Morphological study on rupture of posterior capsule in RLC mouse lens.
OBJECTIVE
To clarify the causative factor underlying rupture of the posterior capsule of the RLC mouse lens as a recessive trait around the 50th postnatal day.


METHODS
The lenses of the RLC mouse were removed in the period from birth to 50th postnatal day. Some specimens were observed by light microscopy and transmission and scanning electron microscopy. Others were examined as flat preparations of the lens epithelium.


RESULTS
There was an abnormal arrangement of lens fibers at the newborn stage, and lens fibers of the perinuclear zone ended almost vertical in relation to the posterior capsule. Consequently, the posterior suture was not formed in this mouse lens. On the 10th postnatal day, the ends of the lens fibers that terminated in the posterior capsule became swollen, and the posterior capsule at the posterior polar region became thin. On the 20th day, the area of swollen fibers was so large at the center of the posterior capsule that a vacuolated area was observed under the dissecting microscope. On the 30th day, the posterior cortical fibers in this area showed marked swelling, and the posterior capsule became extremely thin. On the 40th day, the anterior cortex became unusually thick, and the lens nucleus was dislocated towards the posterior capsule. On the 50th day, the posterior capsule ruptured. At this time the lens fibers from the perinuclear zone constituted the central area of rupture, and the cortical fibers from the equator formed the protruded area outside the lens.


CONCLUSIONS
The findings revealed that the RLC mouse lens has an abnormal lens fiber arrangement from the early period of lens development, that the lens fibers from the perinuclear zone cause swelling without forming the posterior suture, and that the thin capsule is ruptured by pushing out of the nucleus by thickening of the anterior cortex.
Teramoto
Y
Y
Department of Ophthalmic Anatomy and Physiology, Graduate School of Medical Sciences, Kitasato University, 1-15-1 Kitasato, Sagamihara, Kanagawa 228-8555, Japan.
Uga
S
S
Matsushima
Y
Y
Shimizu
K
K
Morita
T
T
Shirakawa
S
S
D000375:Aging / Q000473:pathology; D000818:Animals; D004195:Disease Models, Animal; D007903:Lens Capsule, Crystalline / Q000473:pathology* / Q000648:ultrastructure; D007905:Lens Diseases / Q000209:etiology / Q000473:pathology*; D051379:Mice; D012422:Rupture, Spontaneous