#Bear tracks retina free#

In 52% of patients, there is a ring of hypopigmentation or 'halo' surrounding the borders of the lesion. In some cases, lesions may lack pigment entirely (12%) - these are referred to as amelanotic lesions. Lesion borders are well-defined and are smooth or scalloped in appearance. Lesions are flat (or minimally elevated) and highly pigmented, appearing black in color.

Lastly, PO-FLs have been shown to be histologically similar to typical lesions, with both hypertrophic and hyperplastic RPE cells and thickening of the adjacent Bruch's membrane. Īs opposed to its solitary counterpart, GPR has been found to contain histologically normal cells, with no difference in cell size or density compared to normal RPE cells. Instead, its hyperpigmented appearance results from the increased density of melanin granules, which are large and ellipsoid in shape. Bruch's membrane is normal in these cases. The adjacent Bruch's membrane is thickened.

They possess large, spherical intracytoplasmic melanin granules in much higher density than normal RPE cells. Compared to normal cuboidal RPE cells, affected RPE cells are vertically elongated and range from cuboidal to columnar in shape. Īreas of atrophy, known as lacunae, may also occur throughout the lesion and correlate with depigmented funduscopic appearance. Without photoreceptors, there is no production of lipofuscin - waste products secondary to the normal RPE-mediated phagocytosis of photoreceptor outer segments. These changes disrupt the ability of the RPE to support the overlying photoreceptors, resulting in cell loss and thinning. Multiple studies, however, have found that cells also undergo hyperplasia (increase in cell number), resulting in thickening of the RPE layer. RPE cells in typical CHRPEs exhibit various degrees of cellular hypertrophy (increase in cell size) – normal, cuboidal RPE cells are vertically elongated and columnar in shape. These unique characteristics allow the RPE to provide functional support to the neural retina and act to maintain metabolic homeostasis via:Īlthough the term 'CHRPE' exclusively suggests hypertrophic cellular changes, histological analysis shows various morphologic cellular changes of CHRPE and its variants.

#Bear tracks retina free#

Another notable feature of RPE cells is their high concentration of intracellular melanosomes, a cellular organelle that produces pigment granules known as melanin. These molecules act to absorb stray light and neutralize free radical oxygen species. Outer to the neural retina is the retinal pigmented epithelium (RPE), a single (simple) layer of cuboidal epithelial cells joined together by zonula occludens junctions. These tight junctions allow RPE cells to act as a gate, containing bidirectional pumps that regulate the transport of molecules to and from the choroid and neural retina. The neural retina comprises seven layers of various photosensitive neurons that synapse on one another along a cascade that ultimately terminates in the visual cortex of the occipital lobe for interpretation. The photoreceptor layer houses the cell bodies of rod and cone photoreceptors these cells contain visual pigments responsible for absorbing light and triggering the conversion of light photons into neurochemical signals, a process known as phototransduction. Disruption of the homeostatic balance between the RPE and neural retina is the basis for many of the most common retinal diseases. The underlying choroid and its blood supply also play a crucial role in this process these three structures must work together to maintain homeostatic balance and function properly.

Truly, it comprises two distinct entities that work in concert with each other: the neural retina and the retinal pigmented epithelium. The retina is an ocular structure responsible for gathering gross visual stimuli that enter the eye and transforming them into neuronal signals transported to the brain for interpretation.