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At least 19 recordsLinked to original sources
PubMed2006

Identification of steroidogenic enzyme mRNAs in the human lacrimal gland, meibomian gland, cornea, and conjunctiva.

PURPOSE: Sex steroids exert a significant influence on the health and well-being of the ocular surface and adnexa. These hormones affect multiple aspects of the lacrimal and meibomian glands, conjunctiva, and cornea, and have been linked to the development of many ocular surface pathologies. We hypothesize that these hormone actions, as in other tissues, occur predominantly after the local synthesis of androgens and estrogens from adrenal precursors. To begin to test this hypothesis, we analyzed whether human ocular surface and adnexal tissues and cells contain the steroidogenic enzyme mRNAs necessary for the intracrine synthesis and metabolism of sex steroids. METHODS: Total RNA was isolated from human lacrimal and meibomian glands and immortalized corneal and conjunctival epithelial cells. Samples were reverse transcribed to cDNA and analyzed for the presence of enzyme mRNAs by real-time PCR. Positive and negative controls included human placental cDNA and the absence of template, respectively. RESULTS: Our results show that human lacrimal and meibomian glands and corneal and conjunctival epithelial cells contain the mRNAs for steroid sulfatase, 3beta-hydroxysteroid dehydrogenase (HSD)-Delta-Delta-isomerase type 1, 17beta-HSD types 1 and 3, aromatase, and glucuronosyltransferase. In contrast, only lacrimal and meibomian tissues appeared to contain detectable mRNA for sulfotransferase. CONCLUSIONS: If the corresponding mRNAs are translated, our results indicate that human ocular surface and adnexal tissues contain the enzymatic machinery necessary for the intracrine synthesis and metabolism of sex steroids.

17-Hydroxysteroid Dehydrogenases↗
PubMed1989

Meibomian gland dysfunction. III. Meibomian gland lipids.

The lipid components of meibomian gland excreta were evaluated in rabbits after they received 2% topical epinephrine dropped into their eyes daily for a period of 6 months to a year to induce meibomian gland dysfunction (MGD). Changes were compared to excreta obtained from seven age-matched, untreated control rabbits. Comparison of the lipids from MGD lids with lipids obtained from control rabbits revealed, for clinically evident MGD, a marked increase in the lipids that are uniquely characteristic of epidermal tissue. These epidermal lipids are free sterols (large amounts) and a group of seven types of ceramides. The data are consistent with the hypothesis that the initiating factor of rabbit MGD is hyperkeratinization of the ductal epithelia. For clinically apparent MGD some hydrolysis of the sterol esters of the meibomian gland lipids also seems to have occurred. This was evidenced by the formation of an 8-fold increase in a cluster of anteiso fatty acids with chain lengths longer than C20 in the free fatty acid fraction. This group of free fatty acids was the same as the acids esterified to the sterol esters. We could detect no change in the lipid excreta obtained from rabbits that developed only subclinical MGD, consisting of orifice plugging and dilation of the duct.

Animals↗
PubMed1982

In vivo biomicroscopy and photography of meibomian glands in a rabbit model of meibomian gland dysfunction.

The usefulness of transillumination and biomicroscopy of the lid margin in assessing meibomian gland dysfunction was studied in a rabbit model. Transillumination of rabbit lids treated with topical epinephrine for 2 to 3 months revealed plugging of the meibomian gland orifice. Plugging appeared to be correlated histopathologically with increased thickness and hyperkeratinization of the ductal epithelium at the orifice. Continued treatment resulted in microcystic changes within the duct, which were not easily discernible by routine examination without the aid of a transilluminator. Cystic changes were correlated with dilation of the duct by retained desquamated cornified cells. Biomicroscopy proved valuable in identifying and documenting early lesions associated with epinephrine-induced meibomian gland dysfunction.

Animals↗
PubMed1992

Age-related morphological changes in lid margin and meibomian gland anatomy.

Meibomian gland dysfunction (MGD) is responsible for recurrent irritative symptoms. Attempts to characterize MGD have largely concentrated on microbial and lipid abnormalities in meibomian gland secretions. Few reports describe histological abnormalities in this disease, and fewer still morphological changes. This article follows a previous study that established a classification for MGD. This was based on morphological changes in the meibomian gland and lid margin. Using this classification, we studied the age-related changes in 80 subjects, between 5 and 87 years of age without ocular disease. The lid margin became thicker after childhood. Lid margin vascularity and cutaneous hyperkeratinization increased with age in both lids, whereas, telangiectasia increased with age in the lower lid and squamous blepharitis and posterior lid margin rounding were more common after 50 years of age in the upper lid. Multiple rows of meibomian gland orifices occurred more frequently in the upper than lower lid, and orifice narrowing and pouting increased with age. No age-related changes in the shape or form of the mucocutaneous function, gland ducts, or acini were found. Meibomian gland secretions were less easily expressed in the elderly. We have attempted to define a normal range of lid morphology in healthy children and adults that we believe to be important for the subsequent definition of lid disease, and in particular, posterior blepharitis.

Adolescent↗
PubMed2003

Minocycline effect on meibomian gland lipids in meibomianitis patients.

The objective of this research was to determine the effect of oral minocycline on the meibomian gland nonpolar and free fatty acid lipids of chronic blepharitis patients. Patients--seborrheic blepharitis (SBBL), acne rosacea (AR) without ocular involvement, and acne rosacea with meibomianitis (AR-MKC). Minocycline treatment--50mg orally for 2 weeks followed by 100mg to the end of 3 months; this was followed by 3 more months with no treatment. Meibomian gland secretions (meibum) were collected before treatment, at the end of the 3 months on treatment, and 3 months after stopping treatment. Lipids were separated and analyzed for wax and sterol esters, triglycerides, diglycerides, free cholesterol and free fatty acids. Data were analyzed statistically by ANOVA. Minocycline treatment resulted in decreased diglycerides and free fatty acids in the group AR-MKC, which continued into the second 3 months (off treatment) and was significant. Cholesterol decreased, but triglycerides initially decreased with treatment and then increased when treatment in the group was discontinued (second 3 months); these results, however, were not significant. Thus, minocycline has its greatest effect on lipid types, which result from degradation (lipase) reactions, suggesting a lipase inhibition effect and/or direct effect on ocular flora. This minocycline effect continues even after treatment is discontinued, suggesting a more lasting effect on ocular microflora. Minocycline may be most effective when the treatment period is longer than 3 months. These results give insight into disease mechanisms associated with chronic blepharitis.

Analysis of Variance↗
PubMed1989

Meibomian gland dysfunction. I. Keratin protein expression in normal human and rabbit meibomian glands.

The expression of keratin proteins from meibomian glands and their correlation with skin epidermal keratins were determined. Keratin proteins were localized in both human and rabbit meibomian glands by indirect immunofluorescence using mouse monoclonal antibodies AE1, AE2 and AE3, which are known to react with human epidermal keratins as well as with keratins from other sources. Keratin proteins from rabbit meibomian glands were further isolated and characterized by SDS-PAGE and immunoblot using mouse monoclonal antibodies AE1 and AE3. Meibomian glands from human and rabbit showed similar immunofluorescent staining with each monoclonal antibody. AE1 antibody, which stains human basal epithelial cells of skin, stains all duct epithelial cells in the human but only the superficial duct epithelial cells in the rabbit meibomian gland. AE2 antibody, which stains human suprabasal epithelial cells of skin and is a marker for fully keratinized epithelia, stains the suprabasal epithelial cells of the central duct and ductules in both the human and rabbit meibomian gland. AE3 antibody, which stains all human epithelial cells of skin, stains all epithelial cells of the duct and ductules, as well as the basal epithelial cells of the acinus in both the human and rabbit meibomian gland. Keratins isolated from whole rabbit meibomian glands contained a 65-67 kD and 58 kD AE3-positive, and a 56.5 kD and 50 kD AE1-positive keratin protein. Expression of 65-67 kD/56.5 kD keratin proteins, and the immunofluorescent staining of the duct epithelium by the AE2 antibody, indicate that the meibomian gland duct epithelium is committed to the process of keratinization.

Animals↗
PubMed1991

Intracranial extension of meibomian gland carcinoma.

Meibomian gland carcinomas are rare, slow-growing masses that clinically mimic several benign and malignant processes. We report a patient with sebaceous carcinoma of the meibomian gland with intracranial extension and dural invasion, and discuss the clinical and pathological features of this uncommon entity.

Brain Neoplasms↗
PubMed2000

Immunohistochemical evidence for estrogen receptors in meibomian glands.

PURPOSE: To look for sex hormone receptor distribution in three structures contributing to the normal human tear film: the conjunctiva, the accessory lacrimal glands, and the meibomian glands. DESIGN: An immunohistochemical study. TISSUES AND CONTROLS: Forty-one upper eyelid specimens were collected from 15 male and 26 female patients (age range, 1.5-85 years) during blepharoptosis surgery via posterior tarsoconjunctival mullerectomy (Fasanella-Servat or Gavaris). In addition, control sections of histologically normal breast, prostate, and skin tissue were obtained. METHODS: Immunohistochemical staining using mouse monoclonal antibodies against estrogen, progesterone, and androgen receptors was performed on all tissues and controls. Quantitation of the receptors was performed and expressed as percentage nuclear positivity. Specimens were divided into three groups based on the age of the patient: <12 years (n = 9); 18-55 years (n = 1); >55 years (n = 12). RESULTS: Forty-one specimens contained conjunctiva. All were negative for estrogen, progesterone, and androgen receptors. Twenty-four specimens contained accessory lacrimal glands of Wolfring. All were negative for the three receptors. Twenty-two specimens contained meibomian glands. All were positive for estrogen receptors; one was positive for progesterone receptors and one for androgen receptors. Using Minitab statistical software (Minitab Inc. State College, PA), analysis of variation revealed no statistical difference between sexes or between age groups studied. The sebaceous glands of skin were uniformly positive for androgen receptors. Sebaceous glands of the face and scalp (3 of the 15 skin samples) were also positive for estrogen receptors. CONCLUSIONS: Estrogen receptors are present in the meibomian glands of the upper eyelid. Unlike sebaceous glands elsewhere on the skin, the meibomian glands lack androgen receptors. Estrogen receptors may play a role in modulation of the lipid layer of the tear film, and their activity may be linked to meibomian gland dysfunction and dry eye syndrome.

Adolescent↗
PubMed1985

In vivo transillumination biomicroscopy and photography of meibomian gland dysfunction. A clinical study.

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.

Eyelid Diseases↗
PubMed1996

Meibomian gland phospholipids.

The content of the meibomian gland lipid exprimate is known, but little is known about the phospholipids that comprise the glandular cells. The purpose of the present study is to identify and quantitate the phospholipid complement of the meibomian gland cells that produce the lipid secretion of meibomian oil and which is vital to tear film stability. Eyelids (n = 50) were excised from rabbits, and after surgical removal of surrounding tissues, the tarsal plates with and without expressing meibomian oil were extracted and phospholipids of the plates quantified by 31P nuclear magnetic resonance (NMR). Seventeen phospholipids were quantified from tarsal plates expressed of oil and tarsal plates containing meibomian oil: alkylacylphosphatidylcholine (AAPC), dihydrosphingomyelin (DHSM), dimethylphosphatidylethanolamine, diphosphatidylglycerol (cardiolipin), ethanolamine plasmalogen (EPLAS), lysoethanolamine plasmalogen, lysophosphatidylcholine, lysophosphatidylethanolamine, lysophosphatidylserine, phosphatidic acid, phosphatidylcholine (PC), phosphatidylethanolamine (PE), phosphatidylglycerol, phosphatidylinositol, phosphatidylserine, sphingomyelin (SM), sphingosylphosphorylcholine. The six zwitterionic and neutral phospholipids, DHSM, EPLAS, PE, SM, AAPC, and PC together comprise 79.5% of the total meibomian gland phospholipid profile (in meibomian oil this value is 84.2%). The zwitterionic and neutral phospholipids dominate meibomian gland phospholipid profiles. Since the meibomian gland cells undergo holocrine secretion and form the meibomian glad secretion, such a composition is consistent with the hypothesis that a chemically stable lamellar surfactant layer phospholipids bind non-polar meibomian oil to the aqueous layer of the tear film.

Animals↗
PubMed1985

Biosynthesis of lipids by bovine meibomian glands.

Isolated bovine meibomian glands incorporated exogenous [1-14C]acetate into lipids. Thin layer chromatographic analysis of the lipids showed that wax esters and sterol esters contained 61% of the total label. Radio gas liquid chromatographic analysis of the acid and alcohol moieties of both ester fractions showed the label was distributed equally between the two portions of the ester in both cases. Cholesterol and 5-alpha-cholest-7-en-3 beta-ol were the major labeled sterols, and anteiso-C25, anteiso-C27 and anteiso-C23 were the most highly labeled alcohols. The major labeled fatty acids in the wax esters were anteiso-C15, n-C16, anteiso-C17 and n-C18:1, whereas anteiso-C25 and anteiso-C27 were the major labeled acids in the sterol esters. The diester region with 6% of the total label contained labeled fatty acids and fatty alcohols each with anteiso-C25 as the major component and omega-hydroxy acids in which n-C32:1 was the major labeled component. The triglyceride fraction which contained 8% of the total lipids was composed of labeled fatty acids similar to those found in both sterol and wax ester fractions. Chromatographic analyses of the labeled lipids derived from exogenous labeled isoleucine showed that anteiso-branched products were preferentially labeled. The labeled triglyceride fraction derived from [U-14C] isoleucine also contained esterified C15, C13, C11, C9, C7 and possibly shorter anteiso-branched acids.

Acetates↗
PubMed2002

Anatomy and histopathology of human meibomian gland.

PURPOSE: To investigate histopathologic changes in human meibomian gland. METHODS: Human meibomian gland samples were obtained at autopsy from 50 men and 33 women aged from 17 to 87 years with a mean age (+/- SD) of 61 +/- 13 years. Pieces of tarsal plate measuring 3 x 3 mm including meibomian glands were excised from the center of both upper eyelids, then fixed and embedded in paraffin. Sections 4-microm thick were stained with hematoxylin and eosin and periodic acid-Schiff. Light microscopy was used to observe any histopathologic changes. RESULTS: The following histopathologic changes were observed: (1) cystic dilatation of acini and/or ducts, (2) atrophy of acini, (3) basement membrane thickening of acini, (4) granulation tissue, and (5) lipogranulomatous inflammation. CONCLUSION: Various histopathologic changes were observed in the human meibomian gland. Hyperkeratinization of ductal epithelium and atrophy of acinar cells may cause meibomian gland dysfunction.

Adolescent↗
PubMed2006

Canine meibometry: establishing baseline values for meibomian gland secretions in dogs.

Meibomian lipid secretions are essential in preventing tear evaporation. Disorders of the meibomian glands may therefore play an important role in the pathogenesis of some forms of keratoconjunctivitis sicca (KCS). Until now, meibomian lipid secretions have never been quantitatively evaluated in dogs. With the aim of establishing baseline values of canine meibomian lipid secretions, meibometry was conducted in 42 healthy dogs, 16 of which were Miniature Schnauzers. The mean meibomium level in 84 eyes of the 42 dogs was 179+/-60 Meibometer units. Age, gender and side did not affect the results. However, meibomium levels were significantly lower in the Miniature Schnauzers, a breed that is susceptible to KCS, compared to other breeds. This report demonstrates that meibometry is a simple and minimally invasive technique that may be readily used in conscious dogs to quantify meibomian gland secretions and explicate tear film dynamics in normal and dry canine eyes.

Animals↗
PubMed1985

Fatty acid chain elongation by microsomal enzymes from the bovine meibomian gland.

The composition of meibomian gland lipids suggested that fatty acid chain elongation might play a major role in the synthesis of such lipids. A fatty acid synthase preparation from the bovine meibomian gland catalyzed the formation of C16 acid and the enzyme was immunologically quite similar to that in the mammary gland. The microsomal fraction from the gland, on the other hand, catalyzed elongation of endogenous fatty acids in the presence of ATP and Mg2+ and of exogenous C18-CoA using malonyl-CoA and NADPH as the preferred reductant. The elongated products, ranging up to C28 in chain length, were found mainly as CoA esters and products derived from them. With C18-CoA as the exogenous primer, the elongation rate was linear with incubation time up to 20 min but the rate changed in a sigmoidal manner with increasing protein concentration. The elongation rate was maximal at a pH around 7.0. Typical Michaelis-Menten-type substrate saturation patterns were observed with both malonyl-CoA and NADPH. From linear double-reciprocal plots, the Km values for the two substrates were calculated to be 52 and 11 microM, respectively, with a V of about 340 pmol min-1 mg protein-1 with respect to malonyl-CoA. Exogenous CoA esters of C16 to C22 fatty acids were elongated to give products up to C28 without exhibiting any preference for the primer. The present elongation system could account for the formation of most of the very long chains found in meibomian lipids.

Adenosine Triphosphate↗
PubMed1993

Ocular evaporation in meibomian gland dysfunction and dry eye.

BACKGROUND: Secretions from the meibomian gland are believed to be important in reducing ocular surface water evaporation and preventing dry eye. Patients with blepharitis frequently have meibomian gland dysfunction with loss of meibomian glands (drop out). The authors hypothesized that dry eye that often occurs in patients with chronic blepharitis is secondary to increased evaporation associated with gland loss. METHODS: The authors measured the ocular surface water evaporation and tear osmolarity of patients with meibomian gland drop out and patients with gland drop out with a low Schirmer test. These findings were compared with those of a control group. RESULTS: The authors found that eyes with meibomian gland drop out and those with drop out and a low Schirmer test had a significantly higher evaporative rate at 30% relative humidity (average, 49.9 +/- 21 x 10(-7) g/cm2/second, or 0.49 +/- 0.29 microliters/minute evaporative loss per eye, and 59.1 +/- 28 x 10(-7) g/cm2/second, or 0.58 +/- 0.23 microliters/minute, respectively) when compared with those in the control group (average, 14.8 +/- 6 x 10(-7) g/cm2/second, or 0.15 +/- 0.07 microliters/minute [P < 0.05]). There was a significant correlation between evaporative rate and gland drop out (r = 0.522). CONCLUSION: Patients with meibomian gland drop out, and especially those with low tear production by Schirmer test, have an increased risk of dry eye developing through increased evaporation.

Adult↗
PubMed2004

[Ocular surface temperature of meibomia gland dysfunction patients and the melting point of meibomian gland secretions].

PURPOSE: Since meibomian gland dysfunction (MGD) is thought to be caused by raising of the melting point and degeneration of lipid secretions, the melting point of secretions and the temperature of the ocular surface were investigated. SUBJECTS AND METHODS: Twenty-three patients with MGD [mean age 69.3 +/- 7.2 (mean standard deviation) years) were examined. Seven subjects without MGD (mean age 32.5 +/- 5.8 years) were also observed as controls. METHODS: Solid secretions obtained from MGD patients were heated and the melting point was measured. The weight ratio of lipids and cell components was also determined. RESULTS: Corneal temperature was 32.3 +/- 0.5 (mean +/- standard deviation) degrees C and eyelid temperature was 33.1 +/- 0.5 degrees C in the control subjects. Corneal temperature was 31.1 +/- 0.8 degrees C and eyelid temperature was 32.7 +/- 0.6 degrees C in MGD patients. However, the melting point of the secretions was 34.0 +/- 1.3 degrees C, which was higher than the temperature of the ocular surface and eyelid in both patients and controls. The cell components constituted about 60% of the secretions and the lipid composition, about 40%. CONCLUSION: The cause of MGD is thought to be solid ification of lipids because of elevation of the melting point and the increase in the cell components of the secretions.

Adult↗