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Feature Review | Previous Articles
July 2005


Contact Lens Papillary Conjunctivitis – An Update

Cheryl Skotnitsky, OD

Cheryl Skotnitsky graduated from the School of Optometry at The University of Waterloo in 1985 and worked in private practice for several years before joining the Cooperative Research Centre for Eye Research and Technology, Sydney Australia as a Research Optometrist. Cheryl’s main focus is contact lens research and she has several publications in this area and has made numerous presentations at international conferences. Currently, Cheryl is engaged in a PhD on contact lens induced papillary conjunctivitis at the Vision Cooperative Research Centre and the School of Optometry and Vision Science, UNSW, Sydney Australia.


The high-Dk silicone hydrogel lens is now a significant player in the contact lens field. Despite this, there is much that is not known on the characteristics of this lens type and the development of contact lens-induced papillary conjunctivitis (CLPC), also known as giant papillary conjunctivitis (GPC).

In 2003 Peter Donshik from the University of Connecticut Health Center published (Eye & Contact Lens: Clinical & Laboratory Science; 2003, 29:S37-9) a broad and concise overview of GPC with an emphasis on contact lens polymers and with reference to high-Dk silicone hydrogel lenses. This article will summarise Peter Donshik’s review and introduce the latest findings in this area.

What is CLPC

CLPC is an inflammatory reaction of the upper tarsal conjunctiva that is typically characterised by enlarged papillae (>0.3mm), hyperaemia of the upper tarsal conjunctiva and mucus secretion in the tear film and between papillae. Subjects may be asymptomatic or have symptoms ranging from foreign body sensation, itching, blurred vision and excessive lens movement. The condition can be serious enough to cause intolerance to lens wear.

As acknowledged by Donshik, CLPC was most often reported as a bilateral event, with only 10% of cases being unilateral, however since the introduction of high-Dk silicone hydrogels, we are seeing a greater proportion of unilateral events. As described in Donshik’s review, silicone hydrogels are associated with two types of CLPC, which can be differentiated with respect to the location of papillae on the palpebral conjunctiva. Events with papillae spread across the entire conjunctiva are termed 'general' and when papillae are confined to 1 or 2 regions of the conjunctiva, mainly near the lid margin and central areas they are termed 'local' (1, 2). Recent analysis of data from collaborative clinical trials conducted in India and Australia involving 1,820 subjects have confirmed that these two types of CLPC occur with both high- Dk silicone hydrogels and with low-Dk hydrogels, and have shown that a significantly greater proportion of events that occur with silicone hydrogels are local compared to low-Dk hydrogels (see poster, (3)).

Aetiology of CLPC

CLPC is a complex disease with strong evidence for an allergic aetiology (increased IgE and IgG levels in tears of active CLPC patients) in response to contact lens materials or coatings (eg deposits) and also for a mechanical aetiology involving lens-induced trauma at the conjunctiva (4). Donshik illustrates how both trauma to the conjunctiva and antigenic stimuli contribute to the release of inflammatory mediators and describes how contact lens coatings may exacerbate the antigenic response or may contribute further to trauma at the conjunctival surface.

The case for hypersensitivity includes evidence that CLPC is associated with individuals who are susceptible to allergy, that more events occur in spring, and that greater numbers of mast cells, basophils and eosinophils are observed in the epithelial conjunctiva of CLPC patients compared to asymptomatic lens wearers. The ability for deposits to cause increased risk is supported by data showing that regular replacement of lenses or regular use of enzyme cleaners increases tolerance to lens wear. However it is not yet understood how and what type of lens coatings contribute to CLPC. Ballow, Donshik, Rapacz and colleagues’ study (5) of the effects of worn contact lenses in monkeys suggests that lens coating formed during active CLPC stimulates the papillary response via an allergy response. In their study, lenses taken from subjects with and without CLPC and unworn lenses were placed onto monkey eyes. Elevated levels of IgE, which is a mediator of allergic reactions, were found in tears when worn lenses from subjects with CLPC were placed in the monkey eye, but not when those from asymptomatic subjects or unworn lenses were used.

Low-Dk hydrogel lenses have been classified by the US Food and Drug Administration (FDA) into four groups based on ionicity and water content of the material:

  • Group I lenses are non-ionic and low water content,
  • Group II lenses are non-ionic and high water content,
  • Group III lenses are ionic and low water content, and
  • Group IV are ionic and high water content.

In general high water content lenses (Groups II and IV) accumulate greater amounts of deposits compared to low water content lenses (Groups 1 and III) and ionic lenses (Groups III and IV) tend to accumulate higher levels of protein deposits, such as lysozyme, compared to non-ionic lenses. Despite these differences all lens types to some degree are associated with CLPC; there is no correlation between the amount of protein on lenses and development of CLPC, and the surfaces of contact lenses from CLPC and asymptomatic wearers can be very similar (6, 7).

In 1994, Donshik reported results from his study of over 100 patients wearing different classes of lenses. Although there was no significant difference in the incidence of CLPC among the different groups or type of deposits (8) the signs and symptoms of CLPC in wearers of Group I lenses were less severe than those wearing Group III lenses. This differs somewhat to Hart et al. (7) and Sankaridurg (9) who reported a greater incidence of CLPC with polymacon lenses (Group 1) compared to etafilcon A lenses (Group IV). These conflicting studies indicate that in addition to the state of the lens coating, other factors associated with lens material and design also contributes to CLPC.

High-Dk silicone hydrogel lenses are made from low water content materials and have been classified into Group I (non-ionic) and sometimes Group III (ionic). It is not clear how useful the FDA classification is for silicone hydrogels as there are major differences in chemical composition and on-eye performance between this lens type and low-Dk hydrogels. Silicone hydrogel lenses accumulate relatively little protein deposits during wear compared to low-Dk hydrogels (10, 11) and higher levels of lipid. In addition silicone hydrogels have a greater degree of lysozyme denaturation compared to ionic lenses (11) which may contribute to development of CLPC.

In his review Donshik explored whether local CLPC is unique to high-Dk silicone hydrogel lenses with extended wear, and whether it occurs because of mechanical factors, lens coating or frequency of replacement. The papillary response arising from trauma to the conjunctiva such as that produced by sutures (12, 13), ocular prostheses (14) or epithelialised foreign bodies (15) provides evidence for the mechanical aetiology of CLPC. It is postulated that mechanical interaction of a contact lens edge or material, particularly with stiffer high-Dk silicone hydrogel lenses, causes chronic irritation of the upper lid and may be responsible for initiating the reaction (16). This is supported by the higher proportion of local cases with silicone hydrogels recently confirmed by Skotnitsky (see poster, (3)). Further evidence for a mechanical effect comes from the differences in the location of papillae that occur between soft and RGP lenses. In low-Dk soft lenses papillae form along the tarsal plate and progress to the lid margin whereas in RGP lenses, papillae occur along the lid margin when first observed and tend to progress to the central area of the palpebral conjunctiva, (17) which is similar to that observed with high Dk silicone hydrogels.

Management of CLPC

Management options for CLPC include changing lens material either to another soft lens or an RGP lens material, instituting a regular cleaning regimen, reducing wear time, or more rarely pharmacological intervention in severe cases.

Lens wear should be discontined until symptoms have resolved and the upper palpebral conjunctiva is quiet (usually between 3 and 4 weeks). If patients resume lens wear they are less likely to have a recurrence if they are refit with another soft lens material or an RGP lens. For low-Dk hydrogel lenes, the recurrence of CLPC is 20% when patients are refitted from one hydrogel material to another or to an RGP material as opposed to 40% when refitted with the same material. However a change in replacement schedule appears to be of most benefit in reducing the risk of developing CLPC. In a retrospective study, Porazinski and Donshik (18) found the incidence of CLPC in a group of daily wearers to be 36% in those who replaced their lenses every 4 weeks or longer, and was 4.5% in those who replaced their lenses more frequently (1 day to 3 weeks).

Skotnitsky and colleagues have recently examined the recurrence of CLPC in silicone hydrogel EW subjects and found a high recurrence rate when subjects were refit with the same high-Dk silicone hydrogel lenses and maintained their EW schedule (see poster, (3)). If subjects were refit with silicone hydrogels but switched to a daily disposable schedule then the recurrence rate was significantly reduced (Skotnitsky PhD thesis 2005, in progress). Silicone hydrogel lens wearers who develop CLPC need to discontinue lens wear until the eye is quiet once more and can resume lens wear on a daily disposable or frequent replacement schedule (up to two weeks) with a low-Dk hydrogel lens.


Antigenic challenge and mechanical irritation of the conjunctival surface are clearly involved in the development of CLPC. Although accumulation of lens coatings during wear appears to be a key contributing factor, other factors including lens chemistry and modulus of elasticity, edge design, surface properties, fitting characteristics and replacement cycle also play a role.

When managing CLPC patients practitioners need to be aware of the high risk of recurrrence if they resume extended wear with silicone hydrogels.


  1. Sankaridurg PR, Sweeney D, Naduvilath T, et al. Papillary reponse in contact lens papillary conjunctivitis is either general or localised. [ARVO abstract] Invest Ophthalmol Vis Sci 2001;42:S596.
  2. Skotnitsky C, Sankaridurg PR, Sweeney DF, et al. General and local contact lens induced papillary conjunctivitis (CLPC). Clin Exp Optom 2002;85:193-197.
  3. Skotnitsky C, Sweeney DF, Naduvilath T, Sankaridurg, P. The incidence of local and general contact lens induced papillary conjunctivitis in silicone hydrogel contact lenses. Invest Ophthalmol Vis Sci. 2005 46: E-Abstract 2064.
  4. A llansmith MR, Korb DR, Greiner JV, Henriquez AS, Simon MA. Giant papillary conjunctivitis in contact lens wearers. Am J Ophthalmol 1977;83:697-708.
  5. Ballow M, Donshik PC, Rapacz P, Maena R, Yamase H, Muncy L. Immune responses in monkeys to lenses from patients with contact lens induced giant papillary conjunctivitis. CLAO J 1989 15:64-70.
  6. Tripathi PC, Tripathi RC. Analysis of glycoprotein deposits on disposable soft contact lenses. Invest Ophthalmol Vis Sci 1992; 33 (1):121-125.
  7. Hart DE, Schkolnick JA, Bernstein S, et al. Contact lens induced giant papillary conjunctivitis: a retrospective study. J Am Optom Assoc 1989;60:195-204.
  8. Donshik PC. Giant papillary conjunctivitis. Trans Am Ophthalmol Soc 1994;92:687-744.
  9. Sankaridurg PR. Corneal infiltrative events with extended wear of disposable hydrogel contact lenses [Doctor of philosophy]. Sydney: University of New South Wales; 1999.
  10. McKenney C, Becker N, Thomas S et al. Lens deposits with a high Dk hydrophilic soft lens. Optom Vis Sci 1998;75:276
  11. Jones L, Senchyna M, Glasier, MA et al. Eye Contact Lens 2003;29:575-579
  12. Jolson AS , Jolson SC. Suture barb giant papillary conjunctivitis. Ophthalmic Surg 1984;15:139-140.
  13. Skrypuch OW, Willis NR. Giant papillary conjunctivitis from an exposed prolene suture. Can J Ophthalmol 1986;21:189-192.
  14. Meisler DM, Krachmer JH, Goeken JA. An immunopathologic study of giant papillary conjunctivitis associated with an ocular prosthesis. Am J Ophthalmol 1981;92:368-371.
  15. Greiner JV. Papillary conjunctivitis induced by an epithelialised corneal foreign body. Ophthalmology 1988;196:82-86.
  16. Holden BA, Sankaridurg PR, Jalbert I. Adverse events and infections. In: Sweeney D.F., editor. Silicone hydrogels: the rebirth of continuous wear. Oxford: Butterworth Press; 2000. p. 150-213.
  17. Korb DR, Allansmith MR, Greiner JV, et al. Prevalence of conjunctival changes in wearers of hard contact lenses. Am J Ophthalmol 1980; 90: 336-341.
  18. Porazinski AD, Donshik PC. Giant papillary conjunctivitis in frequent replacement contact lens wearers a retrospective study. CLAO J 1999;25:142-147.
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