composition of your tear film is defective or if any part of the tear production system stops working properly.
For example:. As you age, your lacrimal glands begin to secrete fewer tears, which may cause your eyes to feel uncomfortable and dry. This is called meibomian gland dysfunction MGD.
There are many treatments for dry eye , ranging from eye drops that replace the tear film to antibiotics, anti-inflammatory medications and other treatments like punctal plugs. Retinol, a vitamin A derivative, is secreted by the lacrimal gland and is important for the flow rate of tears and for the health of the eyes.
Vitamin A deficiency has been linked to the development of corneal ulcers and an increased risk of eye infection. If you notice any new feelings of dryness in your eyes or any drastic difference in your ability to see clearly, schedule an appointment with an eye doctor. The main lacrimal gland is situated superotemporally in the orbit within the lacrimal fossa of the frontal bone. Grossly, the gland is a pinkish-gray structure composed of small lobules intermixed with connective tissue septations and lacks a true capsule Figure 1.
Its appearance may be mistaken for preaponeurotic fat. The gland is divided into two lobes, the orbital and palpebral lobes, by the lateral horn of the levator aponeurosis.
Although divided, the division is incomplete due to a posterior wall of parenchyma between the lobes [ 5 ]. The gland is bound anteriorly by the orbital septum and the preaponeurotic fat pad, posteriorly by orbital fat, medially by the intermuscular membrane between the superior and lateral recti, and laterally by bone Figure 2. The size of the main lacrimal gland is somewhat variable with the orbital lobe being the larger of the two.
The lacrimal gland is an exocrine gland similar to the mammary gland and salivary gland [ 7 ]. The gland is composed of lobules separated by loose connective tissue Figure 1. Acini are lined with columnar secretory cells, which have been shown to secrete mucopolysaccharides, implying that the gland is a modified mucus gland [ 5 ]. Each lacrimal gland lobule consists of many acini and intralobular ducts that drain into approximately 8—12 excretory ducts or tubules.
The ducts of the orbital lobe pass through the parenchyma of the palpebral lobe making the proximal secretory ducts susceptible to damage distally [ 5 , 7 , 8 ]. The arterial blood supply to the lacrimal gland comes from the lacrimal branch of the ophthalmic artery, a branch of the infraorbital artery, and occasionally from a branch of the recurrent meningeal artery.
The lacrimal artery passes through the gland to feed the upper and lower eyelids. The lacrimal vein follows the course of the artery and drains into the superior ophthalmic vein. The gland is innervated by both myelinated and unmyelinated fibers arising from the trigeminal nerve, the facial nerve, and sympathetic innervation from the superior cervical ganglion [ 5 ].
Stimulation of the ocular surface activates tear production from the main lacrimal gland reflex tearing. The lacrimal nerve is a sensory branch of the ophthalmic trigeminal nerve V 1 , which provides the sensory afferent pathway. This lacrimal nerve travels in the superotemporal orbit and enters the gland with the major vessels.
This nerve courses through the gland to innervate superficial eyelid structures. Sympathetic nerves travel with the lacrimal artery along with parasympathetics in the zygomatic nerve [ 5 ]. The efferent pathway originates with parasympathetic fibers from the superior salivary nucleus of the pons, which exit the brain stem with the facial nerve.
Lacrimal fibers depart from the facial nerve as the greater superficial petrosal nerve and travel to the sphenopalatine ganglion to join the zygomatic nerve. Prior to dividing into the zygomaticotemporal and zygomaticofacial branches, the zygomatic nerve may give off a lacrimal branch, which may anastomose with a branch of the lacrimal nerve or travel independently along the periorbita [ 5 ].
It is unclear if the anastomosis between the zygomaticotemporal and lacrimal nerves is uniformly present [ 8 ]. The role of the sympathetic nervous system is thought to stimulate basal tear secretion, but its role in lacrimation is not well understood. Lacrimal gland hyposecretion is seen in syndromes of central autonomic dysfunction, such as Riley-Day syndrome [ 9 ].
There are approximately 20 glands of Krause located in the superior conjunctival fornix and approximately half as many in the inferior fornix. The glands of Wolfring are found along the nonmarginal border of the both tarsal plates Figures 2 and 3 [ 5 ].
Accessory lacrimal glands may also be found in the caruncle and in the plica semilunaris. Although the accessory lacrimal glands of Krause and Wolfring are structurally and histologically similar to the main lacrimal gland and may develop identical types of metaplasia, they differ in their innervation [ 7 ].
Although heavily innervated, the accessory lacrimal glands lack parasympathetic innervation [ 5 ], and most of the innervation is unidentified [ 8 ]. Jones states that the main lacrimal gland is responsible only for reflex tearing and the accessory glands of Kraus and Wolfring, providing basal tear secretion [ 10 ]. This distinction has been debated. The volume of tears secreted from these glands is unclear. Studies show mixed results whether or not the accessory glands are able to provide adequate tear volume to prevent keratoconjunctivitis sicca [ 7 ].
Noted age-related changes of the lacrimal gland include atrophy of the glandular parenchyma, increased interstitial connective tissue, increased fat content within glandular tissue and epithelial secretory cells, and increased lymphocyte content within the gland including plasma cells [ 11 — 13 ]. The incidence and uniformity of these changes have not been agreed upon, as many reports note conflicting data.
Obata et al. It is unknown if structural and functional differences exist between the orbital and palpebral lobes or if these differences represent continuum of changes versus distinct pathophysiologic changes. The most common abnormal findings included chronic inflammation and periductular fibrosis. The authors also observed massive ductular ectasia extending into lobules. The combination of periductular fibrosis, inflammation, and dilated, inspissated ducts may lead to retention of tears within the lacrimal gland and contribute to age-related dry eye [ 12 ].
Another study by Obata et al. Glands in which acinar atrophy is apparent show a lack of lysozyme immunoreactivity and are probably related to a decrease of tear proteins as a consequence of aging [ 7 ]. Atrophy of acinar elements may result in fibrosis, but in certain conditions, such as chronic graft-versus-host disease, stromal fibroblasts are actively involved in the pathogenic process of periacinar fibrosis [ 14 ]. The health of the conjunctival epithelium is essential for normal lacrimal gland function.
Stenosis or obstruction of flow of the excretory ducts in the superior conjunctival fornix may cause cystic dilatation of the interlobular ducts in the palpebral lobe. Damage to the excretory ducts in the superior conjunctiva may occur with severe ocular surface diseases with keratinization such as Stevens-Johnson syndrome and ocular cicatricial pemphigoid, or iatrogenically after surgery, which may damage the orifices of the excretory ducts thereby reducing the volume of aqueous bathing the ocular surface [ 7 , 15 ].
As previously suggested, the components of the tear film produced by the lacrimal gland are critical in several processes related to ocular surface health. The first is in protection of the ocular surface from invading pathogens with a local population of IgA-secreting plasma cells that reside within the lacrimal gland itself. While tear firm contains other immunoglobulins, secretory IgA is the predominant antibody and is the only immunoglobulin whose concentration significantly increases during infection, suggesting its critical role in host defense of the ocular surface [ 16 ].
The ability of the lacrimal gland to specifically select for IgA secreting plasma cells is not well understood but likely resides in the recruitment and proliferation of a specific subset of helper T cells. These T cells are recruited by an ILlike peptide known as lacrimal gland-derived lymphocyte proliferation potentiating factor [ 17 , 18 ].
These T cells then recruit and promote B cell differentiation into IgA-secreting plasma cells. Once produced by plasma cells, dimeric IgA is translocated into the tear film by a cell surface antibody receptor to inhibit pathogen adherence to the host surface as seen at other mucosal sites [ 19 ]. The production of this translocation receptor is exquisitely sensitive to endocrine and nervous and immune system regulation [ 20 , 21 ].
Consequently, the host invests significant energy into the production and secretion of IgA into the tear film to reduce ocular surface susceptibility. The lacrimal gland also secretes several bacteria i. These substances greatly reduce susceptibility of the ocular surface due to cytotoxicity to invading pathogens. While it is still controversial, the lacrimal gland may also be an additional source of soluble mucin production, which acts to clear debris and hold fluid on the surface of the eye [ 24 — 26 ].
This glycoprotein also serves as an infectious deterrent by acting as a decoy receptor for invading pathogens [ 27 ]. As such, these cytotoxic agents, mucin, and IgA transform a susceptible, warm, moist, nutrient rich epithelial surface into an inhospitable environment unlike other colonized mucosal surfaces. The second major contribution of the lacrimal gland is in the aqueous produced by acinar cells that add significant volume to the tear film.
The fluid is transported from the interstitial space into the lumen of the gland by way of osmosis and released onto the ocular surface [ 2 ]. The addition of high volumes of water from the gland helps to keep the ocular surface moist, maintain an important component of light refraction in the air-water-corneal interfaces, and dilute proteins within the tears to keep them solubilized.
Water is also transported in conjunction with other important electrolytes required in cellular processes and has been extensively reviewed elsewhere [ 2 ].
With the addition of lipocalin and lipids from the meibomian gland, tears become a highly viscous, low surface tension solution critical in tear film stability and health of the ocular surface [ 28 ].
As such, water serves to dilute substances in the tear film and maintain an interface critical for normal visual acuity. The lacrimal gland is also responsible for producing several other proteins and products necessary in growth and maintenance of host tissue found in the tear film.
Several of these proteins are growth factors. While the defined role of each in corneal regeneration is unclear, these factors promote proliferation and migration of epithelial cells following disruption of the corneal surface and maintain an avascular cornea necessary for transparency of the tissue [ 29 — 34 ]. If these factors decline or are replaced for others, neovascularization of the cornea ensues [ 35 , 36 ].
Retinol, a vitamin A derivative, is also secreted by the lacrimal gland. Retinol is required in maintenance of goblet cells within the conjunctiva and controls corneal epithelial desquamation, keratinization, and metaplasia [ 37 — 39 ]. Vitamin A is also a positive feedback molecule as its deficiency results in a decrease in flow rate of lacrimal gland fluid in rabbits [ 40 ].
In humans, vitamin A deficiency can result in corneal ulcers, melt, and even perforation [ 41 ]. This loss of corneal integrity is felt to be the result of an increased risk of infection, decreased tear film, alterations in corneal wound healing, and changes in leukocyte function [ 42 ]. Consequently, the ocular surface role of secreted vitamin A from the lacrimal gland is multifactorial. The previously mentioned products of the lacrimal gland are only a select few of the known proteins in the tear film and there are likely several unidentified proteins at this point in time.
In summary, the lacrimal gland secretes a complex aqueous milieu rich in antibodies, cytotoxic agents, and growth factors onto the ocular surface to protect the cornea from desiccation, infection, and vascularization while promoting wound healing and transparency.
Dysfunction of the lacrimal gland may result from inflammation, aging, radiation, or infection. The end result of many of these pathologies rests in insufficient tear production and changes in osmolality and increased osmotic stress of the ocular surface [ 43 ].
This results in increased susceptibility of the ocular surface that we hypothesize is due to the loss of the previously mentioned antimicrobial tear film products [ 44 ]. Unfortunately, in inflammatory dry eye, this is further exacerbated by relatively high concentrations of proteins within the tears that induce apoptosis of surface epithelium and a vicious, self-perpetuated cycle of increased expression of proinflammatory cytokines from the ocular surface [ 45 , 46 ].
The proinflammatory state further worsens dry eye by leading to apoptosis and decreased mucin production from conjunctival goblet cells [ 47 , 48 ]. Matrix metalloproteinases MMPs , a family of proteins required in wound healing and degradation of extracellular matrix, are one such proinflammatory product highly expressed in dry eye conditions and known to cause epithelial barrier dysfunction [ 45 , 49 ].
As such, tests such as InflammaDry by Rapid Pathogen Screening have been developed to evaluate tear concentrations of MMPs as surrogates for inflammation in the clinical realm [ 50 ].
Several diseases cause multiple types of pathology making gross categorization difficult. Aging takes a toll on the entire body and the lacrimal gland is no different resulting in decreased tear production with increasing age [ 51 ]. Progressive acinar atrophy and fibrosis and lymphocytic infiltrates are more common within the lacrimal glands of the elderly [ 52 ].
While the exact pathophysiological changes are not well understood, mice lacking a major antioxidant pathway have been shown to have more extensive acinar atrophy and a larger leukocyte infiltrate within the lacrimal gland compared to controls [ 53 ]. Unfortunately, this study did not correlate pathology of the gland with this immune infiltrate [ 54 ]. As such, the exact role of this T cell infiltrate into the lacrimal gland of the elderly is undefined; however, speculation would surmise that this may result in an inflammatory dry eye disease process with lacrimal gland destruction similar to SS.
This is supported in part in that the tear film of older mice contains higher concentrations of pro-inflammatory cytokines than younger mice [ 55 ]. In humans this is further supported by the upregulation of inflammatory markers with decreased aqueous production in the elderly [ 56 ]. In total, lacrimal gland hypofunction in the elderly is likely the result of oxidative damage and an ongoing autoimmune, inflammatory event. SS is a systemic, chronic inflammatory state of the exocrine glands predominately seen in women that results in dry eyes and mouth.
The initiating environmental factor or pathogen trigger for glandular inflammation defining the disease is unknown. In regard to the lacrimal gland itself, imaging studies have shown an accelerated fat deposition within the gland during SS and histopathologic changes such as intralobular fibrosis and a disorganized arrangement of the ducts occurs in even mild cases [ 60 , 61 ].
Furthermore, inflammation involving the lacrimal ducts likely complicates aqueous outflow but little is known on the subject. The role of each of these changes in the overall reduction in tear production is still debatable as the degree of tissue destruction and lymphocytic infiltrate does not correlate with the level of gland dysfunction [ 62 — 64 ]. Despite extensive research, the exact pathophysiology of the disease remains unclear.
What is clear, however, is that the tear film of patients with SS contains an inflammatory proteomic profile compared to normal controls [ 65 ].
This presumably results in epithelial decompensation and loss of goblet cells as previously described resulting in severe dry eye. In mouse models, the lacrimal and submandibular glands are the first affected in the disease process, and MMPs and other proinflammatory cytokines are upregulated in tear film [ 66 — 68 ].
As the disease progresses, lacrimal gland production wanes necessitating increased ocular lubrication and the addition of topical anti-inflammatories such as cyclosporine [ 69 ]. While the mechanism is likely similar to SS with an abnormal immune response, it is worth at least mentioning a fairly new entity, IgG4-related disease, that can cause lacrimal gland dysfunction and is a current, popular topic in the clinical and scientific realm [ 70 , 71 ].
These changes within the lacrimal gland can induce dry eye. Consequently, IgG4-related disease is a known inflammatory disorder of the lacrimal gland but not as well understood as that of SS.
Smoking and video displays have been implicated in lacrimal gland dysfunction [ 73 , 74 ]. While the mechanism of gland dysfunction is unclear in both, cytochrome Ps and signals of oxidative damage are upregulated in the lacrimal glands of rats exposed to cigarette smoke [ 73 ]. We hypothesize that this likely results in destruction of the gland as seen with an aging lacrimal gland; however, no study has specifically evaluated the underlying pathophysiology.
In regard to video displays, lacrimal gland hypofunction and decreased tear production are dependent on the amount of time the monitor is used at work. Unfortunately untested, the authors speculate that proper lacrimal gland function is dependent on number of eyelid blinks [ 74 ].
Regrettably, environmental causes of lacrimal gland dysfunction are poorly understood and there are likely many other factors responsible for decreased tear production that have not been identified. A portion of patients clearly show a reduction in tear production [ 78 ] and this is hypothesized to be due to a lymphocytic infiltrate similar to SS [ 79 ]. This is most evident in those HIV-infected patients who develop diffuse infiltrative lymphocytosis syndrome, a rare entity since the introduction of HAART.
As such, lacrimal gland dysfunction during infectious diseases is likely a similar pathophysiological event as that found in SS. Therapeutic options are few as topical cyclosporine suppresses local immunity and is likely a poor choice for this case of inflammatory dry eye.
While radiation is an effective treatment of rapidly dividing cancerous cells, this therapy has well known toxic effects on local and regional tissues resulting in side effects reviewed extensively elsewhere [ 80 ]. Xerostomia is the most common presentation of glandular dysfunction of the head and neck; however, the lacrimal gland is also affected by radiation [ 83 ]. In rabbits, loss of smooth muscle and decreased aqueous secretion occur within 3 days of irradiation of the lacrimal gland and persist beyond thirty days [ 84 ].
Unfortunately, the long-term histopathological effects of radiation on the lacrimal gland have been poorly studied in animals and humans. In patients receiving local radiation, lacrimal gland dysfunction results in a dose-dependent increase in severity of dry eye following radiation treatment [ 85 ].
Consequently, pathological changes occur within days of radiation therapy inducing both temporary and permanent lacrimal gland dysfunction and resultant dry eye. While dry eyes are an unfortunate side effect, radiation therapy of head, neck, and orbit remains a commonly used treatment modality due to its success in treating such tumors making radiation-induced dry eye an issue for the foreseeable future [ 80 ].
Lastly, there are idiopathic causes of lacrimal gland dysfunction that cannot be linked to any specific cause that may represent subclinical presentations of those previously mentioned above or an altogether undefined entity.
Regrettably, the treatment of dry eye related to tear film insufficiency has made little progress in recent years.
Most current therapies aim to reduce drainage of tears from the eye, that is, punctual occlusion with cautery or plugs, or to replace insufficient aqueous production from the lacrimal gland with artificial tears.
Each of these therapies reduces dry eye symptoms but each has significant drawbacks. For example, punctal plugs have poor retention rates; can migrate into the lacrimal system; predispose the eye to infection; and cause epiphora [ 86 ]. Punctal cautery can cause similar issues but is much more difficult to reverse with patient intolerance.
Artificial tears are a more benign therapeutic option but the preservatives within them can be toxic to the cornea with frequent dosing [ 87 ]. This issue has been circumvented by the production of preservative-free preparations. While the ingredients have significantly changed, artificial tears were first described nearly 3, years ago and are unfortunately rapidly removed from the ocular surface [ 88 ].
It was not until the s that natural or synthetic polymers were added to preparations increasing viscosity and retention time. Even with these advancements, artificial tears are only a temporary measure and do not provide important proteins produced by the lacrimal gland for ocular health as previously discussed and are short-lived.
As such, artificial tears and punctal occlusion remain viable options for dry eye treatment but do not address the underlying lacrimal gland dysfunction. Further advancements have been made with the introduction of cyclosporine. The compound was initially isolated from the fungus Tolypocladium inflatum , a potent inhibitor of T cell activity [ 90 , 91 ].
It has also been shown in mice to better reduce epithelial staining compared to prednisone in an inflammatory dry eye model [ 92 ]. However, this therapy is presumably most effective in an inflammatory dry eye minimizing its therapeutic use to these specific conditions. Additionally, poor patient compliance further reduces its widespread application due to ocular irritation and prolonged use necessary to see any appreciable benefit frustrating even the most compliant patients.
Multiple surgical attempts have been made to bypass the lacrimal gland altogether by transposing the parotid gland duct onto the lower conjunctiva, a technique developed in the s [ 93 ]. We, as well as others, have all but abandoned the technique due to lack of any appreciable benefit, excessive tear secretion, and high rates atrophy of the gland following surgery [ 95 ].
Consequently, this technique is rarely used today except in animals due to inconsistent results and significant side effects. There are several emerging modalities that have shown at least some promise in the basic science realm.
Unfortunately, many of these treatments are still in their infancy and have not made significant progress beyond the basic science realm. Exogenous compounds are delivered to host tissue through either topical or oral routes. Many of these new agents directly inhibit proinflammatory cascades. The list of targets includes vascular cell adhesion inhibitors, immune modulators, and immune suppressants [ 96 — 98 ]. These inhibitors have shown efficacy in mouse models of inflammatory dry eye but have not been used in humans.
One of these agents is delivered in an adenoviral vector, which would theoretically reduce the need for reapplication but raises concerns for inducing an innate immune response that could worsen inflammation [ 35 , 98 ]. Moreover, immune suppression of the ocular surface could result in frequent infectious complications. The recently described nonimmune compound, pituitary adenylate cyclase-activating polypeptide-derived peptide, has been shown to promote corneal wound healing and lacrimal gland secretion in mice [ 99 ].
With the adenoviral vector as the exception, these compounds would likely be an improvement from artificial tears but would reduce ocular immunity. Patient compliance as seen with other topical eye medications would also be an issue. Consequently, the untested role of these topical therapies may be of some benefit in few select populations.
With increasing success in stem cell-based tissue regeneration, tissues and organs such as functioning photoreceptors and the liver can now be grown in vitro [ , ]. Attempts of a bioengineered lacrimal gland have seen recent success in mouse models as well [ ].
Stem cells are isolated using specific lacrimal cell markers, tissue grown ex vivo , and transplanted into the host resulting in increased tear production [ — ]. While promising, it remains to be seen whether these results can be reproduced in humans and provide a feasible, long lasting therapeutic option.
There has also been some suggestion of using lacrimal gland xenografts as healthy tissue, but this theoretical idea remains untested [ ]. Furthermore, these transplant models have not evaluated the effect of transplantation with ongoing diseases such as SS that may reduce graft transplantation rates and efficacy such as seen with a significantly higher rejection rate of herpes-infected corneas compared to noninflammatory corneal transplants [ ].
While clinical promising and would address gland dysfunction and restore normal tear production, lacrimal gland regeneration or xenograph transplantation remains to be years from clinical use.
More recently, sublingual, labial, and submandibular glands have been transplanted into the subconjunctival space as an additional means to treat severe dry eyes due to underlying basal secretion of these glands that does not require innervation [ , ]. The transplanted glands have shown a reduction in dry eye symptoms for at least five years and reduce the need for tear supplementation [ ]. In addition, saliva contains many of the same contents as the lacrimal gland including secretory IgA but the two have not been specifically compared [ ].
Unfortunately, the long-term efficacy beyond 5 years is currently unknown. As such, the surgery has not gained widespread use at this point in time. While transplantation of these glands has shown great effect on dry eye and produce more natural tears than artificial instilled ones, the complicated surgery and risk of graft failure are staggering complications to overcome making them less than ideal.
Lastly, there is ongoing work on an implantable device to that stimulates the lacrimal nerve to increase tear production within the lacrimal gland and this small animal study has shown promising results [ ].
Furthermore, will this device be able to stimulate a diseased gland enough such as in SS to overcome the symptoms of dry eye? In summary, there are several new modalities emerging for severe dry eye; however, many of these options remain unproven or require extensive, technically difficult microsurgery. There are multiple disease entities that can affect the lacrimal gland and cause its dysfunction. Untreated pathologies and downstream effects of reduced production from the lacrimal gland can result in decompensation of the ocular surface and gross deterioration of visual acuity.
The role of this gland cannot be overstated in ocular surface health and proper light refraction from the air-tear interface. It will be interesting to see if the untested, but promising, therapies discussed become viable treatment modalities in dry eye therapy beyond the temporary measures of ocular lubricants.
The authors would like to thank Dr. Nick Mamalis for images of the lacrimal gland and Lane Bennion for the medical drawings. The authors would also like to thank Research to Prevent Blindness for their unrestricted grant to the Moran Eye Center. Conrady et al. This is an open access article distributed under the Creative Commons Attribution License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Article of the Year Award: Outstanding research contributions of , as selected by our Chief Editors. Read the winning articles. Journal overview. Special Issues. Conrady, 1 Zachary P. Joos, 1 and Bhupendra C. Received 24 Dec Accepted 04 Feb Published 02 Mar Abstract The human tear film is a 3-layered coating of the surface of the eye and a loss, or reduction, in any layer of this film may result in a syndrome of blurry vision and burning pain of the eyes known as dry eye.
Introduction The human tear film coats the anterior surface of the eye and is composed of three distinct layers: an inner mucin coating, a middle aqueous component, and a lipid overlay. Anatomy, Physiology, Innervation, and Histology A proper review of the anatomy of the lacrimal gland and accessory lacrimal tissues is important for understanding the pathophysiology of dry eye syndrome and secondary causes of dry eye.
Anatomy, Blood Supply, Innervation Embryologically, the main lacrimal gland develops from an outpouching of the conjunctiva. Figure 1. Lacrimal gland histopathology. The gland is composed of lobules separated by loose connective tissue. The lobules are composed of multiple acini lined by columnar secretory cells.
Figure 2. Oblique view of the right orbit. Oblique view of the right orbit showing the main lacrimal gland divided into the orbital lobe OL and palpebral lobe by the lateral horn of the levator aponeurosis LA. Note the excretory ducts coursing through the palpebral lobe and draining into the superior conjunctival fornix arrow.
Figure 3. Sagittal view of the upper and lower eyelids. The glands of Krause arrow are located in the superior conjunctival fornix. The glands of Wolfring arrowhead are found at the nonmarginal border of the tarsal plate. Table 1. Causes of lacrimal gland dysfunction and their proposed pathological mechanism. Grosscategorization of the most common causes of lacrimal gland dysfunction based on underlying pathology most typical of the disease. References T. Millar and B. View at: Google Scholar A.
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