LAUSR

To the Editor, The pathogenesis of posterior capsule opacification (PCO) is most likely multifactorial, but comparative studies among new products and their novel structures, and/or biomaterials are commonly performed.1 Current frequencies of PCO are considerably low and would appear to make any further progress in structural design that much more difficult. One other plausible recourse is to focus on immune regulation or dysregulation that may concomitantly arise and which may be open to modulation either through preventative biological treatments or further change in the bioactive chemistry of IOLs. Foreign bodies are generally renowned for inciting reactions from both innate and adaptive immunity. In the midst of such post-surgical response, the mast cell has a key potential role in both direct or indirect healing and immune processes.2 Whereas ophthalmological interests in the mast cell were historically and predominantly aimed at conjunctival allergic phenomena, the mast cell is known to exist as an effector cell in the choroid stroma, uvea, and corneoscleral limbus. Roles in corneal graft alloimmunity and specific macular diseases have been postulated even though the retina appears to be a privileged site where mast cells do not reside. Mast cell granules harbor various products, and mast cell subsets can be established based on granule content heterogeneity and other effector functions.2 In the uvea, for example, such heterogeneity has been shown to compartmentalize.3 Apart from immune or neural influences, mast cell activity has been associated with inflammation and healing, and may produce connective tissue or fibroblast growth factors. Whether PCO pathogenesis is considered for the fibrotic and remodeling outcomes that arise, the mast cell can conceivably have some role in either. A potential role for such growth factors in PCO causation has been proposed.4 Furthermore, as shown for odontogenic cysts, mast cell serine proteases (e.g. chymase, tryptase) can be documented in contiguous body cavities which in theory may include ocular chambers after surgical procedures.5 The latter does not exclude other mast cell effector functions from entering similar chambers whether aqueous or vitreous. As is well-known for the time-dependency for initiation and furtherance of PCO, time-dependent associations of PCO and mast cell presence are yet to be well-studied. In essence, the potential for the mast cell to play a pivotal role in PCO evolution in the context of a foreign body has scientific appeal. There is analogy to the mast cellrelated immunomodulation and activation that may occur in the presence of several other foreign body substances such as silicone.6 In the context of intraocular lenses, such material diversity and mast cell relationships merit further investigation. Introduction of an immune aspect of pathogenesis for PCO may also give credence to the concept of genetic heterogeneity and hence diverse patient susceptibility and phenotypic expression of disease. Contributions of any such interactions also remotely enters dialogue in regard to focal mast cell activation in the context of systemic disease.7 Such immunological arms of PCO pathogenesis deserves a renewed consideration given the availability and plethora of current and complex molecular biology tools.