A historical note on the aetiology of phossy jaw shows that present-day knowledge is little greater than it was a century ago. The varied clinical course of the disease is described together with a report of 10 classical cases not previously reported. Six cases, not amounting to true necrosis but in which healing after dental extraction was delayed, are described, and mention is made of the noticeable differences in the oral state and appearances of tartar of healthy workmen exposed to phosphorus compared with healthy workmen not exposed. But no systematic differences of any kind were found in the incidence of general infections, fractures of bones, haematological findings, and biochemical studies of blood and urine in two groups of healthy men most exposed and least exposed to phosphorus in the same factory. An intensive study in hospital of a case of classical necrosis showed no departure from normal, except delayed healing following bone biopsy from the iliac crest, and a reversed polymorphonuclear/lymphocyte ratio. In the discussion the time of onset of necrosis after first exposure to phosphorus, clinical and radiological diagnosis, the organisms present, personal susceptibility, the appearance of the sequestra, and regeneration of bone are considered. An up-to-date note on prevention of the disease is given, although this has met with only partial success. Some persons are highly susceptible and, whilst complete protection is impossible in the light of our present knowledge, early diagnosis and modern treatment have robbed the disease of its terrible manifestations of Victorian times and turned it into a minor, although often uncomfortable complaint, with little or no resulting disability.

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CORRESPONDENCE MEDICAL JOURNAL bleeding point was found. She recovered. There was no mention of toxaemia of pregnancy in this case. In the absence of high blood pressure and arteriosclerosis the heart is incapable of raising the blood pressure sufficiently high to cause rupture of a normal artery, and some congenital or developmental defect must precede spontaneous rupture. Bruce (1937) suggested that the haemorrhage in this group may be due to rupture of a miliary aneurysm or a "junctional area." Bruce's suggestion was soon confirmed by Schuster (1937), who described a case of multiple aneurysms of the splenic artery which she believed were of congenital or developmental origin in a case of familial haemorrhage telangiectasis. Shallow, Herbut, and Wagner (1946) demonstrated defects in the muscle coat of the inferior pancreatico-duodenal artery associated with a ruptured congenital saccular aneurysm at the first bifurcation and three small fusiform dilatations in the more distal parts. At post mortem it is often difficult to demonstrate the bleeding point in this type of massive spontaneous intraperitoneal haemorrhage. However, careful dissection of the affected part and sectioning of the neighbouring vessel will demonstrate the cause-a ruptured miliary aneurysm or congenital defect of the arterial wall.-We are, etc., A. C. BREwER. Liverpool. R. MARcus.

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