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Woo Chan Park, Scheffer C. G. Tseng; Modulation of Acute Inflammation and Keratocyte Death by Suturing, Blood, and Amniotic Membrane in PRK. Invest. Ophthalmol. Vis. Sci. 2000;41(10):2906-2914.
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purpose. To investigate the role of acute inflammation in keratocyte death, which may influence corneal haze after photorefractive keratectomy
methods. Transepithelial PRK was performed on both eyes of 30 rabbits.
Twenty-six rabbits were divided into 4 groups receiving autologous
blood, suturing alone, suturing with amniotic membrane graft, or no
treatment as the control. Twenty-four hours later, the ablated zone was
analyzed for keratocyte death by TdT-dUTP terminal nick-end label
(TUNEL) staining and transmission electron microscopy, for
polymorphonuclear cell (PMN) infiltration by hematoxylin–eosin
staining, and for oxygen radical–induced lipid peroxidation by
malondialdehyde immunohistochemistry. The remaining four rabbits were
subjected to PRK or mechanical scraping and analyzed immediately or
after culturing for 24 hours.
results. Compared with the control group where TUNEL-positive keratocytes were
found only in the superficial ablated stroma, blood application or
suturing caused more and deeper keratocyte death and PMN infiltration
(P < 0.05). The amniotic membrane graft group had less
keratocyte death and PMN than the control or the suture group
(P < 0.05 and P < 0.01,
respectively). There was a strong correlation between keratocyte death
and PMN infiltration (P < 0.01, correlation
factor = 0.786). Transmission electron microscopy revealed that
the majority of keratocyte death was due to necrosis. Amniotic membrane
stroma trapped and prevented PMN infiltration into the stroma.
Malondialdehyde-modified antigen was found on the ablated surface and
around infiltrated PMN.
conclusions. Transepithelial PRK causes oxygen radical–mediated lipid peroxidation
on the superficial stroma and may contribute to superficial keratocyte
death even in the absence of inflammation. Mechanical scraping leads to
apoptosis without the participation of inflammation. Keratocyte death
by necrosis spreads to the deeper part of the stroma and correlates
with additional acute inflammation. Amniotic membrane precludes PMN
infiltration and decreases lipid peroxidation and keratocyte death.
Future studies are needed to discern whether prevention of
inflammation-mediated keratocyte necrosis can reduce unwanted scarring
caused by PRK.
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