Lacritin proteoforms prevent tear film collapse and maintain epithelial homeostasis.

Lipids in complex, protein-enriched films at air/liquid interfaces reduce surface tension. In the absence of this benefit, the light refracting and immunoprotective tear film on eyes would collapse. Premature collapse, coupled with chronic inflammation compromising visual acuity, is a hallmark of dry eye disease affecting 7 to 10% of individuals worldwide. Although collapse seems independent of mutation (unlike newborn lung alveoli), selective proteome and possible lipidome changes have been noted. These include elevated tissue transglutaminase and consequent inactivation through C-terminal cross-linking of the tear mitogen lacritin, leading to significant loss of lacritin monomer. Lacritin monomer restores homeostasis via autophagy and mitochondrial fusion and promotes basal tearing. Here, we discover that lacritin monomer C-terminal processing, inclusive of cysteine, serine, and metalloproteinase activity, generates cationic amphipathic α-helical proteoforms. Such proteoforms (using synthetic peptide surrogates) act like alveolar surfactant proteins to rapidly bind and stabilize the tear lipid layer. Immunodepletion of C- but not N-terminal proteoforms nor intact lacritin, from normal human tears promotes loss of stability akin to human dry eye tears. Stability of these and dry eye tears is rescuable with C- but not N-terminal proteoforms. Repeated topical application in rabbits reveals a proteoform turnover time of 7 to 33 h with gradual loss from human tear lipid that retains bioactivity without further processing. Thus, the processed C-terminus of lacritin that is deficient or absent in dry eye tears appears to play a key role in preventing tear film collapse and as a natural slow release mechanism that restores epithelial homeostasis.

Ectodysplasin-A signaling is a key integrator in the lacrimal gland-cornea feedback loop.

A lack of ectodysplasin-A (Eda) signaling leads to dry eye symptoms, which have so far only been associated with altered Meibomian glands. Here, we used loss-of-function (Eda-/-) mutant mice to unravel the impact of Eda signaling on lacrimal gland formation, maturation and subsequent physiological function. Our study demonstrates that Eda activity is dispensable during lacrimal gland embryonic development. However, using a transcriptomic approach, we show that the Eda pathway is necessary for proper cell terminal differentiation in lacrimal gland epithelium and correlated with modified expression of secreted factors commonly found in the tear film. Finally, we discovered that lacrimal glands present a bilateral reduction of Eda signaling activity in response to unilateral corneal injury. This observation hints towards a role for the Eda pathway in controlling the switch from basal to reflex tears, to support corneal wound healing. Collectively, our data suggest a crucial implication of Eda signaling in the cornea-lacrimal gland feedback loop, both in physiological and pathophysiological conditions. Our findings demonstrate that Eda downstream targets could help alleviate dry eye symptoms.

Not All Dry Eye in Contact Lens Wear Is Contact Lens-Induced.

OBJECTIVES: To compare subjective and clinical outcomes in three study groups: (1) asymptomatic contact lens (CL) wearers (ASYM); (2) symptomatic CL wearers who become asymptomatic on lens removal; and (3) symptomatic CL wearers who do not resolve on lens removal. METHODS: Ninety-two subjects completed the Berkeley Dry Eye Flow Chart with and without lenses, ocular surface examinations, and a battery of questionnaires. RESULTS: Thirty-seven subjects (40%) were ASYM, 30 (33%) had contact lens-induced dry eye (CLIDE), and 25 (27%) had underlying physiological DE. Visual Analog Scale ratings, OSDI score, and SPEED score were significantly better for the ASYM group (P<0.001) but did not distinguish CLIDE from DE. The DE group was significantly worse than CLIDE and ASYM, which were similar, in precorneal noninvasive tear breakup time (8.2 sec DE vs. 12.3 sec CLIDE and 14.3 sec ASYM; P=0.002), anterior displacement of the Line of Marx (P=0.017), and superior conjunctival staining (P=0.001). CONCLUSIONS: Many CL wearers presenting with dryness symptoms have an underlying DE condition and will not respond to treatments aimed at changing lenses or solutions. Contradictory results from research studies of DE in CL wearers could be due in part to a failure to distinguish subjects with symptoms due specifically to CL wear from those whose symptoms have underlying causes unrelated to CL wear.

Comparative Analysis of Age-Related Changes in Lacrimal Glands and Meibomian Glands of a C57BL/6 Male Mouse Model.

It is not known how biological changes in the lacrimal (LGs) and meibomian (MGs) glands contribute to dry eye disease (DED) in a time-dependent manner. In this study, we investigated time-sequenced changes in the inflammation, oxidative stress, and senescence of stem cells in both glands of an aging-related DED mouse model. Eight-week (8W)-, one-year (1Y)-, and two-year (2Y)-old C57BL/6 male mice were used. MG areas of the upper and lower eyelids were analyzed by transillumination meibography imaging. The number of CD45+, 8-OHdG+, Ki-67+, and BrdU+ cells was compared in both glands. Increased corneal staining and decreased tear secretion were observed in aged mice. The MG dropout area increased with aging, and the age-adjusted MG area in lower lids was negatively correlated with the National Eye Institute (NEI) score. Increased CD4+ interferon (IFN)-γ+ cells in LGs were found in both aged mice. An increase in 8-OHdG+ cells in both glands was evident in 2Y-old mice. Reduced Ki-67+ cells, but no change in CD45+ cells, was observed in the MGs of 1Y-old mice. Increased BrdU+ cells were observed in the LGs of aged mice. This suggests that age-dependent DED in C57BL/6 mice is related to inflammation of the LGs, the development of MG atrophy, and oxidative stress in both glands.

The function and morphology of Meibomian glands in patients with thyroid eye disease: a preliminary study.

BACKGROUND: To investigate function and morphology of the meibomian gland (MG) in patients with thyroid eye disease (TED). METHODS: In this prospective case series study, patients with unilateral or bilateral TED were consecutively enrolled. The diagnosis of TED was based on the typical orbital findings and/or radiographic evidence. The disease activity of TED was classified according to the clinical activity score (CAS). Degrees of lagophthalmos and exophthalmos, blinking rates, and results of the Schirmer test 1 were also recorded. All patients completed the SPEED questionnaire and underwent MG assessment, including lipid layer thickness (LLT), MG dropout (MGd), and MG expression. RESULTS: In total 31 eyes from 17 patients with unilateral or bilateral TED were included. Patients were divided into inactive TED (CAS 0-1; 20 eyes from 11 patients) and active TED (CAS 2-3, 11 eyes from 6 patients) groups. MGd was significantly more severe in the active TED than the inactive TED group [Median (Inter-quartile region): 3.0 (2.0-3.0) vs. 2.0 (1.0-2.0) degree, P = 0.04]. However, patients with active TED had thicker LLT than those with inactive TED (90.0 [80.0-100.0] vs. 65.0 [47.8-82.5] nm, P = 0.02), and LLT was positively correlated with lagophthalmos (r = 0.37, P = 0.04). CONCLUSIONS: Patients with active TED had more severe MGd, but thicker LLT. Active TED may cause periglandular inflammation of MGs, leading to MGd, but compensatory secretion from residual MGs and lagophthalmos-induced forceful blinking might temporarily release more lipids over the tear film.

The correct diagnosis and therapeutic management of tear dysfunction: recommendations of the P.I.C.A.S.S.O. board.

PURPOSE: To describe a standard approach to manage tear dysfunction (TD), in order to obtain a clinically favourable outcome. TD is a highly prevalent, yet largely underdiagnosed, condition that affects from 5 to 30% of the population above 50 years old. Left untreated, TD is associated with eye discomfort and ocular surface disease, substantially affecting quality of life. Although the prevalence of this problem is increasing significantly, a standard approach to its prevention and treatment is not available yet. METHODS: In September 2015, a team of Ocular Surface Italian Experts convened for a roundtable to discuss on the latest knowledge about diagnosis and treatments for TD and the real issues in the management of these patients. The discussion centred on the appropriate definition of TD, proposing a new classification of risk factors and how to identify them, how to make a correct diagnosis choosing the rational therapy (questionnaires, symptoms' time relation, seasonality, low tech diagnostic manoeuvres, specific tests for the detection of tear film disturbances leading to recognition of the level of disease and of the ocular system elements involved), which artificial tear matches the ideal profile for a rational therapy and which questions should be done to the patient. RESULTS: A multi-item flowchart for tear film dysfunction, with point-by-point explanatory guide, to better identify and manage the patient with this disorder is provided. CONCLUSIONS: The growing prevalence of TD demands increased attention. An appropriate prevention and a treatment pattern for the patient, combined with greater patient-practitioner interaction, and patient education is offered.

Function of meibomian gland: Contribution of proteins.

The meibomian gland is the major contributor to the tear film lipid layer. It is generally accepted that meibomian gland secretions, i.e, meibum, play a critical role in the homeostasis of the tear film. Lipid components of meibum and their structure, as well as functions were intensively studied. However, the proteins from meibum have not attracted enough attention. This review summarizes current knowledge about protein components of the meibum, particularly their function on tear film and ocular surface, and changes in the proteins during meibomian gland dysfunction (MGD).

Proteolytic activity in the meibomian gland: Implications to health and disease.

The function of the meibomian gland in the upper and lower eyelids is critical to maintaining homeostasis at the ocular surface. Highly specialized meibocytes within the gland must differentiate and accumulate intracellular lipid droplets that are released into the tear film following rupture of the cell membrane. Proteases and their inhibitors have been recognized as key players in remodeling extracellular matrices and promoting the normal integrity of glandular tissue. They modulate a wide range of biological processes, such as cell proliferation and differentiation, and can contribute to disease when aberrantly expressed. Deciphering the role of proteolytic activity in the meibomian gland offers an opportunity to gain a more comprehensive and fundamental understanding of the developmental, physiological, and pathological processes associated with this gland.

Meibocyte differentiation and renewal: Insights into novel mechanisms of meibomian gland dysfunction (MGD).

This paper reviews our current understanding of age-related meibomian gland dysfunction (MGD) and the role of the nuclear receptor, peroxisome proliferator-activated receptor gamma (PPARγ), in the regulation of meibomian gland function, meibocyte differentiation and lipid synthesis. The studies suggest that PPARγ is a master regulator of meibocyte differentiation and function, whose expression and nuclear signaling coupled with meibocyte renewal is altered during aging, potentially leading to atrophy of the meibomian gland as seen in clinical MGD. Study of meibomian gland stem cells also suggest that there is a limited number of precursor meibocytes that provide progeny to the acini, that may be susceptible to exhaustion as occurs during aging and other environmental factors. Further study of pathways regulating PPARγ expression and function as well as meibocyte stem cell maintenance may provide clues to establishing cellular and molecular mechanisms underlying MGD and the development of novel therapeutic strategies to treating this disease.

Role of EGF receptor signaling on morphogenesis of eyelid and meibomian glands.

The epidermal growth factor receptor (EGFR) signaling has a pivotal role in the regulation of morphogenesis during development and maintenance of homeostasis in adult eyelid and its adnexa. Studies have demonstrated that during eyelid morphogenesis the EGFR signaling pathway is responsible for keratinocyte and mesenchymal cell proliferation and migration at the eyelid tip. For meibomian gland morphogenesis, EGFR signaling activation stimulates meibomian gland epithelial cell proliferation. EGFR signaling pathway functions through multiple downstream signals such as ERK, Rho/ROCK and integrin and is regulated by a variety of upstream signals including Adam17, GPR48 and FGFR signaling. Herein we review the literature that describe the role of EGFR and its related signaling pathways in eyelid and meibomian gland morphogenesis.

New insights into the morphology and function of meibomian glands.

Meibomian glands secrete meibum, which gives rise to the lipid layer of the tear film and thereby prevents excessive evaporation of tear fluid. Meibomian gland dysfunction (MGD) is a major causative condition of evaporative dry eye, which is more common than the aqueous-deficient type of dry eye. Noninvasive meibography relies on infrared light and an infrared-sensitive camera to reveal the morphology of meibomian glands in both the upper and lower eyelids, whereas tear interferometry allows both qualitative and quantitative evaluation of the lipid layer of the tear film. These two techniques not only provide valuable clinical information related to dry eye but also allow clinical evaluation of MGD. Tear interferometry also has the potential to distinguish the condition of the tear film between normal individuals and dry eye patients. Furthermore, combined evaluation of the noninvasive breakup time of the tear film and the interferometric fringe pattern as determined by tear interferometry allows classification of the subtype of dry eye disease.

[Analysis of structure and function of meibomian glands in healthy population at different ages].

Objective: To observe the structure and function of meibomian glands in normal population at different ages. Methods: From October 2011 to August 2012, meibomian gland information was collected in healthy volunteers without any symptoms of ocular discomfort, aged more than 5 years. The people were grouped by every 10 years of age. The meibomian gland opening, secretion state and characteristics and Max's line were observed by slit lamp microscopic examination, and the meibomian gland dropouts were examined by noncontact infrared meibomian gland microscopy. The changes of meibomian glands were scored from 0 to 3, 0 for a normal state, 1 for mild abnormality, 2 for moderate abnormality and 3 for severe abnormality. The Mann-Whitney U test was used to compare the meibomian scores between male and female, and between left and right eyes. The correlation of these scores and the age of volunteers was analyzed by the Spearman test. Results: Among all the 100 volunteers, there were 47 males and 53 females, aged from 5 to 83 years (mean, 40.9±22.9). The meibomian gland dropouts were gradually increasing with age, significantly faster after 40 years old (scores for each age group were 2(1), 2(1), 2(1), 2(1), 3(2), 3.5(1.75), 4(3), 6(2). Meibomian gland opening, secretion traits and secretor status gradually became poorer with age, and changes were dramatically fast in the group of 40-49 years of age [scores of this group were 3(1.5), 3(3) and 2(2)], but slowed down after age of 50 years. Moreover, the Max's line position moved to the front gradually with age, with a marked change in the group of 40-49 years of age [scores for each age group were 0(1), 1(1), 2(2), 2(2), 3(2), 2(2), 3(2)], 4 gland changes showed a significantly positive relation to age(r=0.729, 0.635, 0.669, 0.639, 0.470. P<0.01), but not to gender and eye dominance (P>0.05). Conclusions: Meibomian gland opening and meibomian gland secretion become worse with age. The age of 50 years old is the key period for the meibomian gland changes. (Chin J Ophthalmol, 2017, 53: 528-533).

Transcriptome analysis of aging mouse meibomian glands.

PURPOSE: Dry eye disease is a common condition associated with age-related meibomian gland dysfunction (ARMGD). We have previously shown that ARMGD occurs in old mice, similar to that observed in human patients with MGD. To begin to understand the mechanism underlying ARMGD, we generated transcriptome profiles of eyelids excised from young and old mice of both sexes. METHODS: Male and female C57BL/6 mice were euthanized at ages of 3 months or 2 years and their lower eyelids removed, the conjunctival epithelium scrapped off, and the tarsal plate, containing the meibomian glands, dissected from the overlying muscle and lid epidermis. RNA was isolated, enriched, and transcribed into cDNA and processed to generate four non-stranded libraries with distinct bar codes on each adaptor. The libraries were then sequenced and mapped to the mm10 reference genome, and expression results were gathered as reads per length of transcript in kilobases per million mapped reads (RPKM) values. Differential gene expression analyses were performed using CyberT. RESULTS: Approximately 55 million reads were generated from each library. Expression data indicated that about 15,000 genes were expressed in these tissues. Of the genes that showed more than twofold significant differences in either young or old tissue, 698 were identified as differentially expressed. According to the Gene Ontology (GO) analysis, the cellular, developmental, and metabolic processes were found to be highly represented with Wnt function noted to be altered in the aging mouse. CONCLUSIONS: The RNA sequencing data identified several signaling pathways, including fibroblast growth factor (FGF) and Wnt that were altered in the meibomian glands of aging mice.

An evidence-based analysis of Australian optometrists' dry eye practices.

PURPOSE: The aims of this study were to investigate the clinical practices of Australian optometrists as related to the diagnosis, quantification, and management of dry eye and to assess whether these are consistent with research evidence and current guidelines. METHODS: An online survey was distributed to registered optometrists (n = 654). Respondents provided information regarding their preferred diagnostic procedures and management strategies for dry eye, practice modality, year of commencing practice, and whether they possessed an interest in dry eye. RESULTS: Respondents (n = 144) used multiple procedures for diagnosis. Recording patient symptoms ranked as the most important, most valuable, and most commonly used technique. The main objective tests were fluorescein-assisted tear breakup time, corneal fluorescein staining, and meibomian gland evaluation. Optometrists with an interest in dry eye more frequently used lissamine green, phenol red test, interference fringes, and tear osmolarity than nonspecialist practitioners. Dry eye treatment varied with severity. The mainstay of therapy was nonpreserved lubricants and eyelid hygiene; more practitioners recommended topical corticosteroids, systemic omega-3 fatty acid supplementation and increased dietary intake of omega-3 fatty acids for moderate and severe disease, respectively. The primary sources of information used to guide practitioners' management were derived from continuing education conferences. CONCLUSIONS: This study indicates that although Australian optometrists use subjective and objective diagnostic tests and stratify treatment based on dry eye severity, there is a lack of uniformity regarding diagnostic testing, infrequent use of standardized grading scales, and significant variability in clinical care. These findings highlight the potential to improve the translation of dry eye research evidence and evidence-based guidelines into Australian optometric practice.

Long-term (12-month) improvement in meibomian gland function and reduced dry eye symptoms with a single thermal pulsation treatment.

PURPOSE: To determine the 1-year post-treatment dry eye status of subjects with meibomian gland dysfunction and dry eye symptoms after receiving a single LipiFlow Thermal Pulsation System treatment. DESIGN: Single-centre, prospective, observational, open-label, 1-month-registered clinical trial with a 1-year follow-up examination. PARTICIPANTS: Patients with evaporative dry eye disease with meibomian gland dysfunction and dry eye symptoms who had participated in the registered 1-month clinical trial. METHODS: Eighteen of 30 subjects initially enrolled were able to return for a 1-year follow-up. Both eyes of all patients were treated with a single 12-min treatment using the LipiFlow Thermal Pulsation System. Meibomian gland function, tear break-up time and dry eye symptoms were measured. Data are presented for pretreatment (baseline), and 1-month and 1-year post-treatment. MAIN OUTCOME MEASURES: Meibomian gland secretion scores, and tear break-up time and dry eye symptoms. RESULTS: Significant improvement in meibomian gland secretion scores from baseline measurements (4.0 ± 3.4) to 1-month post-treatment (11.3 ± 4.7; P < 0.0005) was maintained at 1-year (7.3 ± 4.6; P < 0.05). Baseline tear break-up time (4.9 ± 3.0) was significantly increased at 1-month (9.5 ± 6.9; P < 0.05); however, this improvement was no longer evident at 1-year post-treatment (6.0 ± 4.4). The significant improvement in symptom scores on Ocular Surface Disease Index and Standard Patient Evaluation of Eye Dryness questionnaires observed at 1-month (P < 0.0005) was maintained at 1-year (Ocular Surface Disease Index [P < 0.05]; Standard Patient Evaluation of Eye Dryness [P < 0.0005]). CONCLUSION: A single 12-min treatment with the Lipi Flow Thermal Pulsation System offers an effective treatment for evaporative dry eye and meibomian gland dysfunction resulting in significant and sustained improvement in signs and symptoms for up to 1 year.

Addressing excessive evaporation: an unmet need in dry eye disease.

Dry eye disease (DED) is a common condition in which tear film abnormalities result in a damaging cycle of tear hyperosmolarity, desiccating stress, inflammation, and ocular surface injury. In a healthy tear film, meibum produced by the meibomian glands forms a lipid layer that stabilizes the tear film and protects against aqueous tear evaporation. Excessive tear evaporation due to a deficient lipid layer is believed to be the most common cause of DED, and most evaporative DED is associated with meibomian gland dysfunction (MGD); this highlights the pathophysiologic importance of the dysfunctional tear lipid layer. Current treatments for DED may be used to supplement hyperosmolar aqueous tears, lubricate the ocular surface, increase meibum flow, decrease inflammation, promote tear production, or otherwise decrease clinical signs of ocular surface damage and/or improve symptoms. Until now, no prescription eye drop has directly addressed the excessive evaporation that occurs in most patients with DED. Perfluorohexyloctane (PFHO) ophthalmic solution (MIEBO™; Bausch + Lomb) is a preservative-free eye drop that has demonstrated the ability to form a long-lasting barrier that inhibits evaporation in preclinical studies. FDA approval of PFHO was based on results from 2 pivotal clinical trials (GOBI [NCT04139798] and MOJAVE [NCT04567329]) in patients with DED and clinical signs of MGD which demonstrated consistent improvements in both signs and symptoms of disease, with a safety profile similar to that of saline eye drops. PFHO is the first and only FDA-approved eye drop that directly targets tear evaporation in patients with DED, thereby promoting ocular surface healing and providing symptomatic relief.

Fluids of the ocular surface: concepts, functions and physics.

General adoption of the ocular surface (OS) concept has advanced the therapy of the external eye. Fresh physical findings have prompted new concepts; examples taken from each section of the text are: (i) ever-present lipid sealant bridges the palpebral fissure capping the three-dimensional 'OS' sac. The muco-aqueous pool (MAP) is thus enclosed, secluded from atmosphere, evaporation mitigated. Hence, the OS is conceptually, a compartment. The term 'dacruon' (otherwise 'tear film') has been coined for the combined fluids of the OS, viz. lipid film and MAP. (ii) Investigative techniques of physics yield data on (say) surface tension and viscosity, and on functions such as anchorage of dacruon base to the varied mucosae of the OS, lubrication, renovation of intermarginal fluid layers as the eye opens after each blink, and refinement of optics and vision by the fluids attached to the cornea. (iii) Physical events in the opening eye produce the unique 'black line' phenomenon in which capillary force induces subsurface flows into thirsty menisci, bringing about parameniscal dark grooves, pupil-ward of each meniscus. Attenuation of fluorescein in the shallowed fluid gaps behind each groove makes the dye appear unilluminated ('black lines') relative to adjacent full-thickness MAP fluid glowing under cobalt-blue illumination. Isolated from cornea by grooves and gaps, the meniscal fluid cannot pass freely over the cornea. It therefore streams through the menisci to nasolacrimal outflow.

Investigations on the conjunctival goblet cells and the characteristics of the glands associated with the eye in chinchillas (Chinchilla Laniger).

OBJECTIVE: To investigate the density and distribution of conjunctival goblet cells (GC) and study the anatomy and microscopic characteristics of glands associated with the eye in chinchillas (Chinchilla Laniger). PROCEDURE: 12 chinchillas were included in the study. Conjunctiva (divided into four regions), eyelids, and glands were embedded in paraffin wax, sectioned, stained, and analyzed. RESULTS: Highest GC densities were found in the palpebral region of the nasal and temporal conjunctiva of both eyelids (GC index: 25.1-18.2%), and lowest densities, in the bulbar and marginal region of the nasal and temporal conjunctiva of both eyelids (GC index: 1.5-0.0%). Meibomian glands extend along the entire length of both eyelids, and the whole glandular complex broadens toward the temporal canthus. This is macroscopically visible through the conjunctiva. The openings of the Meibomian glands are macroscopically not discernible. The light pink, smooth, and crescent-shaped lacrimal gland lies next to the aforementioned broadened part of the Meibomian glands in the temporal canthus. The whitish, 0.9-cm-long, smooth Harderian gland is firmly attached to the posterior part of the globe and extends nasally from the optic nerve to the equator. Furthermore, chinchillas possess two lacrimal puncta, situated on the inner conjunctival surface of both eyelids near the medial canthus. A pigmented lacrimal canaliculus originates from each punctum. The vestigial nictitating membrane is supported by a hyaline cartilage and is pigmented at its free margin. CONCLUSIONS: Chinchillas possess a Harderian gland, a lacrimal gland, and Meibomian glands. The GC density in the nasal and temporal palpebral conjunctiva is higher than in guinea pigs.

Effect of low-level light therapy in patients with dry eye: a prospective, randomized, observer-masked trial.

To evaluate the efficacy of low-level light therapy (LLLT) with near-infrared light-emitting diodes (LED-LLLT) for the treatment of dry eye. 40 patients were randomly assigned with a 1:1 allocation ratio to receive LED-LLLT (LLLT group, n = 20) or placebo treatment (placebo group, n = 20). Patients in the LLLT group received LLLT twice a week for 3 weeks, for a total of 6 treatment sessions. The primary endpoint was the changes in the fluorescein corneal staining (FCS) score. The secondary endpoints were the changes in the ocular surface disease index (OSDI) score, lissamine green conjunctival staining (LGCS) scores, tear film break-up time (TBUT), Schirmer test, and the meibomian gland dysfunction (MGD) index. These were evaluated before treatment and 4 weeks after start of treatment. The mean difference of score change in primary endpoint revealed significant improvement in the LLLT group, compared to the placebo. Among secondary endpoints, LGCS, Schirmer's test, upper meibography scores showed significant improvements, while TBUT, lid debris, lid swelling, lid telangiectasia, meibomian gland secretion and expressibility scores had slight improvement without significant differences. No serious adverse events were observed. The use of LED-LLLT for the treatment of dry eye and MGD appears to be safe and beneficial.

The effect of pregnancy on meibomian gland, tear film, cornea and anterior segment parameters.

AIM: In this prospective study, we aimed to examine the effect of physiological and pathological changes that occur during pregnancy in regard to Meibomian Gland (MG) structure, tear film, cornea and anterior segment parameters. METHODS: The following groups were compared: 49 eyes of 49 pregnant women at 16-20 weeks of pregnancy (P16 Group), 46 eyes of 46 pregnant women at 32-36 weeks of pregnancy (P32 Group) and 51 eyes of 51 participants who were not pregnant (P0 Group). The groups were compared in terms of the first break-up time (NIF-BUT) and average break-up time (NIAvg-BUT) values. Non-contact meibography and MG loss rates were also compared. RESULTS: The groups were found to be compatible in terms of age (P=0.052). The mean NIF-BUT values in the P16, P32 and P0 groups were 4.7 ±2.7, 6 ±3 and 6.7 ±3.1 seconds, respectively (P=0.055). The mean MG loss rates for the upper lid in the P16, P32 and P0 groups were 35.3%±12.6, 33.4%±11.4 and 15.5%±5.4, respectively. The loss rates for the lower lid in the P16, P32 and P0 groups were found to be 40.5%±18.6, 40.5%± 14.4 and 20.1%±8.1, respectively (P=0.000, p=0.000). The mean anterior chamber value (ACV) was found in the P16, P32 and P0 groups with 160.8 ±31.8, 150.9 ±26.5 and 165.9 ±26.5 µm3, respectively (P=0.035). CONCLUSION: MG loss was found to be higher in pregnant groups compared to the non-pregnant groups. We found minimal instability in the tear film of the pregnant groups. We believe that pregnant women should be followed closely in terms of ocular surface diseases.