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Laser iris depigmentation (LID) modifies visible iris color through interaction with pre-existing anterior stromal pigmentation. Its biological effects extend beyond the immediate optical result to pigment-bearing cells, extracellular pigment material, and potentially the aqueous outflow pathway. Selective photothermolysis provides a physical basis for pigment-targeted pulsed irradiation. Histological studies in pigmented rabbit eyes document reduced anterior stromal pigmentation and an increased melanophage response after laser exposure. Pigment-perfusion experiments and trabecular-cell studies identify mechanisms through which pigment burden and cellular processing can influence outflow physiology. Human literature includes a 1,176-eye single-program clinical series and independent reports of secondary pigment dispersion and pigmentary glaucoma. This narrative review integrates iris morphology, laser–tissue interaction, treatment-related pigment dispersion, anterior-segment physiology, sequential clinical assessment, and long-term optical outcomes. It proposes controlled pigment dispersion as an observational construct: pigment liberation is assessed by its distribution, persistence, associated tissue response, and clinical consequences rather than treated as a binary event. A longitudinal response-guided framework connects these biological domains to follow-up, patient selection, and decisions about further exposure. Clinical evaluation rests on the combined assessment of iris appearance, anterior-segment status, pressure, and visual function.
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Mustafa Mete (2026) studied this question.
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