I don't have a subscription but I couldn't help shelling out the $15 to get the full text of this study. If you want to see it all, look for it on this page of the IOVS site under Cornea. It was a very interesting read. MGD patients, while this may not have a practical application for you right now - confocal microscopes are expensive and your local doc probably doesn't have one - it's still fascinating info. And you can always ask.
To me, anything taking a really serious look at the MGs of significantly different dry eye groups is going to be worth reading - they just don't come along often enough. This one ran the gamut, from the classic signs (BUT, Schirmer, staining, etc) to meibography and confocal microscopy.
I find the MG differences between Sjogrens and MGD patients interesting. Clearly the Sjogrens patients are taking a big hit in the MGs - yet their oil is staying clearer and coming out much more easily. But in this study, they hurt a LOT more than the MGD patients.
So, what's still missing from this picture as far as I'm concerned is why SOME patients with MGD experience pain levels rivaling the Sjogrens crowd. On DryEyeTalk, this always seems to be the predominant theme, whether they've been diagnosed with ocular rosacea or classic bleph or demodex or whatever the MG diagnosis du jour in their locale happens to be. These people and the ones I get phone calls from are - from an OSDI score standpoint - completely unlike those represented in studies such as Dr. Villani's. WHY? What are all these outliers? They've got a ton of pain; some have really annoying eyelids and some don't; most don't have really dramatic clinical findings. Many, maybe most get widely varying diagnoses from different doctors.
I find myself more and more frequently wondering if MGD isn't a sort of red herring in many of these cases. On the other hand I don't buy the corneal neuralgia explanation for all of them either (some, just not all). Way back in the day, there were a lot of studies going on that had me thinking that the mucin layer really was key to the differences in pain levels. I don't see too much happening in that world lately. And that may be the wrong tree to bark up. But if so, I'd sure like to know what is. This MGD or pseudo MGD stuff is striking younger and younger people and we need to make more progress in tackling it. What are we going to do in another ten years when there's a whole bunch more kids who have grown up on soda, antidepressants and computers and were fitted with contacts at age 8? They're already showing up in the pediatric docs' offices with MGD. Sigh.
In vivo confocal microscopy of meibomian glands in Sjögren's syndrome.
PURPOSE: To evaluate morphologic changes in meibomian glands (MGs) and the status of periglandular inflammation in patients with primary and secondary Sjögren's Syndrome (SS) using in vivo confocal laser microscopy (LSCM).
METHODS: Twenty patients with primary SS (SSI), 25 with secondary SS (SSII), 20 with MG dysfunction (MGD), and 25 age- and gender-matched control subjects were enrolled consecutively. Each participant completed an Ocular Surface Disease Index questionnaire and underwent a full eye examination, including tear film break-up time (BUT), fluorescein and lissamine green staining, Schirmer test, and an LSCM examination of the MGs, the last to determine acinar unit density and diameter, glandular orifice diameters, meibum secretion reflectivity, inhomogeneous appearance of glandular interstice, and acinar wall.
RESULTS: All parameters indicated statistically significant differences among groups (P < 0.001, Kruskal-Wallis test). LSCM demonstrated no differences between SSI and SSII (Mann-Whitney U test). Compared with control subjects, SS subjects' MGs showed more periglandular inflammation and higher secretion reflectivity (P < 0.001, Mann-Whitney U test). Compared with MGD patients, SS patients' MGs had higher acinar density, smaller diameters, greater density of periglandular inflammatory cells, and lower secretion reflectivity (P < 0.001, Mann-Whitney U test). In SS patients, the two measured confocal signs of inflammation were significantly interrelated and correlated with corneal fluorescein staining (P ≤ 0.01, Spearman correlation coefficient). Acinar density and diameters were strongly correlated among themselves (P < 0.001) and with BUT (P < 0.05).
CONCLUSIONS: LSCM is capable of effectively revealing morphologic and inflammatory changes in MGs and showed discernible patterns of MG abnormalities in SS and MGD not easily distinguishable by the usual clinical exams.
Invest Ophthalmol Vis Sci. 2011 Feb 16;52(2):933-9. Print 2011 Feb.
Villani E, Beretta S, De Capitani M, Galimberti D, Viola F, Ratiglia R.
Università degli Studi di Milano, UO Oculistica Fondazione IRCCS Cà Granda Ospedale Maggiore Policlinico, Milan, Italy. firstname.lastname@example.org