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Annals of the Rheumatic Diseases 2003-Nov

Beta irradiation decreases collagen type II synthesis and increases nitric oxide production and cell death in articular chondrocytes.

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پیوند در کلیپ بورد ذخیره می شود
J Ailland
W U Kampen
M Schünke
J Trentmann
B Kurz

کلید واژه ها

خلاصه

BACKGROUND

When synovitis is proved, intra-articularly injected beta emitting radionuclides like yttrium-90 ((90)Y) are used to treat the inflamed synovium.

OBJECTIVE

To study the viability, matrix production, and NO production during or after (90)Y treatment of chondrocytes.

METHODS

Monolayer, alginate, and explant cultures of primary bovine articular chondrocytes as well as synoviocytes were incubated with 0-3 MBq (90)Y/ml medium for four days from culture day 3 onwards. Cell viability was demonstrated by light and electron microscopy or by trypan blue or ethidium bromide/fluorescein diacetate staining, membrane integrity by measurement of lactate dehydrogenase (LDH) activity in the culture supernatants. Biosynthetic activity was demonstrated by incorporation of [(3)H]proline and immunocytochemical staining of collagen type II. NO production was measured with the Griess reagent.

RESULTS

In chondrocyte and synoviocyte monolayer cultures radiation caused a dose dependent increase in cell death and membrane destruction within four days. In alginate and explant cultures, where proliferation is low, no significantly increased LDH activity was seen, and cell viability was approximately 100% for up to 14 days after irradiation. Collagen type II expression (alginate) and biosynthetic activity (alginate and explants) were decreased dose dependently while there was an increase in NO production. Light and electron microscopy data showed that five weeks after irradiation all cells in alginate and most cells in explants subjected to 3 MBq (90)Y/ml were dead, whereas after lower amounts of irradiation several morphologically intact cells were found.

CONCLUSIONS

beta Irradiation may influence the long term maintenance of cartilage tissue or the aetiology of degenerative joint diseases.

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