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EDITORIAL
Year : 2001  |  Volume : 49  |  Issue : 3  |  Page : 151-152

Ocular surface failure is treatable


Dept. of Ophthalmology, Postgraduate Institute of Medical Education and Research, Chandigarh -160 012, India

Correspondence Address:
Jagiit S Saini
Dept. of Ophthalmology, Postgraduate Institute of Medical Education and Research, Chandigarh -160 012
India
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Source of Support: None, Conflict of Interest: None


PMID: 15887722

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How to cite this article:
Saini JS. Ocular surface failure is treatable. Indian J Ophthalmol 2001;49:151-2

How to cite this URL:
Saini JS. Ocular surface failure is treatable. Indian J Ophthalmol [serial online] 2001 [cited 2019 Nov 20];49:151-2. Available from: http://www.ijo.in/text.asp?2001/49/3/151/22628

The past few years have witnessed significant progress in understanding the cell dynamics of the ocular surface and its clinical applications. Several studies have confirmed that the corneal stem cells probably reside at the limbus in inter-palisade rete ridges, in the basal layer.[1] An intricate neuro-anatomic integration with blind reflex, tear production and clearance complements the continuous self-renewal with both vertical and centripetal horizontal cell kinetics. Application of these concepts is fundamental to understanding diseases of the ocular surface and management principles.

A deficiency of tear film formation (dry eye) is a relatively innocuous clinical problem. Attendant ocular surface failure is a far more serious clinical entity. It is critical however to initiate management of tear film disorders while managing ocular surface failure. Eyes with ocular surface failure generally have chronic symptoms of photophobia, tearing, blepharospasm, and recurrent episodes of pain, chronic inflammation with redness with or without decreased vision. The biomicroscopic findings at slitlamp examination may vary from dull irregular reflex of the corneal epithelium to ingrowth of thickened fibrovascular pannus, chronic keratitis, scarring and calcification. Because conjunctival epithelium is more permeable than corneal epithelium,[2] conjunctivalised corneal surfaces are frequently stained abnormally by fluorescein. The conjunctivalised surface of the cornea always shows a stippled staining pattern with fluorescein, is thinner than adjacent normal corneal epithelium, is irregular, prone to recurrent erosions and attracts new vessels.[3]

Persistent epithelial defects, melting and perforation of the cornea can occur in patients with stem cell deficiency. Corneal stem cell deficiency can be best confirmed histologically by the use of impression cytology[4] which can detect goblet cells containing conjunctival epithelium on the corneal surface. Immunohistochemically, the absence of a cornea-type differentiation (such as absence of keratin CK3), and the presence of mucin in goblet cells, has been shown by monoclonal antibodies.[5] Diagnosis of limbal stem cell deficiency is crucial because patients with this abnormality generally are poor candidates for conventional corneal transplantation. Lamellar or penetrating keratoplasty provides only a temporary replacement of the host's corneal epithelium because the grafted epithelial cells have a limited proliferative capacity and life span. Asymptomatic patients with partial and peripheral conjunctivalisation of the corneal surface may not require intervention.

Corneal and conjunctival epithelial cell phenotypes have been known to co-exist on the corneal surface for prolonged periods without significant extension of the conjunctivalised area nor any transdifferentiation of conjunctival epithelium into corneal phenotype of cells. [6, 7] If the visual axis or most of the corneal surface is covered with conjunctiva-like epithelium, mechanical debridement of conjunctival epithelium can allow adequate corneal epithelial healing to occur from the remaining intact limbal epithelium. In patients with total limbal stem cell deficiency, limbal auto or allotransplantation is indicated for corneal surface reconstruction. Although all techniques used in stem cell transplantation are similar in principle, the source of donor stem cells can vary. Donor tissue can be obtained from the fellow eye (i.e., limbal autograft) in cases of unilateral disease, or from a living related donor (usually gives a better tissue match) or from a cadaver donor (i.e.limbal allograft) when both eyes are affected. Many reports on these procedures have been published. There is a growing body of evidence that limbal transplantation is efficacious in replenishing the stem cells pool when deficient, promoting ocular comfort and improving vision.[8] There is however, limited success with allo-transplants of either fresh or cultured limbal stem cells.

The rediscovery of the virtues of amniotic membrane has provided another surgical tool for restoring the damaged milieu in severely damaged ocular surface disorders. Amnion alone does not restore normal ocular surface epithelium. Residual islands of stem cells or transplanted limbal stem cells are more successful in covering the cornea surface in presence of amnion membrane. [9, 10] There are riddles yet to be solved in completely understanding and modulating the immunobiology of limbal stem cell transplantation. There is hope for a hitherto complex variety of clinical ocular disorders characterised by ocular surface failure and more are likely to fructify in near future. The large number of articles on the subject in peer reviewed mainstream journals testifies to the growing confidence of clinicians and researchers in unfolding newer breakthroughs. Although there are several reviews on the subject in recent years,[11] the authors of the article "New perspectives in ocular surface disorders - an integrated approach for diagnosis and management"[12] published in this issue of the journal are to be complimented for a lucid description for the benefit of practicing ophthalmologists.



 
  References Top

1.
Davanger M, Evensen A. Role of the pericorneal papillary structure in renewal of corneal epithelium. Nature 1971;229:560-61.  Back to cited text no. 1
[PUBMED]  [FULLTEXT]  
2.
Huang AJW, Tseng SCG. Corneal epithelial wound healing in the absence ofs limbal epithelium. Invest Ophthalmol Vis Sci 1991;32:96-105.  Back to cited text no. 2
    
3.
Dua HS, Forrester JV, Cohen EJ, Laibson PR. Clinical observations on corneal epithelial cell migration in humans. Invest Ophthalmol Vis Sci 1993;34(S):1017.  Back to cited text no. 3
    
4.
Kenyon KR, Bulusoglu G, Ziske JD. Clinical pathologic correlations of limbal autograft transplantation. Am J Ophthalmol 1990;31:l.  Back to cited text no. 4
    
5.
Tseng SCG, Prabhasawant P, Barton K, Gray T, Meller D. Amniotic membrane transplantation with or without limbal allografts for severe ocular surface disorders. Ophthalmology 1995;102:1486-96.  Back to cited text no. 5
    
6.
Dua HS. Stem cells of the ocular surface: scientific principles and clinical applications. Br J Ophthalmol 1995;79:968-69.  Back to cited text no. 6
[PUBMED]  [FULLTEXT]  
7.
Dua HS, Gomes JAP, Singh A. Corneal epithelial wound healing. Br J Ophthalmol 1994;78:401-8.  Back to cited text no. 7
    
8.
Basu S, Rao SK. Current status of limbal conjunctival autografts. Curr Opin Ophthalmol 2000;11:224-32.  Back to cited text no. 8
    
9.
Meller D, Tseng SC. Amnion membrane transplantation with or without limbal allografts in corneal surface reconstruction in limbal deficiency. Ophthalmology 2000;97:100-107.  Back to cited text no. 9
[PUBMED]  [FULLTEXT]  
10.
Koizumi N, Fullwood NJ, Bairaktaris G, Inatomi T, Kinoshita S, Quantock AJ. Cultivation of corneal epithelial cells on intact and denuded human amniotic membrane. Invest Ophthalmol Vis Sci 2000;41:2506-13.  Back to cited text no. 10
[PUBMED]  [FULLTEXT]  
11.
Dua HS, Saini JS, Azuara-Bianco A, Gupta P. Limbal stem cell deficiency: Concept, aetiology, clinical presentations, diagnosis and management. Indian J Ophthalmol 2000;48:83-91.  Back to cited text no. 11
    
12.
Sangwan VS, Tseng SCG. New perspectives in ocular surface disorders: An integrated approach for diagnosis and management. Indian J Ophthalmol 2001;49:153-69.  Back to cited text no. 12
    



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