This condition is liable to be confused with rickets on the one hand and simple atrophy on the other. It differs from rickets in being a disease of mature bone, rarely occurring in children. It leads, like rickets, to weakness of the bones, rendering them liable to various curvatures and deformities.
In its causation the disease is often obscure, but pregnancy seems in many cases the determining cause. It may come on during pregnancy and run a rapid course. It has also been observed in cases of insanity, and here the softness of the bones may lead to fractures from compara tively slight violence.
The disease usually begins in the bones of the pelvis, vertebrae, or ribs, but extends to the rest of the skeleton, continuing to progress up till death. The cases present various curvatures and partial fractures. The pelvis is specially liable to deformity, the acetabula being pushed inwards and the cavity narrowed. The bones as seen after death are soft and light so that they may float in water, and they are easily cut with the knife or scissors.
The lesion consists of a solution of the bone with a corresponding increase in the medullary spaces. It begins, as shown in Fig. 271, in a decalcification of the bony trabecule, in the parts next the medullary spaces and Haversian canals, so that instead of these trabecular having in the fresh state a homogeneously opaque appearance, they show at their peripheries a transparent zone in which the bone corpuscles are visible but Avithout their canaliculi. The appearance of these parts is precisely that of bone artificially decalcified by steeping in an acid. The decalcified parts may be rendered prominent by staining with carmine, the unaffected bones remaining uncoloured while the affected parts are stained. The disease advances by the decalcified parts dissolving so that the medullary spaces increase, while the decalcification further encroaches on the bony trabecular.
Fig. 271. - A fragment of bone from a case of osteomalacia. The central part shows the usual appearance of bone, while the marginal parts are transparent, being devoid of lime salts, although still showing bone corpuscles, x 90.
The bone-marrow is in some cases replaced by round-celled tissue as if the process partly partook of an inflammatory character; in other cases the adipose tissue of the marrow seems to undergo increase, so as to fill the enlarged spaces. This appears to have been the case in specimens examined by John Hunter, which he thus describes: "The component parts of the bone were totally altered, the structure being very different from other bones, and wholly composed of a new substance resembling a species of fatty tumour, and giving the appearance of a spongy bone deprived of earth and soaked in soft fat." In these cases the medulla forms a bright yellow, pink, or deep crimson material, and when examined microscopically presents free oil in great quantity with crystals of margarine.
[Necrosis is considered in a special section after inflammation].
John Hunter, quoted by Paget, Lect. on Surg. Path., 1870, p. 103; Stansky, Rech. sur l'osteomalacie, 1851; Rokitansky, Handb. d. path. Anat.; Rindfleisch, Path. Hist.; Cohnheim, Path. Anat., i.; Pommer, Unters. iiber Osteomalacic und Rachitis, 1885: von Recklinghausen, Virchow's Festschrift, 1891; Rehn (a case in childhood), Jahrb. f. Kinderheilk., xii.; Vincent, in Internat. Syst. of Surg., 1886; Shattock, Path, trans., xxxviii., 1887; Ribbert, Biblioth. Medica., 1893, c, Heft 2; Eisenhart (Puerperal osteomalacia), Arbeit. Med.-klin. Inst., Munich, 1893.