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Report of the Subcommittee on Contact Lens Interactions with the Ocular Surface & Adnexa

Report of the Subcommittee on Contact Lens Interactions with the Ocular Surface & Adnexa Membership Nathan Efron (Australia) Lyndon Jones (Canada) Anthony Bron (UK) Erich Knop (Germany) Reiko Arita (Japan) Stefano Barabino (Italy) Alison McDermott (USA) Edoardo Villani (Italy)

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Report of the Subcommittee on Contact Lens Interactions with the Ocular Surface & Adnexa

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  1. Report of the Subcommittee on Contact Lens Interactions with the Ocular Surface & Adnexa Membership Nathan Efron (Australia) Lyndon Jones (Canada) Anthony Bron (UK) Erich Knop (Germany) Reiko Arita (Japan) Stefano Barabino (Italy) Alison McDermott (USA) Edoardo Villani (Italy) Mark Willcox (Australia) Maria Markoulli (Australia) Not pictured: Lyndon JONES David SULLIVAN Mark WILLCOX Nathan EFRON Edoardo VILLANI Stefano BARABINO Reiko ARITA Erich KNOP Alison McDERMOTT Maria MARKOULI Tony BRON Jason NICHOLS

  2. Physiological vs Pathological We concentrated on tissue interactions at the lower end of the severity spectrum

  3. Edema*: SiHys have largely obviated edema (<3% in EW) edema is less towards limbus ('clamping') Shape change*: topography can detect minor shape changes in soft CLs SiHys cause 0.35D central corneal flattening Temperature*: slight temp decrease with CLs 'Whole' Cornea * no proven link with discomfort

  4. Thinning*: rigid > Hys > SiHys Retardation of desquamation*: SiHys cause least interference Irregular basal cell morphology*: observed in long-term Hy wear Staining*: insignificant staining common Microcysts*: indicate metabolic dysfunction Halos*: due to epithelial edema Dendritic (presumed Langerhans) cells*: increase with soft CL wear Corneal Epithelium * no proven link with discomfort

  5. Edema*: striae & folds; orthogonal lines (LSCM) Thinning*: stroma thins 2.1µm/yr with Hy EW Neovascularisation*: limbal vessel penetration with Hy lenses Keratocyte loss*: due to physical impact of CLs Microdots*: dysgenic or apoptotic cells? Infiltrates: may be symptomatic† Corneal Stroma * no proven link with discomfort †Chalmers RL et al. Optom Vis Sci 2012; 89:(3):316-25.

  6. Blebs*: benign artifact swollen cells reflect light away lens Dk/t inversely related to blebs Cell redistribution*: cells to spread out from centre leads to reduced central ECD Polymegethism: caused by cell border straightening severe cases linked to discomfort: ('corneal exhaustion syndrome’)† Corneal Endothelium * no proven link with discomfort †Sweeney DF. Optom Vis Sci 1992; 69:(8):601-8.

  7. Vessel engorgement (redness): 0.13mm in non-lens wearers vs. 0.47mm with Hy lenses SiHy lenses reduce redness driven by hypoxia link to CL discomfort† Stem cell deficiency: can be focal or circumlimbal in 2.4% of soft CL wearers possibly due to hypoxia, toxicity or direct mechanical insult one third of patients symptomatic¥ risk factors: female; length of wear Limbus †Bergenske P et al. Eye Contact Lens 2007; 33:(2):74-80. ¥Martin R. Clin Exp Optom 2007; 90:(1):26-30.

  8. Staining: associated with ‘dryness’† Flaps*: appears to be mechanical Lid parallel conjunctival folds (LIPCOF): associated with ‘dryness’¥ Conjunctivochalasis*: associated long-term soft lens wear? Hyperemia*: due to mechanical effects & hypoxia Reduced goblet cell density*: with soft CL wear Rolling leucocytes in vessels*: indicates sub-clinical inflammation? Bulbar Conjunctiva * no proven link with discomfort †Lakkis C et al. CLAO J 1996; 22:(3):189-94. ¥Pult H et al. Optom Vis Sci 2008; 85:(10):E924-9.

  9. Redness*: increases with CL wear 'Normal' tarsal conjunctiva*: 'satin' or 'smooth' – 14% uniform micropapillae (all <0.3mm) – 85% non-uniform micropapillae (up to 0.5mm) – 1% Papillary changes: low grade changes induce 'itchiness' & discomfort† Palpebral Conjunctiva * no proven link with discomfort †Young G et al. Eye Contact Lens 2009; 35:(2):50-8.

  10. Drop-out (meibography & LSCM)*: caused by rigid lenses Shortening (meibography)*: caused by soft lenses Duct obstruction (LSCM)*: ‘non-obvious MGD’ is symptomatic† Tear foaming*: associated with symptomatic CL wear¥ Inflammation (LSCM)*: impaired lower lid margin integrity Relationship to papillary conjunctivitis*: suggested link in CL wearers Altered meibum composition*: may be related to CL wear Meibomian Glands (MG) * no proven link with discomfort †Blackie CA et al. Cornea 2010; 29:(12):1333-45. ¥Korb DR et al. J Am Optom Assoc 1980; 51:(3):243-51.

  11. Lid wiper epitheliopathy (LWE):Found in: 80% of symptomatic CL wearers† 13% of asymptomatic CL wearers† Lid margin (LM) microbiome*: CFUs on LM swabs range from 0 – 465 coag-negative staph most often found DW – LM microbes increase over time EW – LM microbes decrease over time LM microbiota increase in in dry eye Lid Margins * no proven link with discomfort †Korb DR et al. CLAO J 2002; 28:(4):211-6; Yeniad B et al. Eye Contact Lens 2010; 36:(3):140-3.

  12. Blinking*: facilitates tear exchange flushes out debris promotes gaseous exchange interacts with eye movements Impact of CLs: rigid CL discomfort with blinking (see lens design sub-committee) reduces blink completeness alters blink rate* blinking exerts backwards squeeze pressure & tangential shearing force on CLs* tear exchange: soft 2%; rigid 16%* Blinking * no proven link with discomfort

  13. Good evidence that CLD is linked to: meibomian gland dysfunction lid wiper epitheliopathy Weak evidence that CLD may belinked to: corneal infiltrates limbal vessel redness limbal stem cell deficiency conjunctival staining lid-parallel conjunctival folds papillary conjunctivitis [low grade] Important areas for future research: role of staining, LWE & MGD in CLD CL-induced tissue changes & CLD over time Conclusions

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