Meibomian glands are the oil-producing glands located in both the upper and lower eyelids. They number about 25 to 30 (each: a total of about 100) and normally slowly release oil into the tear film. This oil helps to stop the water in the tears from evaporating, thus helping to prevent dry eyes. Detailed anatomy here.
The meibomian glands (3 Fig above) of the tarsal plate produce the lipid that will line the layer of the tear film. The Meibomian lids empty into ducts that dot the marginal surface of the eyelid and can be seen emanating droplets of oil for the tears.
meibum is a transparent, free-flowing, yellow oil that when expressed resembles a light cooking oil. In a healthy eye, gentle pressure with a finger or cotton swab for as little as 15 seconds in the central portion of each lower lid should produce a small amount of meibum from one or more of the glands in each lid. If no oil is produced, or if a thickened or opaque oily substance issues from the glands, the diagnosis is MGD and appropriate treatment should ensue [Source]
Over time, some of these glands die or otherwise atrophy. See this. Hyperkeratinization of ductal epithelium and atrophy of acinar cells may cause meibomian gland dysfunction.
the natural history of MGD starts with hyperkeratinization of the duct epithelium leading to duct occlusion. This is seen as pouting or plugging of the gland orifices and production of keratin rich expressed material. This plugging causes damming back of the gland secretions that leads to disuse atrophy of the acini. In the advanced stages periductal scaring occurs, it is seen as an exaggerated opaque ring shaped opacity around the ducts or a focal absorption of the gland orifices that ends in total damage and gland loss [Source]
MGD as a MAJOR CAUSE OF DRY EYES (Evaporative dry eyes)
Many people who have dry eye symptoms are treated as though the cause is aqueous deficiency (artificial tear supplementation and punctal plugs), when in fact their primary problem is meibomian gland dysfunction MGD. Some researchers believe that up to 70% of chronic dry eye may actually be MGD, not "classic" dry eye. More broadly, nearly half of the subjects with dry eyes have MGD [Academic paper].
Posterior blepharitis is often called meibomitis or meibomian gland dysfunction [Source]. Meibomian gland dysfunction is quite common and unfortunately it often goes undiagnosed. Even when diagnosed is often not treated or is not treated effectively until it has become chronic or severe.
MGD may be inflammatory (often as a result of blepharitis) or atrophic.
Severe blockage can lead to much enlarged glands (a cyst) or even infection. It is therefore important to firstly, unclog the glands which are blocked and secondly to prevent them from blocking up again as much as possible
Thickening of oil
The oil is supposed to be nice and warm and runny, but sometimes it can get thick and gets stuck. This leads to blockage of the narrow duct which takes the oil from the gland to the tear film. The oil continues to be made and this can lead to filling and swelling of the glands.
Vicious cycle: bacterial infection as a result of MGD
MGD causes reduced lipid production for the ocular surface, leading to tear evaporation and dry eye. Decreased tear production reduces the eye’s ability to flush bacteria from the lid margins, enabling bacteria to infect the meibomian glands and eyelash follicles, in turn further degrading the tear film. In addition to aqueous deficiency dry eye, MGD contributes significantly to ocular surface disease. Since it is not always easy to distinguish the clinical signs and symptoms of MGD from dry eye disease or ocular allergy, the MGD may go untreated. [Source]
Anterior blepharitis is not uncommonly seen in association with MGD due to the abnormal keratinization found mainly with seborrheic blepharitis E161.However it is still unclear whether the keratinization and gland drop out are primary or secondary phenomena [Source]
Anterior blepharitis is commonly found among patients and it was hypothesized that it might play a role in the progression of the disease. [Source]
Age related cause
A neurotransmitter called vasoactive intestinal polypeptide and the hormone androgen control meibum secretion.2 Women's androgen levels drop during and after menopause, and post-menopausal women have an increased prevalence of MGD, so this may indicate a hormonal connection.3 As further proof, topical antiandrogen treatments reduce meibum levels, while topical use of the androgen precursor dehydroepiandrosterone increases meibum levels.4 [Source]
As the natural history of meibomitis advances, the meibomian gland orifices progress from open to stenosed to closed (Figure below). [Source]
Natural history of meibomitis. Meibomian gland inflammation leads first to stenosis and then closure of the meibomian gland orifice.
The clinical presentation of MGD includes, capped meibomian glands and the pathognomonic foamy tear. Expression of the meibomian glands may be difficult. The secretions of the meibomian glands can become extremely thickened and have the appearance of tooth-paste. The plugged glands can become infected and the patient may complain of recurrent styes. The dysfunctional lipid layer that occurs in MGD leads to a rapid tear film breakup and evaporative loss of tears resulting in secondary aqueous tear layer insufficiency. [Source]
Symptoms of MGD include redness on the lid margin, flaky debris or mattering, fluctuating vision, burning and stinging. [Source]
1. Unblock the glands
Lid therapy – particularly heat treatment – helps deal with this by first kind of melting the stuff that’s thickened up, then gently squeezing it out.
The first part of unblocking the glands is to liquefy the thickened oil in the glands. This is achieved by running a face cloth under the hot tap until it is warm, but not hot. (From here)
Hold this against the closed eye for about one minute or so (see figure One).
Then, having liquefied the oils with this warming, press with one finger firmly on your cheek.
Next, with the first-finger, press firmly on the lower lid, pushing upward to push the oil up into the tear film (see figure Two).
Do this a few times over the entire lower eyelid, and then repeat for the upper eyelid.
Repeat the entire procedure for the other eye.
Do this initially once per day for one week. This will help to unclog the blocked glands.
After the first week, doing this once or twice per week should help prevent the glands from becoming reblocked.
2. Kill any bacteria that have collected
Oral antibiotics such as doxycycline 50mg twice a day for one month then once a day for another two months [Source]. And take preservative free artificial tears. Make sure you use warm compressors on daily basis to help disease stability.
Providers have historically considered MGD one of the most difficult diseases to treat because we have lacked a simple, effective therapy. The challenge with “mechanical” therapies (cleansing, hot compresses, massage) is adherence; the challenge with topical antibiotic drops and ointments is efficacy—they do not penetrate the lid margin well, and most lack the needed antiinflammatory effect. While more effective, oral tetracyclines often have unpleasant gastrointestinal side effects. [Source]
The procedure is performed at the doctor’s office and takes about 12 minutes for each eye. LipiFlow delivers heat to the inner eyelid and massage to the outside, which helps unblock the flow of lipids from the cystic meibomian glands. [Source]
[See video below]
Obstructive meibomian gland dysfunction (MGD) is a common source of complaint among patients with dry eye syndrome and its prevalence increases with age. The principal clinical consequence of obstructive MGD is evaporative dry eye syndrome. Moreover, chronic obstruction of the meibomian glands may also result in degeneration of the secretory gland tissue that can lead to a secondary hypo-secretion even if the primary obstruction is later resolved by therapeutic approaches. Risk factors in the pathogenesis of obstructive MGD include age, hormonal disturbances and environmental influences (e.g., contact lenses). Furthermore, qualitative alterations in the composition of the meibum may lead to hyper-keratinization of the ductal epithelium and increased viscosity of the meibum. This can result in obstruction of the duct and orifice leading to a lack of meibum on the eyelid margin and tear film with downstream hyper-evaporative dry eye syndrome. At the same time, obstruction leads to a stasis of meibum inside the meibomian gland with increased pressure and resulting dilatation of the ducts and in atrophy of the acini with rarefaction of the secretory meibocytes and gland dropout. Stasis can also increase the growth of commensal bacteria, their production of oil degrading enzymes and release of toxic mediators. These factors can act as self-enforcing feedback loops that aggravate the primary hyper-keratinization and compositional disturbance of meibum and can hence lead to a progressive MGD (Knop and Knop, 2009b). [Source]
The first global consensus report on meibomian gland dysfunction — a major cause of lid disease and evaporative dry eye — has been published in a special issue of the Investigative Ophthalmology & Visual Science (IOVS) journal. The report is the result of findings from a two-year-long workshop composed of more than 50 leading clinical and basic research experts from around the world.
The workshop participants used an evidence-based approach to develop a worldwide definition: meibomian gland dysfunction (MGD) is a chronic, diffuse abnormality of the meibomian glands, commonly characterized by terminal duct obstruction and/or qualitative/quantitative changes in the glandular secretion. This may result in alteration of the tear film, symptoms of eye irritation, clinically apparent inflammation, and ocular surface disease.
Using the same methodology, the participants developed a universal classification system — based on pathophysiology, rather than anatomical changes or the severity of disease — to meet the needs of clinicians and researchers alike. The consensus paper further proposes recommendations for diagnosing MGD and MGD-related disorders and presents a sequence of diagnostic tests to be performed in an order that will minimize the extent to which one test influences those that follow.
Also included in the report are recommendations for the evaluation and grading of the severity of MGD, management of and therapy for the disease and norms for clinical trials designed to evaluate pharmaceutical interventions for treatment.
The International Workshop on Meibomian Gland Dysfunction was conducted by the Tear Film & Ocular Surface Society (TFOS). While the breadth and depth of the consensus findings are expected to have a far-reaching impact on the clinical care of patients, the group of experts concur that additional research be conducted to further study other aspects of MGD. These include its association with dry eye disease and standardized and validated ways to identify symptoms and signs of MGD.
"IOVS publishes consensus findings on meibomian gland dysfunction." PHYSorg.com. 31 Mar 2011.
The new classi?cation system proposed by the International Workshop on MGD distinguishes among the subgroups of MGD on the basis of the level of secretions and further subdivides those categories by potential consequences and manifestations. On the basis of these proposed classi?cations, obstructive MGD is the most pervasive.
Department of Ophthalmology, University of Iowa Hospitals, Iowa City 52242.
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.
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.
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).
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.