| Domain | Established finding | Suggested ontology terms | Evidence type/strength |
|---|---|---|---|
| Definition | Ocular pigment dispersion syndrome (PDS) is an anterior-segment disorder in which pigment granules are released from the posterior iris, disperse through the aqueous humor, and accumulate in structures including the trabecular meshwork; this can raise intraocular pressure (IOP) and progress to pigmentary glaucoma (PG). (pqac-00000001, pqac-00000002) | Suggested: MONDO pigment dispersion syndrome; MeSH Pigment Dispersion Syndrome; NCIT pigmentary glaucoma; GO aqueous humor outflow | Human clinical + review synthesis; moderate-to-strong |
| Classic triad | The classic ophthalmic signs are typically described as midperipheral iris transillumination defects, a Krukenberg spindle on the corneal endothelium, and dense trabecular meshwork pigmentation on gonioscopy. Pigment deposition in the angle is a key clinical observation. (pqac-00000002) | Suggested HPO: iris transillumination defect; corneal pigmentation/Krukenberg spindle; abnormal trabecular meshwork pigmentation | Established clinical phenotype; moderate |
| Mechanism | The leading mechanism is mechanical contact between lens zonular fibers and the posterior iris, causing release of iris pigment. Progressive pigment loading of the trabecular meshwork contributes to dysfunction, reduced phagocytosis and migration, increased stress fibers/cell contraction, loss of trabecular cells, and increased outflow resistance, producing ocular hypertension and possibly PG. (pqac-00000001) | Suggested GO: phagocytosis; cell migration; actin filament organization; regulation of actomyosin structure organization; aqueous humor outflow; response to mechanical stimulus | Human clinicopathologic + experimental support; strong for mechanical/outflow model, moderate for downstream cellular details |
| Main anatomy/cells | Primary affected structures are the posterior iris, lens zonules, aqueous humor pathway, trabecular meshwork, and Schlemm canal. Key cell types include iris pigment epithelial cells/melanocyte-lineage cells and trabecular meshwork cells. The posterior trabecular meshwork is the more pigmented filtering region clinically. (pqac-00000001, pqac-00000002) | Suggested UBERON: iris, posterior iris epithelium, lens zonule, anterior chamber, trabecular meshwork, Schlemm canal; Suggested CL: trabecular meshwork cell; iris pigment epithelial cell | Anatomy/clinicopathology; strong |
| Progression to pigmentary glaucoma | Not all PDS cases progress, but pigment accumulation can lead to ocular hypertension and PG. One review-level source states that 25-50% of patients with PDS are at risk of developing ocular hypertension. (pqac-00000001) | Suggested HPO: ocular hypertension; open-angle glaucoma; elevated intraocular pressure | Human observational/review evidence; moderate, quantitative estimate should be treated as literature-derived range |
| Risk profile | PDS is associated clinically with pigment accumulation in the angle and can be exacerbated by factors increasing pigment liberation; literature outside the provided context commonly notes younger myopic males as a classic profile, but that demographic detail is not directly supported in the available context set and should be labeled as external if used in the main report. Within available context, the mechanistic risk is posterior iris-zonule contact leading to continued pigment release. (pqac-00000001) | Suggested HPO: myopia; abnormal iris anatomy; pigment dispersion | Mixed evidence; strong for mechanistic risk, insufficient in-context support for detailed demographic profile |
| Diagnosis | Diagnosis relies on slit-lamp examination and gonioscopy, which assess angle openness, amount of pigmentation, and angle anatomy. Newer adjunctive imaging discussed for trabecular assessment includes anterior-segment OCT, gonioscopy-coupled OCT, and adaptive-optics scanning laser ophthalmoscopy, but gonioscopy remains the practical core exam. (pqac-00000002) | Suggested NCIT: gonioscopy; optical coherence tomography; slit-lamp examination; HPO: abnormal anterior chamber angle pigmentation | Standard clinical practice; strong for gonioscopy, emerging for advanced imaging |
| Management | Management is stage-based and centers on lowering IOP when ocular hypertension or PG is present. Options include topical medications, laser trabeculoplasty (especially SLT, targeting pigmented trabecular cells), and surgery for uncontrolled disease. ROCK inhibitors act on trabecular cytoskeleton/ECM pathways; trabeculectomy and nonpenetrating deep sclerectomy lower IOP more substantially than trabecular MIGS but with more risk. (pqac-00000000, pqac-00000002) | Suggested NCIT: prostaglandin analog therapy; Rho kinase inhibitor therapy; selective laser trabeculoplasty; trabeculectomy; minimally invasive glaucoma surgery | Human therapeutic evidence + review synthesis; moderate-to-strong |
| Evidence caveat | The available context strongly supports trabecular/anterior-segment pathophysiology and management principles, but does not provide definitive in-context support for exact disease identifiers, all phenotype frequencies, or genetic loci; those should be sourced separately in the full report. (pqac-00000000, pqac-00000001, pqac-00000002) | Suggested evidence tags: human clinical; review; experimental model | High-confidence limitation statement |


*Table: This table summarizes high-yield, knowledge-base-ready findings for ocular pigment dispersion syndrome, including core definition, mechanisms, anatomy, diagnosis, and management. It also distinguishes supported findings from areas where ontology mappings or evidence remain provisional.*