It is the development of this osteoid tissue thai is the true characteristic histological feature of rickets.

This disease appears to be remarkably wide-spread. Schmorl6 states that histological investigation on 386 children dying before the age of four years showed that 90 per cent had rickets. Dick7 has reported that 80 per cent of the children in the London County Council schools were found to have symptoms of this disease, and Findlay (1. c.) states that evidence points to an incidence of probably not less than 50 per cent in the general population of the industrial areas of Great Britain. Hess found that 90 per cent of the children in a New York orphan asylum were affected. In a recent paper on rickets in Germany, Engel8 asserts that the number of rachitic children constantly increased during the war. These children in many cases were dwarfed, deformed, and in a number of cases unable to walk at the age of three, four and even six or seven years. It is estimated that in the town of Dortmund, where there were about 30,000 children, 10 per cent cannot walk. Dalyell9 reports from Vienna that in one community, which included many breast-fed infants, rickets was diagnosed in 50 per cent of the children of five months and 100 per cent of those of nine months of age.

• Schmidt and Schmorl, Ergeb. d. enn. Med. u. Kind. 4, 403, 1909. 6 Schmorl, Verhand, der. deutsch. path. Gesel. 1909, 58.

7 Dick, Proc. Roy. 8oc. Med. Sect, for Difl. Child., 1915, p. 83.

8 Engel, Lane. 1920, i, 188.

9 Dalyell, Brit. Med. J. July 31, 1920.

Many theories have been advanced to account for the development of rickets. Some of these are now generally discredited and may be dismissed with a word.

Heredity appears to have no direct connection, although Siegert10 believes that the appearance of the disease in breast-fed children may be accounted for on this ground.

The view common at one time that rickets was to be regarded as a manifestation or result of congenital syphilis no longer receives any consideration.

The theory of an infective organism has been held by various authors,11 some of whom claim that they have induced the disease by inoculation or contact with an infected animal. Recent work has not confirmed this view, however, and it seems probable that the observed results are susceptible of other interpretation.

While some writers have maintained that want of breast feeding is the cause of the disease, others have held that too prolonged suckling is responsible. The work of Pindlay12 has eliminated both these possibilities.13

Attempts to establish a direct connection between rickets and deficiency of some internal secretion have been equally unsuccessful.14

Faulty diet or digestion resulting in the production of acidosis of some form of intoxication has been suggested by several writers as the cause of the rachitic condition, but this has never been confirmed and, on the other hand, other forms of acidosis produce no such decalcification of the bones. Lienaux and Huynen15 regard both rickets and osteolmalacia as a special type of acidosis in the broader sense, due to the unsatisfactory proportions of the calcium and the phosphoric acid in the diet. They base their theory on observations made on farm animals and the satisfactory results obtained by addition of lime to a calcium-poor diet. It has been found, however, that abundance of calcium alone, whether supplied in the form of milk or as calcium phosphate, will not necessarily protect against rickets, while a diet low in calcium may not produce rickets even though evidence of the calcium deficiency is found in the softness of the bones.16

10 Siegert, Verhand. d. Gesell. f. Khde. 1903; Jahrb. f. Khde. 58 and 59.

11 Torane and Salvatore Forte, La Pediatria, Sept 1907; Moussu, Bulletin de la Society Centr., Vol. LVTL; Koch, Zeit. f. Hyg. und Infektions-krankheiten, 72, H. 2, 321; Koch, Zeit. f. Hyg. und Infektons-krankheiten, 69, 436; Mircoli, Pathologica, 3, 562 and 566, 1911; Marfan, Le Raehitiame et aa Pathogenic, Paris, 1911; Koch, Arch. wies. prakt. Tierheilkunde, 45, 263, 1919.

12 Findlay, Lane. May 8th, 1915.

13 See also Davidsons, Ztsch. f. Kinderh. 21, 349, 1919.

14 Stoeltsner, Jahrb. f. Khkde, 51 and 53; Basch, 76. 64, 289, 1906; Matti, Ergeb. d. inn. Med. u. Kind. 10, 1, 1913; Klose and Vogt, Beitr. s. klin. Chir. 79, 1910; Renton and Robertson, J. Path. Bact. 21, 1916.

15 Lienaux and Huynen, Bull. acad. roy. med. Belg. 29, 855, 1919.

16 Stoeltzner, Jahrb. f. Kinderh. 60, 268, 1899.