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The potential for eye rubbing to contribute to keratoconus development and progression is well established, but the mechanisms of that association have not been fully elucidated. This review examines mechanisms for rubbing-related corneal trauma from both anterior and posterior surface responses to elevated intraocular pressure. Apart from rubbing-related intraocular pressure elevation, consideration is given to other sources of elevation which may contribute to corneal bulging and cone formation. Mechanisms whereby intraocular pressure-related increased posterior corneal surface distending stress and stromal hydrostatic pressure may alter keratocyte functions and increase susceptibility to such stress are examined. Elevated intraocular pressure (IOP) that is associated with a chronic habit of abnormal rubbing (CHAR) can be a major contributor of keratoconus (KC) development and progression. Anterior corneal surface protection during rubbing due to Bell’s reflex in most patients, at least for the central and para-central cornea, increases the likelihood that IOP distending stress can be an important source of KC pathogenesis, perhaps even in patients who do not have abnormal rubbing habits. That the earliest pathological changes in KC occur at the posterior corneal surface is consistent with the significance of an IOP-related distending force mechanism for KC pathogenesis.

Mechanisms of corneal trauma in response to rubbing and other intraocular pressure elevating activities in keratoconus