Download Lacrimal Gland Pathologies from an Anatomical Perspective

Review Article
Acta Medica Anatolia
Volume 3 Issue 3 2015
Lacrimal Gland Pathologies from an Anatomical Perspective
Dr.Mahmut Sinan Abit
Bingol State Hospital Saray mah. Merkez 12000 Bingol/Turkey
Abstract
Most of the patients in our daily practice have one or more ocular surface disorders including conjunctivitis, keratitis, dry eye
disease, meibomian gland dysfunction, contact lens related symptoms, refractive errors, computer vision syndrome. Lacrimal
gland has an important role in all above mentioned pathologies due to its major secretory product. An anatomical and physiological knowledge about lacrimal gland is a must in understanding basic and common ophthalmological cases. İn this paper
it is aimed to explain the lacrimal gland diseases from an anatomical perspective.
Keywords: lacrimal gland, anatomy
Received: 07.08.2015
Accepted: 30.09.2015
doi: 10.15824/actamedica.96512
Introduction
Lacrimal gland is pinkish-gray, lobulated serous
gland. The aqueous component of tear film is mainly
provided by lacrimal gland (1). In the first trimester
of pregnancy and at 19-21 mm stage of embryologic
development, it appears as epithelial buddings from
superolateral conjunctival fornix ectoderm. The
mesenchymal condensations around these clusters
than turn in to secretory components. These early
epithelial buds with secretory components form the
orbital lobe of lacrimal gland. At the 40-60 mm stage
of fetal development another group of epithelial stalks
appears which form the palpebral lobe of the lacrimal
gland later. Development of lacrimal gland continues
for 3-4 years after birth (2, 3). Congenital alacrima is
characterized by deficient lacrimation from birth as
a result of embryological development disorder and
lacrimal gland hypoplasia (4). Congenital alacrima
Figure 1. Lacrimal gland, anterior view
can also be seen as a component of some syndromes
such as triple A syndrome in which achalasia and
addison disease accompanies alacrima. Besides dry eye,
mental retardation, autonomic dysfunction, deafness
and hyperkeratosis on palms of hands and soles of feet
are additional symptoms of this syndrome (5).
Lacrimal gland is situated in the superotemporal orbit.
It measures about 20 mm long, by 12 mm wide and
by 5 mm thick (6). In normal human population, by
increasing age periductal fibrosis, paraductal blood
vessel loss, aciner cell atrophy and interacinar fibrosis
causes age related primary lacrimal gland deficiency (7).
It is anatomically divided in to two portions as orbital
and palpebral lobe by the lateral horn of levator
aponeurosis. But this separation is incomplete and
around lateral end of aponeurosis, lobes show
continuity (Figure 1, Figure 2). The larger orbital
Figure 2. Lacrimal gland, lateral view
1- orbital lobe 2-secretory ductules 3-palpebral lobe 4-secretory ductules 5-levator aponeurosis.
Correspondence: Bingol State Hospital Saray mah. Merkez 12000 Bingol/Turkey
E-mail: [email protected]
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Review Article
lobe is about the 60-70 % of total mass of lacrimal
gland and situated anterior to levator aponeurosis,
posterior to orbital septum and preaponeurotic
fat pad. The smaller palpebral lobe is about the
30-40 % of total mass of lacrimal gland, located
posterior to levator aponeurosis and anterior to
palpebral conjunctiva (6-9). In upper eyelid surgical
procedures lacrimal gland must be differentiated
from preaponeurotic fat pads, otherwise surgical
removal of lacrimal gland causes severe dry eye
symptoms. This differentiation can be easily made
by color difference; fat pads appear yellowish while
lacrimal tissue appears pinkish (10).
Two to six secretory ductules of orbital lobe pass
through the palpebral lobe at where ductules
of palpebral lobe are joined and finally a total
number of 6-12 tubules empty in to superolateral
conjunctival fornix approximately 4-5 mm above
the tarsus (11) (Figure 1,2). Therefore any damage
to palpebral lobe may cause similar results as any
damage to whole lacrimal gland. Upper conjunctival
fornix damage and obstruction of lacrimal gland
ducts by trachoma, cicatricial pemhygoid, mucous
membrane pemphygoid, erythema multiforme,
trauma, chemical burns and thermal burns lead to
secondary lacrimal gland deficiency and aqueous
deficient dry eye syndrome (12-16).
In addition to supporting function of relation
between lacrimal gland pseudocapsule and
periorbita of frontal bone, Whitnall’s ligament and
lateral horn of levator aponeurosis are other major
supporters stabilizing the gland in shallow lacrimal
fossa. Lacrimal gland prolapsus is not an uncommon
result of upper eyelid surgery procedures when
Whitnall’s ligament disrupted and it should be kept
in mind that refixation of lacrimal gland should be
needed to avoid postoperative cosmetic problems
and dry eye (17).
Lacrimal gland is composed of lobules separated
from each other by loose fibrovascular connective
tissue (Figure 3). This interlobular septa is the
extension of lacrimal gland pseudocapsule, which
is connected to periorbita as mentioned earlier. Of
lobules 80% are secretory acini which are composed
of an inner layer of columnar or pyramidal shaped
epithelium around a central lumen and surrounded
by a basal layer of myoepthelial cells (18, 19).
Contraction of myoepithelial cells aid in secretion.
Columnar epithelial cells of secretory acini have well
developed endoplasmic reticulum, golgi complex,
moderate numbers of mitechondria, free ribosomes,
lipid droplets and vacuoles. Of lobules lacrimal ducts
Acta Med Anatol 2015;3(3): 113-118
Abit M et al.
forms the 10-12 % and composed of one or two
layers of cuboidal cells. The other cellular units of
lacrimal gland are lymphocytes, plasma cells, mast
cells and macrophages (18, 19).
The most common space occupying lesions of
lacrimal gland are cysts (dacryops) which are derived
from cystic dilatation of ductal epithelial cells and
dermoid cysyts (20). The most common benign
primary lacrimal gland tumor of lacrimal gland is
pleomorphic adenoma (benign mixed cell tumor).
This benign tumor is consisted of myoepithelial and
cellular components as well as ductal epithelium.
Very rarely myoepithelioma may appear as another
benign tumor mimicking pleomorphic adenoma (21,
22). The most common epithelial origin malignant
tumor is adenoid cystic carcinoma. Malign mixed cell
tumor, adenocarcinoma, squamous cell carcinoma
are other types of lacrimal gland malignant tumors
(21, 22).
Figure 3. Ultrastructural anatomy of a lacrimal lobule.
1-interlobular septa, 2-basal lamina, 3-myoepithelial cell,
4-pyramidal shaped epithelium, 5-central lumen, 6-lobular
excretory ductile, 7-T and B cells, 8-serous acinus, 9-plasma
cell, 10-macrophage.
Besides aqueous secretion, lacrimal gland also
secretes protein and electrolytes. The mechanism
of this secretions are under neural and hormonal
control. Acetyhcholine and vasoactive intestinal
peptide are parasympathetic and norepinephryne
is the sympathetic neurotransmitter of lacrimal
gland (23). Many hormones take role in regulation
of lacrimal gland functions. By the stimulation of
parasympathetic nerves, acetylcholine released
which activate M3 muscarinic receptors located
at acinar basal and lateral membranes result in
increase in intracellular concentration of calcium
in activation of several protein kinase C. Protein
secretion is stimulated by these biochemical
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pathways .Norepinephrine causes an increase in
protein secretion by the ability of binding both alpha
and β-adrenergic receptors (24-27). Other chemical
mediators that regulate secretion of lacrimal gland
include alpha melanosite stimulating hormone,
adrenocorticotrophic hormon, epidermal growth
factor, substance p, calcitonin gene and androgens.
Ductal epithelial cells modify the secretory product
of acini before reaching to conjunctival fornix and
ocular surface of final composition (28-30).
The final electrolyte composition of lacrimal gland
secretion is similar to plasma except for lower level
of Na and higher levels of K and Cl. It contains many
kind of proteins including lysosime, lactoferrin,
secretory IgA, epidermal growth factors, a lacrimal
gland spesific protein lacrytin, surfactan proteins
A-D (31-33).
Lacrimal gland receives arterial supply from lacrimal
artery,a branch of the ophthalmic artery,with
contributions from the infraorbital artery and
sometimes from the recurrent menengial artery.
Lacrimal artery enters its posterior border pass
through the gland and reaches to conjunctiva where
it takes the name lateral palpebral artery which
anostomoses with medial palpebral artery over the
eyelids.Venous drainage of lacrimal gland is in to the
superior ophthalmic vein then to cavernous sinus.
The lymphatic drainage of lacrimal gland joins with
conjunctival lymphatics to drain in to superficial
parotid lymph nodes.
Lacrimal gland has both sensorial and autonomic
innervations (Figure 4). Lacrimal nerve is the smallest
branch of ophthalmic nerve. Like as lacrimal artery
lacrimal nerve also pass through the gland reaches
to adjacent conjunctiva and eyelid carrying sensorial
innervation.
Preganglionic
parasympathetic
secromotor fibers originate in the lacrimal nucleus
of brainstem, exit from the ventrolateral portion
as the nervus intermedius in company with motor
division of facial nerve and enters the auditory
canal to reach geniculate ganglion (Figure 4). The
greater superficial petrosal nerve arises from the
preganglionic parasympathetic fibers of geniculate
ganglion. Greater superficial Petrosal nerve unites
with the deep petrosal nerve carrying postganglionic
sympathetic fibers and together they form the nerve
of pterygoid canal (vidian nerve). Vidian nerve
reaches to pterygopalatine ganglion (34, 35) (Figure
4).
Pterygopalatine ganglion is the largest parasympathetic ganglion located in pterygopalatine fossa,
suspended by nerve roots from the maxillary nerve.
Acta Med Anatol 2015;3(3): 113-118
Abit M et al.
Here parasympathetic nerve fibers synapse and
continues as postganglionic parasympathetic nerve
whereas sympathetic nerve fibers do not. Postganglionic parasympathetic nerve fibers leave the pterygopalatine ganglion through the branches of zygomatic nerve and finally reach to lacrimal nerve and
lacrimal gland with communicating branches (34,
35).
The postganglionic sympathetic nerve fibers
arising from superior cervical ganglion do not
synapse in pterygopalatine and uses the same way
as postganglionic parasympathetic nerve fibers
to reach lacrimal gland (Figure 4). Disruption in
any part of autonomic system of lacrimal gland
results in deterioration of lacrimal gland fluid and
electrolyte secretion. Familial dysautonomia is a
rare inherited autonomic and sensorial nervous
system malfunction characterized by insensitivity to
pain, reduced lacrimal gland secretion, labile blood
pressure, emotional instability, pupillary function
abnormality and many other symptoms varying
person to person (36).
Figure 4. Sensory and autonomic innervation of lacrimal
gland.
LN: Lacrimal nucleus GG: Geniculate ganglion TG: trigeminal ganglion SSG: Superior cervical ganglion PPG: pterygopalatine ganglion V1:ophthalmic branch of trigeminal nerve
V2: maxillary branch of trigeminal nerve V3: mandibular
branch of trigeminal nerve.
1-Wrisberg nerve (nervus intermedius) 2-greater superficial
petrosal nerve 3-deep petrosal nerve 4-Pterygoid canal
nerve (vidian nerve) 5-ganglionic branches 6-zygomatic
nerve 7-zygomaticofacial nerve 8-zygomaticotemporal
nerve 9-communicating branches of zygomatic nerve 10-lacrimal nerve.
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A decrease in corneal sensitivity (hypoesthesia,
hypesthesia) causes less stimulation of lacrimal
gland and reduced reflex tear production. There
are many factors leading to hypesthesia. Corneal
sensitivity decreases steadily with age like all other
neural transmissions. Topically used proparicaine,
non steroidal anti inflammatory agent’s diclofenac,
ketoralac, timolol maleate, betaxolol are some
commonly prescribed agents by physicians which
may cause reduced corneal sensitivity (37-44).
Contact lens usage is another common mechanism of
lacrimal gland hyposecretion due to reduced corneal
sensitivity.Diabetes mellitus may cause lacrimal
gland hyposecretion by two ways; reduced corneal
sensitivity and microvasculature damage of lacrimal
gland. Herpes simplex keratitis, herpes zoster
ophthalmicus, refractive surgery, extracapsular
cataract surgery, keratoplasty are other common
causes of corneal hypoesthesia and diminished
reflex tears secretion (45-50).
A cerebellopontin angle tumor or any other space
occupying lesion pressing on trigeminal nerve root
may cause unilateral corneal hypoesthesia as a first
sign. The afferent pathway of reflex lacrimation
Abit M et al.
pathway may be affected as the complication of
trigeminal neuralgia surgery (51-55).
Bilateral corneal hypoesthesia is commonly
associated with diabetes, amyloidosis, and vitamin
A deficiency.
Nervus intermedius may be damaged in a
neurosurgery procedure usually for brainstem
pathology such as vestibular schwannoma (56-60).
Secondary lacrimal gland deficiency is the result of
destructive infiltration of lacrimal gland by several
diseases including lymphoma, sarcoidosis, AIDS, graft
versus host disease, hemochromatosis, neurofibroma,
tumors and Sjörgen syndrome (61-64).
Patients admitting with the symptoms of aqueous
deficient dry eye disease make one of the largest
groups of our daily practices. Every ophthalmology
expert should know the major, micrustructural and
neurophysiological anatomy of lacrimal gland to
handle with the problems of different etiological
factors. This paper summarizes the anatomy of
lacrimal gland for the purpose of best systematic
clinical approach.
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