In Vivo Transillumination Biomicroscopy and Photography of Meibomian Gland Dysfunction

In Vivo Transillumination Biomicroscopy and Photography of Meibomian Gland Dysfunction

In Vivo Transillumination Biomicroscopy and Photography of Meibomian Gland Dysfunction A Clinical Study JEFFREY B. ROBIN, MD, JAMES V. JESTER, PhD, JA...

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In Vivo Transillumination Biomicroscopy and Photography of Meibomian Gland Dysfunction A Clinical Study JEFFREY B. ROBIN, MD, JAMES V. JESTER, PhD, JANIS NOBE, MD, NICHOLAS NICOLAIDES, PhD, RONALD E. SMITH, MD

Abstract: Meibomian gland transillumination biomicroscopy and infrared photography were performed on 18 patients with clinically evident meibomian gland dysfunction (MGD) and dermatologic rosacea, 22 patients having MGD without evidence of dermatologic rosacea, and 15 unaffected individuals who served as controls. All patients having clinical signs of MGD demonstrated morphologic abnormalities of their meibomian glands by transilluminated biomicroscopy. Patients without dermatologic rosacea were noted to have varying degrees of gland distortion. Moreover, infrared photography documented a loss of the normal grape-like clusters of dark spots that represent the gland, suggesting a loss of glandular acini. Patients with dermatologic rosacea had more severe alterations, including marked distortion and loss of normal gland anatomy. There were no such abnormalities in clinically unaffected individuals. These data demonstrate that transilluminated biomicroscopy and infrared photography have the ability to identify a spectrum of morphologic alterations of the meibomian glands in MGD patients. The authors suggest that these techniques could be used to classify clinical MGD based upon the presence or absence of identifiable meibomian gland abnormalities. [Key words: blepharitis, chalazia, infrared photography, meibomian glands, ocular lipids, ocular rosacea, rosacea, seborrheic dermatitis, transillumination biomicroscopy.] Ophthalmology 92:1423-1426, 1985

Dysfunction of the meibomian glands has been suggested as an important factor in the pathogenesis of several From the Department of Ophthalmology, University of Southern California, and the Estelle Doheny Eye Foundation, Los Angeles. Presented at the Eighty-eighth Annual Meeting of the American Academy of Ophthalmology, Chicago, Illinois, October 30-November 3, 1983. Supported in part by a Postdoctoral Fellowship Grant from Fight for Sight, Inc., (Dr. Robin) National Institutes of Health grant R01 EY 04455, and Fight for Sight Grant In Aid G 694. Reprint requests to Ronald E. Smith, MD, Department of Ophthalmology, Estelle Doheny Eye Foundation, 1355 San Pablo Street, Los Angeles, CA 90033.

ocular conditions, including chronic blepharitis, t-4 ocular rosacea, 5-8 chalazia, 9 and even contact lens intolerance. 10 Recently, meibomian glands have been implicated in lid margin disease associated with dermatologic conditions involving the sebaceous glands, particularly acne rosacea.2·4 Borrie, 6 in 1953, noted that a blepharitis involving the meibomian glands occurred in nearly I 00% of patients having dermatologic rosacea. Furthermore, ocular abnormalities preceded the development of dermatologic signs in 20% of his patients. The term "meibomian gland dysfunction (MGD)" 11 has been used to describe the spectrum of clinically observed meibomian gland abnormalities previously de1423

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Fig 1. Transilluminati on biomicroscopy and photography of the lower lid meibomian glands were performed by everting the lower eyelid with the transilluminato r probe.

2 scribed as "meibomitis" or "meibomianitis". Although we prefer entities, these terms describe essentially the same no conis there because dysfunction" "meibomian gland sistent evidence of actual glandular inflammation in these conditions. Recently, an experimental model of MGD in rabbits 12 was developed in our laboratory. By modifying a system of transillumination biomicroscopy and infrared photog13 raphy originally described by Tapie, we were able to document in vivo the morphologic alterations of mei12 bomian glands in experimental MGD. Based upon studies using these techniques, we describe the meibomian gland morphologic alterations in a series of clinically identified MGD patients, both with and without dermatologic rosacea.

MATERIALS AND METHODS Fifty-five individuals were included in this study. Forty of these patients had been referred to the Estelle Doheny Eye Foundation/University of Southern California with the diagnosis of blepharitis. Upon routine slit-lamp examinations, they were noted to have clinical signs consistent with a diagnosis of meibomian gland dysfunction: inspissation of the orifices of the meibomian glands, dilatation of the meibomian glands, thickening of the eyelid margins, foamy tears, chalazia, and injection of the palpebral and bulbar conjunctival blood vessels. The remaining 15 subjects were volunteers who had no ocular abnormalities on clinical examination. Of the 40 patients with MGD, 18 also had dermatologic 7 rosacea. Clinical diagnosis of rosacea was established by involving the flush signs following the presence of the areas of the face: erythema, telangiectasia, hypertrophic sebaceous glands, and pustules of the skin. In addition to complete ocular examinations, all subjects in this study underwent transilluminated slit-lamp 1424

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Fig 2. Morphologic characteristics of normal lower lid meibomian glands as demonstrated by transilluminated slit-lamp infrared photography. The gland complexes, which are thin and relatively straight, consist of clusters of small dark spots (arrowhead) surrounding ducts (arrow). Because the ducts transmit light, they are not distinct on infrared photographs. The clusters of small dark spots probably represent acini.

biomicroscopy of their meibomian glands. Using an OS300 1 transilluminator (Medical Instrument Research Associates, Inc., Boston, MA), the lower lid was gently everted using the transilluminator probe, thus allowing direct visualization of the meibomian glands through the palpebral conjunctiva (Fig 1). Meibomian gland morphology was documented photographically under transilluminated biomicroscopy by a Zeiss photo slit lamp using high-speed infrared Kodak film (HIE 135-20) exposed at 1/60 sec at a setting off/32. This system has been previously noted to provide excellent reproduction of mei· bomian gland structure. 12

RESULTS By transillumination biomicroscopy, normal meibo~ mian glands appeared as long, straight, narrow grape-like clusters of numerous, small, dark (hypotransilluminescent) spots (Fig 2), probably representing individual acini. Both the long central duct and the orifice of each gland appeared to transmit light and were therefore not seen by infrared photography. There appeared to be little variation in gland morphology between all 15 normal subjects. There was only minimal distortion of the direction of the glands. By clinical slit-lamp examination, all 18 patients having MGD and dermatologic rosacea had narrowing or occlusion of the gland orifices, as well as dilatation and distortion of the glands. Chalazia were noted in seven patients. Transillumination biomicroscopy of these patients revealed severe morphologic abnormalities of the meibomian glands, including marked loss of visible gland structures, particularly the clustered dark (hypotransilluminescent) spots (Fig 3). Moreover, the remaining discernible glands had indistinct structures and were reduced in size.

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BIOMICROSCOPY OF MEIBOMIAN GLANDS

Fig 3. Slit-lamp infrared photograph demonstrating lower lid meibomian glands in a patient with meibomian gland dysfunction and dermatologic rosacea. The glands that can be seen are dilated and distorted (arrow). However. most of the lid is devoid of visible gland complexes. Several microcysts (arrowhead), appearing as larger round spots, are noted.

Fig 4. Slit-lamp infrared photograph of lower lid meibomian glands in a patient having meibomian gland dysfunction without dermatologic rosacea. The gland complexes are mildly dilated and distorted (arrow). There is, however, no significant area of lid devoid of visible glands. Two microcysts are noted (arrowhead).

Chalazia appeared as large, round, dark (hypotransilluminescent) areas. Milder abnormalities were noted in the 22 MGD patients without dermatologic rosacea. Clinically, lids were characterized by consistent glandular enlargement and occasional orifice narrowing or occlusion. No chalazia were seen in these patients. By transillumination biomicroscopy, some meibomian glands appeared shortened and had fewer dark spots (Fig 4). Other glands appeared enlarged and distorted, particularly at their distal ends. Although no chalazia were noted, several patients had isolated enlarged dark areas that may be microchalazia or microcysts, but their exact histopathologic composition is unknown.

loss of gland visualization by infrared photography strongly suggests an altered function of the gland. We therefore believe that use of the term "meibomian gland dysfunction" (MGD) 14 to describe this entity/condition is appropriate, in spite of the fact that the exact pathophysiology is unknown. Overall, the spectrum of in vivo abnormalities documented in this report corresponds well with the histopathologic meibomian gland alterations noted in clinical 10•14 and experimental 12 MGD. We can only speculate as to the underlying mechanism involved in the loss of normal meibomian gland morphology. Evidence suggests that keratinization of the meibomian duct epithelium may be an important factor. 2·3 • 10- 14 Gutgesell and coworkers, 14 in a histopathologic study of seven patients with MGD, found signs of obstruction and dilatation of meibomian gland ducts, along with acinar enlargement and hyperkeratinization of the duct epithelium. In an experimental model of MGD, we noted similar histopathologic abnormalities, particularly ductal dilatation and hyperkeratinization. 15 Further support for the role of hyperkeratinization in MGD comes from experimental and clinical studies of polychlorinated biphenyl (PCB) intoxication.16 Exposure to PCB appears to result in marked keratinization of the meibomian gland duct epithelium and, clinically, a severe blepharoconjunctivitis is noted. These observations concerning MGD and keratinization of the meibomian gland may be the counterpart to the well recognized relationship between skin disease and sebaceous gland dysfunction. Knutson 17 has shown that keratinization of the sebaceous gland duct leading into the pilosebaceous canal is the critical step in the development of clinical acne vulgaris. In conclusion, meibomian gland transillumination biomicroscopy and infrared photography appear to be sensitive techniques for identifying and documenting morphologic abnormalities of the meibomian glands.

DISCUSSION Using a modified system of transillumination biomicroscopy and infrared photography, we were able to demonstrate a spectrum of morphologic alterations in the meibomian glands of patients with clinical MGI). In the mildest form, these alterations/changes consisted of irregularity and distortion of the distal portion of the glands, along with a mild loss of what appeared to be the acinar component of the meibomian glands. More severe involvement included complete loss of visualization of the gland and development of isolated enlarged dark spots. The latter probably represents either microchalazia or microcysts of the glands. It is not possible to tell by transillumination alone if the loss in visualization of the grape-like clusters of dark spots represents an actual loss of the meibomian glands. However, based on animal studies, 12 areas represented by the small dark spots appear to correlate with the acinar components of the meibomian glands, ie. sites for lipid production. Based on these findings, we conclude that the

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These techniques appear to be less subjective and may provide a greater degree of detail than does slit-lamp examination.

REFERENCES 1. Keith CG. Seborrhoeic blepharo-kerato-conjunctivitis. Trans Ophthalmol Soc UK 1967; 87:85-103. 2. McCulley JP, Dougherty JM, Deneau DG. Classification of chronic blepharitis. Ophthalmology 1982; 89:1173-80. 3. McCulley JP, Sciallis GF. Meibomian keratoconjunctivitis: oculo-dermal correlates. CLAO J 1983; 9:130-2. 4. McCulley JP, Sciallis GF. Meibomian keratoconjunctivitis. Am J Ophthalmol1977; 84:788-93. 5. Cory CC, Hinks W, Burton JL, Shuster S. Meibomian gland secretion in the red eyes of rosacea. Br J Dermatol1973; 89:25-7. 6. Borrie P. Rosacea with special reference to its ocular manifestations. Br J Dermatol 1953; 65:458-63. 7. Brown Sl, Shahinian L Jr. Diagnosis and treatment of ocular rosacea. Ophthalmology 1978; 85:779-86.

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8. Starr PAJ, Macdonald A. Oculocutaneous aspects of rosacea. Proc R Soc Med 1969; 62:9-11. 9. Lempert SL, Jenkins MS, Brown Sl. Chalazia and rosacea. Arch Ophthalmol1979; 97:1652-3. 10. Henriquez AS, Korb DR. Meibomian glands and contact lens wear. Br J Ophthalmol1981; 65:108-11. 11. Jester JV, Nicolaides N, Smith RE. Meibomian gland studies: histologic and ultrastructural investigations. Invest Ophthalmol Vis Sci 1981; 20: 537-47. 12. Jester JV, Rife L, Nii D, et al. In vivo biomicroscopy and photography of meibomian glands in a rabbit model of meibomian gland dysfunction. Invest Ophthalmol Vis Sci 1982; 22:660-7. 13. Tapie R. Etude biomicroscopique des glandes de Meibomius. Ann Oculist 1977; 210:637-48. 14. Gutgesell VJ, Stern GA, Hood Cl. Histopathology of meibomian gland dysfunction. Am J Ophthalmol1982; 94:383-7. 15. Ehlers N. The precorneal film; biomicroscopical, histological and chemical investigations. Acta Ophthalmol 1965; Suppl 81. 16. Ohnishi Y, Kohno T. Polychlorinated biphenyls poisoning in monkey eye. Invest Ophthalmol Vis Sci 1979; 18:981-4. 17. Knutson DD. Ultrastructural observations in acne vulgaris: the normal sebaceous follicle and acne lesions. J Invest Dermatol1974; 62:288307.