Zusammenfassung
Eine obstruktive Dysfunktion der Meibom-Drüsen (MGD) kommt überraschend häufig in der Normalbevölkerung vor und nimmt mit dem Alter zu. Klinisch werden oft nur die unmittelbaren Folgen an der Augenoberfläche im Sinne von Benetzungsstörung und trockenem Auge betrachtet. Zusätzlich führt aber die chronische Obstruktion der Meibom-Drüsen auch zu einer Degeneration von sekretorischem Drüsengewebe, die in einer persistierenden sekundären Mindersekretion resultieren kann, auch wenn die primär auslösende Obstruktion später therapeutisch beseitigt wird.
Entscheidende Einflussfaktoren in der Pathogenese der obstruktiven MGD und ihrer Interaktion beim Forschreiten der Erkrankung werden systematisch analysiert und in einem Flussdiagramm dargestellt. Alter, hormonelle Störungen und Umwelteinflüsse wie Kontaktlinsen sowie qualitative Veränderungen des Meibom-Öls führen zu verstärkter Verhornung des Gangepithels und erhöhter Viskosität des Sekrets, die allein oder zusammen in einer Obstruktion des Ausführungsgangs resultieren. Dies führt zu einem Mangel des Meibom-Öls auf dem Lidrand und Tränenfilm mit nachfolgenden Benetzungsstörungen im Sinne eines evaporativen trockenen Auges. Gleichzeitig resultiert die Obstruktion in einer Stase des Sekrets innerhalb der Meibom-Drüsen mit erhöhtem Druck und nachfolgender Dilatation der Gänge sowie Atrophie der Azini mit Rarefizierung der sekretorischen Meibozyten und klinisch darstellbarem Ausfall von aktivem Drüsengewebe („gland dropout“). Stase kann auch das Wachstum kommensaler Bakterien, die Bildung fettspaltender Enzyme (Lipasen) und die Freisetzung toxischer Mediatoren begünstigen. Diese Faktoren können im Sinne selbstverstärkender „Teufelskreise“ die zugrunde liegende Hyperkeratinisierung und Sekretveränderung erhöhen und zu einer progredienten Erkrankung der Meibom-Drüsen führen.
Abstract
Obstructive dysfunction of the meibomian glands (MGD) is surprisingly frequent in the general population and increases with age. Clinically, the focus is mainly on the consequences at the ocular surface in the sense of an evaporative dry eye syndrome. However, in addition, chronic obstruction of the meibomian glands also leads to degeneration of the secretory gland tissue which can result in a secondary hyposecretion even if the primary obstruction is later resolved by therapeutic approaches.
Important influencing factors in the pathogenesis of obstructive MGDs and their interaction during the progression of the disease are systematically analyzed and displayed in a flow diagram. Age, hormonal disturbances and environmental influences, such as contact lenses, as well as qualitative alterations in the composition of the meibomian oil (meibum) lead to hyperkeratinization of the ductal epithelium and increased viscosity of the meibum which result, either alone or in combination, in obstruction of the duct and orifice. This leads to a lack of meibum on the lid margin and tear film with downstream hyperevaporative 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 (lipases) and release of toxic mediators. These factors can, in return, act as self-enforcing feedback loops in the sense of vicious circles that aggravate the primary hyperkeratinization and compositional disturbance of meibum and can hence lead to a progressive MGD.
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Knop, E., Knop, N. Meibom-Drüsen. Ophthalmologe 106, 980–987 (2009). https://doi.org/10.1007/s00347-009-2044-8
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DOI: https://doi.org/10.1007/s00347-009-2044-8