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ARTICLES
Year : 1978  |  Volume : 26  |  Issue : 4  |  Page : 23-25

Degenerative lesions in retinoblastoma and their significance


1 Department of Pathology, Jawaharlal Nehru Medical College, Aligarh Muslim University, Aligarh, India
2 Reader of Ocular Pathology, Jawaharlal Nehru Medical College, Aligarh Muslim University, Aligarh, India
3 Reader in Ophthalmology, Jawaharlal Nehru Medical College, Aligarh Muslim University, Aligarh, India

Correspondence Address:
Nirmala Tyagi
Department of Pathology, Jawaharlal Nehru Medical College, Aligarh Muslim University, Aligarh
India
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Source of Support: None, Conflict of Interest: None


PMID: 437860

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How to cite this article:
Tyagi N, Hameed S, Gogi R, Ahuja O P, Nath K. Degenerative lesions in retinoblastoma and their significance. Indian J Ophthalmol 1978;26:23-5

How to cite this URL:
Tyagi N, Hameed S, Gogi R, Ahuja O P, Nath K. Degenerative lesions in retinoblastoma and their significance. Indian J Ophthalmol [serial online] 1978 [cited 2021 May 8];26:23-5. Available from: https://www.ijo.in/text.asp?1978/26/4/23/31497

Extensive necrosis and calcification in retinoblastoma have been observed by most of the workers.[2],[4],[5],[8] Necrosis is generally regarded as a result of overgrowth of the tumour mass in relation to its blood supply. Reese[8] has con­sidered calcium deposition as an inhibition of tumour growth and its concentration is related to spontaneous regression of the tumour.

The present study was undertaken to assess the incidence of various degenerative lesions and their correlation with the extent of the tumour.


  Material and Method Top


Surgical material from sixty cases of retinoblastoma diagnosed histopathologically at the Institute of Ophthalmology, Aligarh Muslim University, Aligarh, during the period of 1957 to September 1976 was utilized for the present study. Besides reviewing old slides fresh sections were cut at 4 to 5 microns thickness and stained with haemotoxylin and eosin and von Kossa stain to assess the nature of the degenerative changes.


  Observations and Comments Top


Necrosis and haemorrhage were seen in almost all the tumours (98.33%). This obser­vation was in complete agreement with the findings of other workers [4],[7],[8],[10],[11] who have described necrosis as a very common feature of retinoblastoma. The necrotic area was either sharply demarcated from the viable cells or sometimes the degeneration was gradual and a transitional zone between the viable cells and the necrotic tissue was noticed. Necrosis was variable and at times only a little portion of viable cells around a blood vessel was seen to form pseudorosette [Figure - 1] in the necrotic mass.

Various stages of degeneration were observed in different tumours or in the same tumour. At places the cells were less intensely stained as compared to normal cells while at other sites only acid stain or no stain was taken. The nuclei showed pyknosis and karyorrhexis or fragmentation simulating nuclear dust or leucocytes. This picture may be confused with suppurative endophthalmitis[9] or hypopyon when such material is present in the anterior chamber.[1] Macrophages or foam cells containing nuclear fragments, lipid material or mucin were also present-an observation identical to the findings of Reese[8 and Duke-Elder and Dobree[4]. No infiltration by neutrophils was seen in the necrosed tissue. This confirmed the observa­tions of other workers[1],[8] that the necrotic material is least toxic and does not give rise to inflammation as seen in melanoma.

Calcification was observed in 10 cases (16.67%) either in the form of darkly stained granular material or in clumps [Figure - 2]. This was further confirmed by von Kossa stain which imparted a black colouration to the calcified areas. Parkhill and Benedict[7] and Shivde et al[11] have also noticed calcification in 14.2% and 23.6% of tumours respectively. Calcification in the wall of blood vessels was seen in 3.3% cases [Figure - 3]. This finding was in accord with the observations of Reese' and Shivde et al[11].

Another interesting observation in the present study was the formation of Bone [Figure - 4] in one tumour (1.67%). Though Reese[8] has mentioned that bone could be found in the necrosed area of the tumour the author could not come across any report describing bone formation except that of Das[3].

An attempt was made to correlate the presence of calcification with the extent of the tumour (both intraocular and orbital). The frequency of infiltration of different structure in tumours with calcification and without calcifica­tion is shown in [Figure 5].


  Discussion Top


Calcium deposition is said to be an inhibitor of tumour growth and Reese[8] has suggested that in case of spontaneous regression of tumour the calcium concentration has been sufficient to prevent growth. Though none of the cases with calcification showed spontaneous regression in the present series, significant observation was that in these cases extension of the tumour was less as compared to those without calcifica­tion [Figure 5]. Thus calcification may have some beneficial effect-an observation in conformity with the views of Reeses. Though the invasion of the blood vessels was more frequent in cases with calcification but the low frequency of extra­ocular and distant metatases in retinblastoma has minimised the importance of this observa­tion. Probably the seedlings are destroyed or fail to get proper environment to flourish.


  Summary Top


Degenerative morphological changes were studied in 60 cases of retinoblastoma. Necrosis was seen in more or less all the tumours (98.33%). The degree of necrosis was variable. Calcification was observed in 10 tumours (16.67). In two cases wall of the blood vessels were also calcified. Bone formation was seen in one tumour (1.67%).

Though no spontaneous regression was found in any case, the frequency of spread of tumour both intraocular and extraocular was comparatively low in cases showing calcification in the necrosed area.

 
  References Top

1.
Ashton, N., 1958, Cancer, edited by Raven, R.W., 2, London, Batterworth Medical Publication, 599.  Back to cited text no. 1
    
2.
Cook, A.G., 1966, Systemic Pathology, 2, edited by Wright., G.P. and Symmers, W.St.S, Ed. 1st, London, Longmans Green & Co. Ltd., 1636.  Back to cited text no. 2
    
3.
Das, S.P., 1964, Jour. All India Ophthal. Soc. 12, 128.  Back to cited text no. 3
    
4.
Duke-Elder, S. and Dobree, J.H., 1967, Diseases of the Retina in Duke-Elder's System of Ophthalmology 10, St. Louis, The C.V. Mosby & Co., 692.  Back to cited text no. 4
    
5.
Evans, R.W., 1968, Histological Appearances of Tumours, 2, London, E. & S. Livingstone Ltd., 448.  Back to cited text no. 5
    
6.
Hogan, M J. and Zimmerman, L.E., 1962, Ophthalmic Pathology, 2, Philadelphia, W.B. Saunders Co., 516.  Back to cited text no. 6
    
7.
Parkhill, E.M. and Benedict, W.L., 1941, Amer. Jour. Ophthal., 24, 1354.  Back to cited text no. 7
    
8.
Reese, A,B., 1963,Tumours of the Eye, 2, New York, Harper & Row, 84.  Back to cited text no. 8
    
9.
Scullica, L., 1959, Ann. Ottae e Clin., 85, 395.  Back to cited text no. 9
    
10.
Sinha, A.K., 1975, Indian Jour. Ophthal., 23, 20.  Back to cited text no. 10
    
11.
Shivde, A.V., Kher, N., Hardas, Usha D. and Sharma, K.D., 1975, Indian Jour. Cancer, 12,144.  Back to cited text no. 11
    


    Figures

  [Figure - 1], [Figure - 2], [Figure - 3], [Figure - 4]



 

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