Studies on the effect of acute doses of indomethacin [prostaglandin inhibitor] during induced liver failure

54 male mice were divided into 3 main groups: Control group [6 mice], Schistosoma mansoni infected group [24 mice] and carbon tetrachlorid [CCl4] treated group [24 mice]. The last 2 groups were further subdivided into [4] subgroups [6 mice/each]. One of them served as a control while the other 3 subgroups received [0.75, 1.25 and 2.5 mg/100 g BW] of indomethacin, respectively. Indomethacin made the liver functions deteriorate. Schistosomiasis did not affect kidney functions while urea and creatinine were elevated in CCl4- treated group. Indomethacin led to more elevation of both. Histological studies of liver treated by CCl4 revealed portal venous congestion, granular cytoplasm and cellular infiltration while schistosomiasis produced the classic granulomatous reaction. Indomethacin treatment led to distortion of hepatic cell arrangement as well as marked cellular infiltration and congestion. On the other hand, kidney treated with CCl4 showed cellular infiltration around glomeruli, indomethacin caused marked congestion and cellular infiltration. Schistosoma infection did not produce any historical changes. All recorded changes could be attributed to the toxic effect of indomethacin, inhibition of prostaglandins and weakness of the immunological cells of liver

Bilharzial arthropathy of the temporomandibular joint

Bilharziasis was experimentally induced in Swiss albino mice in order to study the histopathological changes in the TMJ in case of bilharzial infection. The bony components of the joint showed massive chronic inflammatory cell infiltration. The articular disk [meniscus] showed thickening and hyperplastic changes with narrowing of the joint space. The articulating surfaces showed erosions and irregularity. It was concluded that bilharziasis can cause arthropathy of the temporomandibular joint [TMJ]