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

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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) Mark Willcox (Australia) Maria Markoulli (Australia) Reiko ARITA David SULLIVAN Nathan EFRON Stefano BARABINO Edoardo VILLANI Mark WILLCOX Erich KNOP Alison McDERMOTT Maria MARKOULI Tony BRON Jason NICHOLS Not pictured: Lyndon JONES

Subcommittee on Contact Lens Interactions with the Ocular Surface & Adnexa We concentrated on tissue interactions at the lower end of the severity spectrum Physiological vs Pathological

Subcommittee on Contact Lens Interactions with the Ocular Surface & Adnexa 'Whole' Cornea 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 * no proven link with discomfort

Subcommittee on Contact Lens Interactions with the Ocular Surface & Adnexa Corneal Epithelium 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 * no proven link with discomfort

Subcommittee on Contact Lens Interactions with the Ocular Surface & Adnexa Corneal Stroma 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† * no proven link with discomfort †Chalmers RL et al. Optom Vis Sci 2012; 89:(3):

Subcommittee on Contact Lens Interactions with the Ocular Surface & Adnexa Corneal Endothelium 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’)† * no proven link with discomfort †Sweeney DF. Optom Vis Sci 1992; 69:(8):601-8.

Subcommittee on Contact Lens Interactions with the Ocular Surface & Adnexa Limbus 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 †Bergenske P et al. Eye Contact Lens 2007; 33:(2):74-80.¥Martin R. Clin Exp Optom 2007; 90:(1):26-30.

Subcommittee on Contact Lens Interactions with the Ocular Surface & Adnexa Bulbar Conjunctiva 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? * no proven link with discomfort †Lakkis C et al. CLAO J 1996; 22:(3): ¥Pult H et al. Optom Vis Sci 2008; 85:(10):E924-9.

Subcommittee on Contact Lens Interactions with the Ocular Surface & Adnexa Palpebral Conjunctiva 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† * no proven link with discomfort †Young G et al. Eye Contact Lens 2009; 35:(2):50-8.

Subcommittee on Contact Lens Interactions with the Ocular Surface & Adnexa Meibomian Glands (MG) 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 * no proven link with discomfort †Blackie CA et al. Cornea 2010; 29:(12): ¥Korb DR et al. J Am Optom Assoc 1980; 51:(3):

Subcommittee on Contact Lens Interactions with the Ocular Surface & Adnexa Lid Margins 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 * 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.

Subcommittee on Contact Lens Interactions with the Ocular Surface & Adnexa Blinking 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%* * no proven link with discomfort

Subcommittee on Contact Lens Interactions with the Ocular Surface & Adnexa Conclusions Good evidence that CLD is linked to: – meibomian gland dysfunction – lid wiper epitheliopathy Weak evidence that CLD may be linked 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