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EDITORIAL
Year : 2002  |  Volume : 50  |  Issue : 3  |  Page : 169-170

Amniotic membrane transplantation


Correspondence Address:
Virender S Sangwan


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Source of Support: None, Conflict of Interest: None


PMID: 12355689

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How to cite this article:
Sangwan VS. Amniotic membrane transplantation. Indian J Ophthalmol 2002;50:169-70

How to cite this URL:
Sangwan VS. Amniotic membrane transplantation. Indian J Ophthalmol [serial online] 2002 [cited 2020 Jun 3];50:169-70. Available from: http://www.ijo.in/text.asp?2002/50/3/169/14791

The management of patients with severe ocular surface disease has always been a challenge for ophthalmologists. Ocular surface reconstruction techniques have advanced considerably during the last few years moving away from the bare sclera techniques, through free conjunctival autograft, oral and nasal mucosal grafts, to the more potent and physiologic - limbal transplantation.[1] The role of limbal stem cells in maintaining the integrity of ocular surface and the clinical manifestations of limbal stem cell deficiency (LSCD) are now well documented.[2] The strategies for managing limbal deficiency include cadaveric or living related limbal transplantation in bilateral LSCD; simple debridement, amniotic membrane transplantation (AMT) and allotransplantation for unilateral LSCD.[2] Cultivated limbal epithelium on denuded human amniotic membrane has been developed as a new treatment for limbal stem cell deficiency. This new technology has great potential for a group of diseases otherwise considered to be incurable.[3] Recently AMT has been used for a variety of ocular surface problems including persistent corneal epithelial defects, for pterygium surgery, conjunctival defects after removal of surface tumours, acute and chronic chemical injuries, and shield ulcer of vernal keratoconjunctivitis.[2]

The amniotic membrane has an avascular stromal matrix and a thick basement membrane composed of collagen type IV, V and laminin. The basement membrane reinforces the adhesion of the basal epithelial cells, facilitates epithelial migration, and prevents epithelial and fibroblast apoptosis.[2] Also, thanks to its property of not expressing human leukocyte antigens, it is well tolerated and does not cause any rejection reaction in the host. Recent reports indicate that the potential mechanism of action might include the following: The basement side of the membrane is an ideal substrate for supporting the growth of epithelial progenitor cells by prolonging their life span and maintaining their clonogenicity.[4] This action supports the use of amniotic membrane transplantation to expand the remaining limbal stem cells and corneal transient amplifying cells in the treatment of partial limbal deficiency[4] and to facilitate epithelialization for persistent corneal epithelial defects with stromal ulceration. The amniotic membrane can also be used to promote non-goblet cell differentiation of the conjunctival epithelium and conjunctival goblet cell differentiation is further promoted by co-culturing with conjunctival fibroblasts on the same side of the basement membrane.[2]

The stromal side of the membrane contains a unique matrix component that suppresses TGF-β signaling, and proliferation and myofibroblast differentiation of normal human corneal and limbal fibroblasts.[2] This explains why amniotic membrane transplantation reduces scars during conjunctival surface reconstruction, prevents recurrent scarring after pterygium removal, and reduces corneal haze following phototherapeutic keratectomy (PTK) and photorefractive keratectomy (PRK).[2] The stromal matrix of the membrane can also exclude inflammatory cells and contains various forms of protease inhibitors.[5] This is why stromal inflammation is reduced after amniotic membrane transplantation and corneal neovascularisation is mitigated, actions important for preparing the stroma to support limbal stem cells to be transplanted at the same time or later.[5]

When appropriately processed and preserved, amniotic membrane can be used in a number of indications (as listed above), either as a graft to replace the damaged ocular surface stromal matrix or as a patch to prevent unwanted inflammatory insults from gaining access to the damaged ocular surface. In this issue of the Journal, Madhavan et al[6] describe the preparation and preservation of human amniotic membrane (HAM). The method has been described well in the reported literature but Madhavan et al have simplified the procedure and explained the process in detail.[6]

It is critical for safety that the procurement, processing, and preservation have to be aseptic. Do we have to use only preserved HAM? Is it safe to use fresh HAM? There are few studies addressing this issue and it seems that it may be reasonably safe to use fresh HAM provided all aseptic precautions are observed while procuring and processing it. A recent study[1] reported that the outcome using non-preserved HAM is similar to preserved HAM. They found non-preserved HAM to be a good alternative; it is also easily obtained in places where preserved HAM is not available or is too expensive to procure.

The main argument against fresh HAM use is lack of facilities, such as the need for a -70C refrigerator, which precludes its use outside big institutions and in developing countries.[1] This obviously limits the accessibility of the tissue for wider application. What is the advantage of preservation? Preserved HAM is widely used for ophthalmic indications and reported safety and success.[2] Preservation significantly impairs viability and impairs proliferative capacity.[7] It is believed that the immunogenicity of cryopreserved tissue is lower than that of fresh tissue. The immunogencity of cryopreserved HAM is not fully understood and still controversial.[8] Preservation offers the advantages of repeat serology after several months' non-viability of epithelial cells, and convenience in situations of high volume usage.

 
  References Top

1.
Mejia LF, Acosta C, Santamaria P. Use of nonpreserved human amniotic membrane for the reconstruction of ocular surface. Cornea 2000;19:288-91.  Back to cited text no. 1
    
2.
Sangwan VS, Tseng SCG. New Perspectives in ocular surface disorders. An integrated approach for diagnosis and management. Indian J Ophthalmol 2001;49:153-68.  Back to cited text no. 2
    
3.
Koizumi N, Inatomi T, Suzuki T, Sotozono C, Kinoshita S. Cultivated corneal epithelial transplantation in ocular surface disorders. Ophthalmology 2001;108:1569-74.  Back to cited text no. 3
[PUBMED]  [FULLTEXT]  
4.
Grueterich M, Tseng SCG. Human limbal progenitor cells expanded on intact amniotic membrane ex-vivo. Arch Ophthalmol 2002;120:783-90.  Back to cited text no. 4
    
5.
Shimmura S, Shimazaki J, Ohashi Y, Tsuboto K. Anti-inflammatory effects of amniotic membrane transplantation in ocular surface disorders. Cornea 2001;20:408-13.  Back to cited text no. 5
    
6.
Madhavan HN, Priya K, Malathi J, Joseph PR. Preparation of amniotic membrane for ocular surface reconstruction. Indian J Ophthalmol 2002;50:227-31.  Back to cited text no. 6
[PUBMED]    
7.
Kruse FE, Joussen AM, Rohrschneider K, You L, Sinn B, Baumann J, et al. Cryopreserved human amniotic membrane for ocular surface reconstruction. Graefes Arch Clin Exp Ophthalmol 2000;238:68-75.  Back to cited text no. 7
[PUBMED]  [FULLTEXT]  
8.
Kubo M, Sonoda Y, Muramatsu R, Masahiko U. Immunogenicity of human amniotic membrane in experimental xenotransplantation. Invest Ophthalmol Vis Sci 2001;42:1539-46.  Back to cited text no. 8
    




 

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