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Review
. 2011 Mar 30;52(4):1938-78.
doi: 10.1167/iovs.10-6997c. Print 2011 Mar.

The international workshop on meibomian gland dysfunction: report of the subcommittee on anatomy, physiology, and pathophysiology of the meibomian gland

Erich Knop  1 , Nadja Knop, Thomas Millar, Hiroto Obata, David A Sullivan
Affiliations
Review

The international workshop on meibomian gland dysfunction: report of the subcommittee on anatomy, physiology, and pathophysiology of the meibomian gland

Erich Knop et al. Invest Ophthalmol Vis Sci. .
No abstract available

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Figures

Figure 1.
Figure 1.
Heinrich Meibom, the younger (1638–1700). In 1666, he published the first detailed description of the tarsal glands in the eyelid, which later became known as the meibomian glands. Reprinted with permission of the Herzog August Bibliothek, Wolfenbüttel, Germany, Signatur B 100.
Figure 2.
Figure 2.
Topography of the meibomian glands within the tarsal plates of the upper and lower eyelids. The extension of a single meibomian gland follows the shape of the tarsal plate, which is different in both lids. The drawing depicts a posterior view with the anterior part of the lid removed, and the tarsal connective tissue made translucent so that the glands are exposed. The proximal ends of the glands extend toward the proximal margin of the tarsal plates and the secretum (meibum) is delivered at the distal end of the tarsus via a short excretory duct through the orifice onto the lid margin. Reproduced from Sobotta Đ. Atlas der Anatomie des Menschen. Ferner H, Straubesand J, eds. Ed. 18, Vol. 1, p. 215, Urban & Schwarzenberg 1982, with the kind permission of Elsevier.
Figure 3.
Figure 3.
Morphology of a single meibomian gland. A single meibomian gland (located within the tarsal plate near the conjunctiva) is composed of multiple holocrine secretory acini that are arranged circularly around a long central duct to which they are connected via short, lateral, connecting ductules. The terminal part of the central duct is lined by an ingrowth of the epidermis (ep) that covers the free lid margin and hence forms a short excretory duct that opens as an orifice at the posterior part of the lid margin just anterior to the mucocutaneous junction (mcj) near the inner lid border. The oily secretum (meibum) is synthesized within the secretory acini and transported (yellow arrows) in a distal direction toward the orifice. Knop N, Knop E. [Meibomian glands. Part I: anatomy, embryology and histology of the Meibomian glands] Meibom-Drüsen Teil I: Anatomie, Embryologie und Histologie der Meibom-Drüsen. Ophthalmologe. 2009;106:872–883, with the kind permission of Springer Science and Business Media.
Figure 4.
Figure 4.
Structure of the acini and ductal system of a normal meibomian gland. (A) The holocrine acini of the meibomian gland are filled with the secretory cells (meibocytes) and surrounded by a basement membrane (bm). In the periphery of the acinus, a capillary (c) and a small nerve fiber (n) are seen. From the basal cells (b) at the peripheral margin, differentiating meibocytes (d) start with the production and accumulation of lipids within lipid droplets that occur as vacuoles in routine histology, because the lipids are dissolved in the histologic preparation. Toward the center of the acinus, there is an increase in the number and size of their internal lipid droplets as the cells differentiate into mature meibocytes (m). These remain vital, as indicated by their intact nucleus (arrowhead). In the very large hypermature meibocytes (h), the nucleus becomes pyknotic (double arrowheads) [compare with Fig. 7]. The cytoplasmic membrane of these cells disintegrates, and the components of the whole cell form the secretory product, termed meibum, in the disintegration zone (des) close to the connecting ductule (de). Remnants (arrow) of the meibocytes are still found inside the ductule and sometimes in the central duct. (B) In the area of the disintegration zone, located at the transition of the acinus to the ductule, the basal cell layer is replaced (open arrows) by the multilayered squamous epithelium of the ductule, which is about four cell layers thick. If the ductal epithelium is observed in an oblique plane of section, it is seen to contain keratohyalin granules (arrowheads) in the luminal cell layer that represent an incipient stage of keratinization. (C) Numerous acini of spherical to elongated shape are radially arranged around the central duct (cd) of a gland, seen here in a longitudinal section. Ductules enter (B, C, arrows) the central duct, typically in an oblique direction, which results in the formation of a sharp tissue spur (C, arrowheads) toward the central duct. The direction of flow of the meibum inside the gland is indicated by a large arrow in (B) and (C). Light microscopic images of paraffin-embedded sections stained with hematoxylin and eosin (H&E); size markers are shown in the images. Reprinted from Knop N, Knop E. [Meibomian glands. Part I: anatomy, embryology and histology of the Meibomian glands] Meibom-Drüsen Teil I: Anatomie, Embryologie und Histologie der Meibom-Drüsen. Ophthalmologe. 2009;106:872–883 with the kind permission of Springer Science and Business Media.
Figure 5.
Figure 5.
Driving forces for the delivery of meibomian oil onto the lid margin and tear film. A schematic drawing of a single meibomian gland inside the connective tissue of the tarsus at the posterior lid margin. The driving forces that result in the eventual delivery of meibomian oil (meibum) onto the lid margin and tear film are (1) the continuous secretion of meibum by the secretory acini, which generates a secretory pressure that pushes the meibum (yellow arrows) into the ductal system and further toward the orifice and (2) the mechanical muscular action by muscle fibers (red dots) of the pretarsal orbicularis muscle (M. orbicularis), located on the outside of the tarsus, and of the marginal muscle of Riolan (M. Riolan), which encircles the terminal part of the meibomian gland. During a blink, these muscles may exert a compression (red arrows) of the meibomian gland that drives the oil out of the orifice into the marginal lipid reservoir, where it eventually constitutes the tear film lipid layer (TFLL), as observed clinically [compare with Figs. 3, 7, and 18]. Reprinted from Knop E, Knop N, Schirra F. [Meibomian glands. Part II: physiology, characteristics, distribution and function of meibomian oil] Meibom-Drüsen Teil II: Physiologie, Eigenschaften, Verteilung und Funktion des Meibom-Öls. Ophthalmologe. 2009;106:884–892, with the kind permission of Springer Science and Business Media.
Figure 6.
Figure 6.
Stem cells in the hair follicle as a potential model for the meibomian gland. Stem cells (SCs) are located in the bulge area (Niche) of the outer root sheet (ORS) of the hair follicle. Two different populations of transient amplifying (TA) cells arise from this stem cell source and migrate (solid arrows) into two directions: hair-forming TA cells (hTA) migrate downward, whereas epidermis-forming TA (eTA) cells migrate upward. Both of them gradually differentiate and mature via different intermediate stages (TA1, TA2… to TAn) into the terminally differentiated cornified cells (TDcc) of the epidermis and hair, respectively. Inner root sheet (IRS) and (I); upper follicle (UF); hair medulla (M); hair shaft (HS); cortex (C); skin epidermis (E). In the bulge region and epidermis further differentiated cells generally move upward (dashed arrows) to the lumen. Schematic drawing of a section through the skin and a hair follicle. Reprinted from Taylor G, Lehrer MS, Jensen PJ, Sun TT, Lavker RM, Involvement of follicular stem cells in forming not only the follicle but also the epidermis, Cell, 102, pp. 451–461, ©2000 with permission from Cell Press.
Figure 7.
Figure 7.
Structural and functional domains of the meibomian glands. The human meibomian glands are composed of at least three different structural and functional compartments. These are (1) the holocrine acinus with its basal cycling and luminal differentiating, lipid-producing meibocytes (yellow); (2) the four-layered stratified squamous epithelium of the ductal system (connecting ductules and long central duct), which has physiological incipient (pink) keratinization; and (3) the epidermis of the excretory duct, which represents an ingrowth of the stratified squamous, fully cornified (red) epidermis of the skin from the free lid margin. It can be assumed from studies of stem cells of the epidermis and of hair-associated sebaceous glands that each of these compartments is provided with lineage-committed progenitor cells. The basement membrane that separates the epithelial tissues from the underlying connective tissue is indicated by a dotted line. Schematic drawing of a section through a meibomian gland and the posterior lid margin, mcj, mucocutaneous junction [compare with Fig. 3]. Modified from Knop N, Knop E. [Meibomian glands, Part I: anatomy, embryology and histology of the meibomian glands]. Meibom-Drüsen, Teil I: Anatomie, Embryologie und Histologie der Meibom-Drüsen. Ophthalmologe. 2009;106:872–883 with the kind permission of Springer Science and Business Media.
Figure 8.
Figure 8.
Location of sebaceous gland progenitors in the mouse skin. The expression of sebaceous gland–committed progenitor cells was found to be restricted to the transition zone between the acinus and the hair follicle in skin sebaceous glands. Such progenitor cells, labeled by retroviral transfer (A–C), are seen in a hair met in longitudinal section (A) as well as in cross-sections (B, C). Another marker (BLIMP1) that is assumed to characterize lineage-committed sebaceous gland progenitors indicates respective cells at the same position in a schematic drawing (D). (A–C) Reprinted by permission from Macmillan Publishers Ltd: EMBO J, Ghazizadeh S, Taichman LB. Multiple classes of stem cells in cutaneous epithelium: a lineage analysis of adult mouse skin. 2001;76:1215–22, © 2001. (D) Reprinted from Cell, 126, Horsley V, O'Carroll D, Tooze R et al., Blimp1 defines a progenitor population that governs cellular input to the sebaceous gland, 597–609, © 2006 with, permission from Cell Press.
Figure 9.
Figure 9.
Transfer of carbons for lipid synthesis from the mitochondria to the cytoplasm. When the tricarboxylic acid (TCA) cycle in the mitochondria is blocked due to an excess of the high-energy molecule NADH, there is a buildup of mitochondrial acetyl-CoA that indicates to the cell that it has a surfeit of energy and therefore does not need to oxidize carbons to obtain more energy. Instead, it is more desirable to store the carbons as fats until the energy is needed. The acetyl group (2C) of acetyl-CoA is passed to oxaloacetate (4C) to form citrate (6C), and citrate is transferred across the mitochondrial membrane into the cytoplasm. It is then lysed (citrate lyase) and coupled to cytoplasmic CoA to form cytoplasmic acetyl-CoA, which is used for fatty acid synthesis, and oxaloacetate, which is cycled back (indirectly) to the mitochondrial matrix. Figure courtesy of Tom Millar.
Figure 10.
Figure 10.
Formation of malonyl-CoA. Figure courtesy of Tom Millar.
Figure 11.
Figure 11.
Various activities of fatty acid synthase. The functional enzyme is a dimer with multiple functions in different regions. On each cycle, the growing chain is transferred to a malonyl-loaded acyl carrier protein domain of the protein, and in so doing displaces CO2, which increases the chain length by 2C. Figure courtesy of Tom Millar.
Figure 12.
Figure 12.
β-Hydroxy-β-methyl glutaryl-CoA (HMG-Co A). HMG-CoA synthase 1 (4.1.3.5) is located in the cytoplasm, unlike HMG-CoA synthase 2 (4.1.3.4), which is located in the mitochondria. Figure courtesy of Tom Millar.
Figure 13.
Figure 13.
Formation of 3-phospho-5-pyrophosphomevalonate. 3-Hydroxy-3-methyl glutaryl-CoA is converted on the endoplasmic reticulum to the energetically activated 3-phospho-5-pyrophosphomevalonate. Figure courtesy of Tom Millar.
Figure 14.
Figure 14.
Formation of 10C geranylpyrophosphate. The 5C isopentenylpyrophosphate and its isomer are formed from 3-phospho-5-phosphomevelanate, which are then joined to form 10C geranylpyrophosphate. Figure courtesy of Tom Millar.
Figure 15.
Figure 15.
Formation of cholesterol. Formation of 15C farnesyl pyrophosphate, followed by 30C squalene, which is then converted through a variety of reactions to 27C cholesterol. Figure courtesy of Tom Millar.
Figure 16.
Figure 16.
Major biosynthetic and inactivation pathways of androgens and estrogens in humans. Direction of enzymatic action is shown by arrows. Abbreviations include Sulfatase, steroid sulfatase; ST, sulfotransferase; Sulf Met, sulfated metabolites; HSD, hydroxysteroid dehydrogenase; DHEA, dehydroepiandrosterone; DHEA-S, DHEA sulfate; Estrone S, estrone sulfate; DHT, dihydrotestosterone; 5-diol, 5-androstene-3β,17β-diol; ADT-G, androsterone-glucuronide; 3α-diol-G, androstane-3α, 17β-diol-glucuronide. Reproduced from Schirra F, Suzuki T, Dickinson DP, Townsend DJ, Gipson IK, Sullivan DA. Identification of steroidogenic enzyme mRNAs in the human lacrimal gland, meibomian gland, cornea, and conjunctiva. Cornea. 2006;25:438–442 with permission from Wolters Kluwer/Lippincott Williams & Wilkins.
Figure 17.
Figure 17.
A schematic diagram of the two major lipogenic pathways, which result in the synthesis of cholesterol (and steroid hormones) and fatty acids (and triglycerides and phospholipids). Both pathways typically require the generation and secretion of acetyl-CoA from mitochondria, the transcriptional control by SREBPs in the nucleus, and the action of lipogenic enzymes in the cytosol. The extent of the androgen upregulation of specific genes for SREBPs and enzymes is shown within the diagram. Reprinted from Exp Eye Res, 83, Schirra F, Richards SM, Liu M, Suzuki T, Yamagami H, Sullivan DA, Androgen regulation of lipogenic pathways in the mouse meibomian gland, 291–296, © 2006, with permission from Elsevier.
Figure 18.
Figure 18.
Comparison of the structure of a normal and an obstructed human meibomian gland. (A, B) A histologic section through a normal meibomian gland at the inner lid border. (A) The terminal part of the central duct (cd) and the terminal acini are encircled by fibers of Riolan's muscle (riol), which represents the marginal inner part of the orbicularis muscle (orb) and is split by the downgrowth of the ciliary (c) hairs [compare with Fig. 5]. The free lid margin is covered by the keratinized epidermis (ep), which transforms at the inner lid border into the conjunctival mucosa (conj). The section does not pass through the orifice of the central duct (cd). (B) In a magnification of (A), it is seen that the connecting ductules (de) from the acini (a) of a normal gland are typically narrow and enter the central duct in an oblique direction. (C–E) Section through a meibomian gland with obstructive MGD. (C) The orifice (open arrow) is in the typical position, still within the keratinized epidermis, which extends for about half a millimeter into the central duct and forms an excretory duct. Even though the obstruction is not very advanced, as judged from the moderate dilatation of the central duct (cd), there are distinct alterations of the gland structure. The cd is already partly dilated, the epithelium of the wall is thinner than in the normal gland, and the wall is partly undulated. (D) The orifice is obstructed by numerous keratin lamellae (small arrows). (E) The secretory acini (a) are distinctly smaller and more roundish than in a normal gland, whereas the ductules (de) are dilated and enter the central duct (cd) at about right angles (small arrows). An atypical lumen (asterisk) has formed within the acini, and the secretory meibocytes are reduced in number and form only a few remaining cell layers (arrowhead). In one location, the residual meibocytes of a presumably disrupted acinus appear integrated into the wall of the central duct (double arrowhead). Inflammatory leukocytes are not apparent. Taken together, these findings indicate atrophy of the dilated meibomian gland. Light microscopic images of paraffin-embedded sections stained with hematoxylin and eosin (H&E); size markers are shown in the images. Reprinted from Knop E, Knop N, Brewitt H et al. [Meibomian glands, Part III: meibomian gland dysfunction (MGD)—plaidoyer for a discrete disease entity and as an important cause of dry eye.] Meibom-Drüsen, Teil III: Meibomdrüsen Dysfunktionen (MGD)—Plädoyer für ein eigenständiges Krankheitsbild und wichtige Ursache für das Trockene Auge. Ophthalmologe. 2009;106:966–979 with the kind permission of Springer Science and Business Media.
Figure 19.
Figure 19.
Cystic dilatation of a human meibomian gland. In cystic dilatation due to obstruction of the meibomian gland orifice, the ductal system is distinctly dilated, together with a dilation of the connecting ductules and atrophy of the acini. Figure reprinted from Obata H, Horiuchi H, Miyata K, Tsuru T, Machinami R. Histopathological study of the meibomian glands in 72 autopsy cases (in Japanese). Nippon Ganka Gakkai Zasshi. 1994;98:765–771 with permission from the Japanese Ophthalmological Society.
Figure 20.
Figure 20.
Epinephrine-induced MGD in rabbit. (A) The lumina of the dilated ducts are filled with keratinized material, representing keratin lamellae that are shed from the hyperkeratinized ductal wall. (B) The epithelium of the orifice was also hyperkeratinized and obstructed. Figure courtesy of Hiroto Obata.
Figure 21.
Figure 21.
Features of pathologic meibum. (A) Yellowish white, turbid meibum from a 72-year-old woman. (B) Impression cytology of yellowish white, turbid meibum from a 71-year-old man. An orange, keratinized material is seen on the nitrocellulose membrane. Cellular components such as inflammatory cells are not seen. Papanicolaou staining. Figure courtesy of Hiroto Obata.
Figure 22.
Figure 22.
Acinar atrophy of human meibomian gland. (A) Acinar atrophy: Atrophic acini show a small and irregular, not rounded, shape (arrows); the duct appears slightly dilated. No inflammatory cell infiltration is seen. Figure reprinted from Obata H, Horiuchi H, Miyata K, Tsuru T, Machinami R. Histopathological study of the meibomian glands in 72 autopsy cases (in Japanese). Nippon Ganka Gakkai Zasshi. 1994;98:765–771 with permission from the Japanese Ophthalmological Society. (B) Basement membrane thickening of the acini: Basement membrane thickening (arrows) is frequently associated with atrophy of acini. Periodic acid-Schiff (PAS) staining. Figure courtesy of Hiroto Obata.
Figure 23.
Figure 23.
Capillary vessels in a normal human meibomian gland. Immunostaining of factor VIII, a marker of vascular endothelial cells, reveals capillary vessels surrounding the acini. Figure courtesy of Hiroto Obata.
Figure 24.
Figure 24.
Course of structural alterations of the meibomian glands in obstructive MGD. Schematic drawing of a meibomian gland and the posterior lid margin. (A) Normal: In the normal meibomian gland, the secretory product (meibum, yellow arrows) that is produced inside the acini is transported through the connecting ductules into the central duct and is finally delivered through the excretory duct and orifice that is located within the keratinized epidermis (red) at the posterior lid border. The ductal system has an incipient stage of keratinization (pink). The acini are spherical to elongated, and the connecting ductules are narrow. (B) Obstruction: When the orifice and excretory duct are obstructed by hyperkeratinization of the epithelium and/or increased viscosity of the meibum, the delivery of meibum onto the lid margin is reduced or completely inhibited. (C) Additional dilatation: The continuing secretion of meibum in the acini generates an increasing pressure inside the glands that leads to a gradual dilatation, first of the central duct. (D) Additional atrophy: After a prolonged time, the increased pressure inside the gland leads to dilatation of the connecting ductules and a pressure atrophy of the acini with rarefaction of secretory meibocytes. This effect causes shrinkage of the whole acini that may represent the histopathologic equivalent of the clinically detectable gland dropout and results in a presumed secondary hyposecretion. (E) Additional cornification of the glandular epithelium: In late stages the whole ductal epithelium can become cornified and the meibocytes replaced by a stratified squamous cornified epithelium. Reprinted from Knop E, Knop N. [Meibomian glands. Part IV: Functional interactions in the pathogenesis of meibomian gland Dysfunction (MGD).] Meibom-Drüsen, Teil IV: Funktionelle Interaktionen in der Pathogenese der Dysfunktion (MGD). Ophthalmologe. 2009;106:980–987 with the kind permission of Springer Science and Business Media.
Figure 25.
Figure 25.
Pathways and proposed sequence of events that lead to self-enforcing vicious circles in MGD. Mechanisms and interactions (arrows) in MGD occur as a result of underlying causative factors (colored square boxes located in the periphery). The core mechanisms of gland obstruction due to ductal hyperkeratinization and increased viscosity of the meibomian oil (meibum) are shown in the center of the figure on a yellow underlay and result in two effector limbs (wide shadowed downstream arrows, also on yellow underlay). Associated functional complexes, such as progenitor cell differentiation, bacterial growth, inflammation, and seborrhea, are shown on color-shaded spherical zones around the core mechanisms. Dashed arrows depict likely interactions; functional complexes of likely but insufficiently clarified importance are shown in dashed circles. Vicious circles that result in a progressive process of dysfunction are indicated by red bent arrows. Hyperkeratinization of the epithelium of the excretory duct and orifice is the main factor that leads to obstruction of the meibomian glands. This effect is influenced by endogenous factors such as age, sex, and hormonal disturbances as well as by exogenous factors, such as topical medication. These may act, at least in part, via the release of a physiological inhibition of full keratinization and via an aberrant differentiation of progenitor cells. Increased viscosity of meibum through qualitative changes of its composition is the other important causative factor that contributes to the obstructive process. It may occur independently, because of the influence of endogenous or exogenous factors or a preexisting obstructive stasis of secretum. Obstruction leads on the one hand (left effector limb arrow) to the immediate clinically observable low delivery of meibum onto the lid margin and tear film that results in an evaporative dry eye condition. On the other hand (right effector limb arrow), obstruction also results in several consecutive negative effects directly inside the meibomian glands, because of an internal stasis of meibum. Stasis can be associated with increased viscosity of the meibum, which reinforces the obstruction in a vicious circle. The continuous secretory activity of the meibocytes leads to a progressive increase in pressure within the glands. This increased pressure can, in another vicious circle, induce an activation of the epithelial cells that reinforces hyperkeratinization. Pressure further leads to a dilatation, first of the ductal system and, after a prolonged time, also to atrophy of the acini, with rarefaction of their secretory meibocytes, and thus results in a secondary hyposecretion with low secretion of lipids. Atrophy may be the reason for the clinically detectable gland dropout, and CL wear is, by presently unknown mechanisms, associated with gland dropout. Stasis of meibum also promotes the growth of bacteria on the ocular surface and possibly inside the glands, usually pre-existing commensals, that produce lipid-degrading enzymes. Their action on the meibomian lipids leads to the production of toxic mediators, such as free fatty acids, that may initiate subclinical inflammatory reactions with release of inflammatory cytokines. Toxic and inflammatory mediators may promote subclinical inflammatory events inside the gland, in the periglandular conjunctiva, on the lid margin, and on the ocular surface, as suggested by observations in dermatology (e.g., in acne pathogenesis and skin irritation). Toxic mediators are also assumed to have negative effects on tear film stability. Furthermore, they can lead to qualitative changes in the composition of meibum that increase its viscosity or, through activation of epithelia on the lid margin and possibly inside the gland, they can reinforce keratinization. Altogether, these events can give rise to several vicious circles (red arrows) that increase the preexisting obstruction, if not limited by timely diagnosis and therapeutic intervention. There is evidence from a mouse model that acinar atrophy may also occur due to the aging process. If MGD occurs in conjunction with systemic skin diseases such as seborrheic dermatitis, possibly accompanied by blepharitis, an increased amount of oil (seborrhea) with decreased viscosity can be observed on the lid margin. Seborrheic blepharitis, similar to stasis, can be associated with increased bacterial growth and its downstream negative effects. The seborrheic oil has a different composition than that of normal meibum and thus may have negative effects on the tear film. All major mechanisms of the schematically depicted process are supported by findings in the literature. Reprinted from Knop E, Knop N. [Meibomian glands, Part IV: functional interactions in the pathogenesis of meibomian gland dysfunction (MGD).] Meibom-Drüsen, Teil IV: Funktionelle Interaktionen in der Pathogenese der Dysfunktion (MGD). Ophthalmologe. 2009;106:980–987 with the kind permission of Springer Science and Business Media.
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