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Recurrent granular corneal dystrophy.

J C Stuart, M L Mund, T Iwamoto

    American Journal of Ophthalmology
    |January 1, 1975
    PubMed
    Summary
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    Granular corneal dystrophy recurs in transplanted corneas due to host cell invasion, not donor tissue issues. This infiltration affects the graft, confirming recurrence mechanisms in corneal transplantation.

    Area of Science:

    • Ophthalmology
    • Corneal Disease Research
    • Histopathology

    Background:

    • Granular corneal dystrophy is a hereditary condition affecting corneal clarity.
    • Recurrence of granular corneal dystrophy in corneal grafts is a significant clinical challenge.
    • Understanding the pathogenesis of recurrence is crucial for improving graft survival.

    Purpose of the Study:

    • To investigate the histological basis of recurrent granular corneal dystrophy in transplanted corneas.
    • To differentiate between host-derived and donor-derived contributions to graft recurrence.
    • To elucidate the cellular mechanisms underlying recurrence at the microscopic level.

    Main Methods:

    • Analysis of corneal buttons and lamellar keratoplasty tissue from four patients with recurrent granular corneal dystrophy.

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  • Utilized light microscopy and transmission electron microscopy for detailed tissue examination.
  • Examined tissue interfaces, including epithelium, Bowman's membrane, and stroma.

    • Main Results:

    • Observed fibrous tissue infiltration between the epithelium and Bowman's membrane in all studied grafts.
    • Deposits characteristic of granular dystrophy were identified within this fibrous tissue using both microscopy techniques.
    • The native donor corneal stroma remained unaffected, showing no signs of dystrophy.
    • The observed fibrous tissue lacked vascularization.

    Conclusions:

    • Recurrence of granular corneal dystrophy in corneal grafts is primarily caused by the invasion of host cells into the donor tissue.
    • The host's cellular infiltration, rather than intrinsic donor abnormalities, drives the recurrence process.
    • The donor stroma is resistant to the dystrophic changes, with recurrence localized to the anterior graft layers.