Disease relevance of Meibomian Glands

• In the eyelid, Meibomian glands were uniformly negative for 15-lipoxygenase-2 in all cases examined (n = 9), and sebaceous carcinomas apparently derived from Meibomian glands were also negative (n = 12) [1].
• 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 [2].
• At a speed similar to that of leucocyte traffic in the retina, normal mucins caused a decrease in neutrophil cathepsin G fluorescence, a decrease that was not observed with mucins from patients with Meibomian gland disease or Sjogren syndrome [3].
• In this study, we analyzed the triglyceride fraction of human meibomian gland secretions to determine whether specific fatty acids were significantly associated with specific chronic blepharitis disease groups [4].
• CONCLUSION: Our results suggest that androgen insensitivity may promote meibomian gland dysfunction and an increase in the signs and symptoms of dry eye [5].

High impact information on Meibomian Glands

• In addition to atrophic sebaceous glands, the meibomian glands were also found to be severely atrophic in APOC1 transgenic mice [6].
• These findings suggest that intact ocular surface health is EDA dependent and that Tabby corneal abnormalities are not solely dependent on meibomian gland lipid secretion [7].
• The FAR2 mRNA was more restricted in distribution and most abundant in the eyelid, which contains wax-laden meibomian glands [8].
• Effect of androgen deficiency on the human meibomian gland and ocular surface [9].
• Moreover, meibomian gland secretions were obtained from each eye and analyzed by high-performance liquid chromatography/mass spectrometry for the relative content of cholesterol, cholesterol esters, wax esters, diglycerides, triglycerides, and specific molecular species in the diglyceride fraction [9].

Chemical compound and disease context of Meibomian Glands

• The effects of tetracycline and meibomian gland expression therapy also were investigated in patients with ocular rosacea [10].
• OBJECTIVE: To investigate the efficacy of topical cyclosporine A 0.05% (tCsA) (Restasis, Allergan Pharmaceuticals) in the treatment of meibomian gland dysfunction (posterior blepharitis) [11].
• We are unaware of any previously reported cases of DLE presenting with discoid eyelid lesions associated with staphylococcal blepharitis and Meibomian gland dysfunction [12].

Biological context of Meibomian Glands

• Strikingly, both corneal defects and inflammation were prevented in Tabby mice bearing a transgene for the Eda-A1 isoform, but meibomian glands were restored little if at all [7].
• Consistent with the composition of the meibomian gland secretion, exogenous acyl-CoA longer than C14 and shorter than C20 gave maximal rates of esterification of hexadecanol [13].
• Moreover, androgens appear to modulate lipid production and gene expression in mouse and/or rabbit meibomian glands; and (2) androgen deficiency may lead to meibomian gland dysfunction, altered lipid profiles in meibomian gland secretions, tear film instability, and evaporative dry eye [14].

Anatomical context of Meibomian Glands

• We conclude that hyperkeratinization of the duct epithelium leading to plugging and dilation of the meibomian gland underlies the development of MGD following topical epinephrine treatment [15].
• On slit-lamp examination severe meibomian gland dysfunction, loss of eyelashes, decreased tear meniscus, diffuse corneal vascularization, and delayed punctate fluorescein staining of corneal epithelium were detected [16].
• Lacrimal secretion is under cholinergic control and modulated by sympathetic adrenergic, peptidergic (VIP) and humoral influences; the meibomian glands are innervated, but the goblet cells are not [17].
• The changes in the eyelids were characterized by hyperkeratosis, with accumulations of keratin in hair follicles of the epidermis and squamous metaplasia with keratin cysts in the tarsal glands [18].
• RESULTS: Our findings showed that androgen, estrogen and/or progesterone receptor mRNAs are present in the lacrimal gland, lacrimal gland acinar epithelial cells, meibomian gland, lid, palpebral and bulbar conjunctivae, cornea, iris/ciliary body, lens, retina/uvea, retina/choroid and retinal pigment epithelial cells of rats, rabbits or humans [19].

Associations of Meibomian Glands with chemical compounds

• Dry-eye signs, including tear-film breakup time, Schirmer test result, score for fluorescein staining of the cornea, and meibomian gland dysfunction, were assessed [20].
• Biomicroscopy proved valuable in identifying and documenting early lesions associated with epinephrine-induced meibomian gland dysfunction [21].
• The model supports previous observations by the authors that systemic 13-cis-retinoic acid affects meibomian gland structure in a laboratory animal [22].
• CONCLUSIONS: These findings demonstrate that testosterone regulates the expression of numerous genes in the mouse meibomian gland and that many of these genes are involved in lipid metabolic pathways [23].
• Lipids secreted form the bovine meibomian glands were assigned to following classes: cholesteryl esters (A) (fatty acyl chain lengths from 15 to 27 carbon atoms), 41%; wax esters, 29%; triacylglycerols, 10%; and cholesteryl ester (B) (fatty acyl chain lengths from 14 to 18 carbons), 15% [24].

Gene context of Meibomian Glands

• 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 [25].
• PURPOSE: Phospholipase A2 (PLA2) hydrolyzes phospholipids, one of the important constituents of human meibomian gland secretions [26].
• A region of strong labelling for aggrecan, dermatan sulphate and chondroitin 6 sulphate immediately surrounded the Meibomian glands [27].
• Whereas in the skin, hyperkeratinization is followed by follicular hyperkeratosis and dermal cyst formation, in the meibomian gland, ductal hyperkeratinization appeared to lead to loss of well developed acini followed by atrophy of the gland at 1 year as confirmed by immunostaining for keratin proteins [28].
• The expression of keratin proteins from meibomian glands and their correlation with skin epidermal keratins were determined [25].

Analytical, diagnostic and therapeutic context of Meibomian Glands

• Transillumination of rabbit lids treated with topical epinephrine for 2 to 3 months revealed plugging of the meibomian gland orifice [21].
• Identification by gas chromatography/mass spectrometry of long-chain fatty acids and alcohols from hamster meibomian glands using picolinyl and nicotinate derivatives [29].
• Once corneal scarring has developed, perforating keratoplasty has a poor prognosis due to the ectodermal dysplasia, the absence of the meibomian glands and the defective tear film [30].

References