By definition, the multifactorial etiology of involutional ectropion is generally attributed to aging changes in the lid and orbit.¹,²,³ Because several anatomic and ultrastructural features are shared between both entropion and ectropion,⁴ an understanding of the vector forces involved in maintaining lower eyelid stability is paramount to appreciate the abnormalities that would eventually lead to either one or the other, and therefore these factors should be discussed together. Unfortunately, the question that has eluded researchers for decades—“Why would some eyelids turn in, while others turn out?”—still lingers unanswered in the literature,⁵,⁶,⁷,⁸ and the ultimate decisive factor or more accurate factors remain elusive.⁴,⁸ It should be realized, however, that for the eyelid margin to turn inward or outward, two critical etiologic events should occur: horizontal lower eyelid laxity and retractor dehiscence.⁶ Although the other factors that are also discussed below reportedly play a less significant role, nevertheless, they might tip the scale toward either ectropion or entropion.

The normal lower eyelid position depends on firm anchoring of the lateral and medial canthal tendons to the bony orbital rim,⁹ and therefore a primary etiopathogenetic event is canthal tendon laxity, which more commonly involves the lateral canthal tendon,¹⁰ and allegedly plays a more significant role in ectropion than entropion.³,¹¹ The lateral canthal tendon is more frequently involved because it is inherently weaker than the medial,¹² more anatomically susceptible to clinically significant displacement, and is more exposed to chronic repetitive trauma.⁹

The second crucial anatomic event is disinsertion or attenuation of the lower eyelid retractors, which also makes the lid unstable.²,¹³,¹⁴ However, in contrast to the ligamentous weakening outlined above, lower lid retractor dehiscence plays a more significant role in entropion than ectropion,²,⁷,¹⁵ although the location and extent of the disinsertion of the retractors will determine clinically whether the patient will have isolated punctal eversion or frank tarsal ectropion.¹⁴ In patients with tarsal ectropion, retractor disinsertion allegedly plays a more important pathogenetic role than horizontal lid laxity, which is also present but is not the striking feature.¹³,¹⁴,¹⁶,¹⁷,¹⁸ It was Jones in 1960 who first theorized that retractor disinsertion would allow the inferior border of the tarsus to rotate either outward or inward and likened it to levator aponeurosis dehiscence in the upper eyelid.¹⁹

An unchecked orbicularis oculi muscle that overrides the lower border of the tarsus is another vital event involved in the pathogenesis of entropion, but not in ectropion where it remains well tethered and does not roll upward.²⁰ Atrophy and hypertrophy of the orbicularis muscle have been demonstrated in involutional entropion and ectropion, respectively.²¹,²² Earlier authors hypothesized that this is a primary pathogenetic event and that the variability in muscle bulk could explain the ability or failure of the orbicularis muscle to contract and override the tarsus, consequently causing either pathology.²¹,²² An arteriosclerotic or a partially occluded marginal artery has been implicated in the atrophy of the muscle.²¹ It should be noted, however, that more recent studies failed to reproduce those earlier results, and
accordingly, these studies do not support the hypothesis that a primary change in orbicularis muscle fibers is responsible for either disease.²³,²⁴

Tarsal size may also play an important role in turning the eyelids to the inside or out. In the presence of lateral canthal tendon laxity, a large or thickened tarsus overcomes the tone of the preseptal orbicularis resulting in ectropion, while a small, shrunken, or atrophic tarsus may be overcome by the same muscle resulting in involutional entropion.⁵,²⁴,²⁵

A larger globe or an increase in axial length correlates directly with involutional ectropion, while smaller eyes are more prone to develop entropion.⁴ Another factor of significance is the globe position. The consensus is that an increase in exophthalmometry measurements also correlates directly with the development of ectropion, while enophthalmos correlates more with involutional entropion.⁴,⁶,²⁶ However, other researchers have failed to observe a direct causal relation between axial length and globe position,²⁷,²⁸,²⁹ and some authorities argue that this postulated association with globe position or size only demonstrates that a tighter eyelid-globe apposition simply prevents the eyelid from rotating inward or outward.²⁰ Midface descent is an often overlooked factor that may also mechanically aggravate preexisting ectropion due to downward gravitational vectors.³⁰,³¹,³²

Ultrastructurally, the composition of the “younger” tarsus is mostly collagenous fibers with scattered elastic fibers. Collagen fibers are essential for tensile strength, while elastic fibers are a source of tarsal resilience.²⁵,³³,³⁴ With advancing age, there is a significant and generalized reduction in both collagen and elastic fibers throughout all eyelid layers including the skin, orbicularis, and the tarsal stroma.²¹,²²,²⁵,³³,³⁴ There is a relative increase in collagen fiber content in eyelid specimens from patients with involutional ectropion compared to patients with involutional entropion.³³,³⁴ Whether this is the underlying factor explaining the greater tendency toward tarsal hypertrophy in patients with involutional ectropion is unknown.³⁵ Upregulation of key elastolytic enzymes like matrix metalloproteinase MMP-2, MMP-7, and MMP-9 in eyelid tissues is responsible for enzymatic degradation of elastic tissue, and consequently, a significant reduction in elastic fiber content, as well as substantial ultrastructural abnormalities in the residual elastin tissue, has been demonstrated both in ectropion and entropion.³³,³⁴ The cause of this overexpression of elastin-degrading enzymes with advancing age is unknown but may be the consequence of local ischemia resulting from arteriosclerosis of the marginal arcade, chronic mechanical stress, or local inflammation.³³,³⁴