Know Your Pathology: Osteomalacia and Rickets

Osteomalacia, literally softening of the bones, is a metabolic disorder of the adult skeleton that is usually defined in terms of its major causes: deficiency of phophorus or vitamin D. Osteomalacia is characterised by accumulation of excess, unmineralised and presumably unmineralisable osteoid on trabecular surfaces. Osteomalacic bones have a diminished resistance to pressures and tensions, and increased susceptibility to the stresses and strains of ordinary activity. As a result, there is excess deposition of matrix where mechanical stimuli are strongest, such as at insertions of tendons and fascia, places of angulation and curvature, and on stress-oriented epiphyseal trabeculae. When the disease is advanced, bones break easily, the marrow cavity is enlarged and the cortex is thin, spongy and soft. Deformities are often present.

Osteomalacia due to deficiency of phosphorus is uncommon in animals except in areas of the world, such as South Africa, northern Australia and the North Island of New Zealand, where the pasture is low in phosphorus and supplemental feeding is rare. Cattle are more susceptible than sheep, and horses seem to be remarkably resistant to phosphorus deficiency. Osteomalacia due to vitamin D deficiency occurs in grazing animals where the combination of relatively high latitudes and relatively mild climates allow them to be pastured for much of the year. Critical factors are probably the unavailability of sun-cured hay, the demands of pregnancy and lactation, and inadequate exposure to ultraviolet light.

Whereas osteomalacia is a disease of mature bones, rickets is a disease of growing bones. The causes and pathogenesis are the same, but the vitality of youthful tissue and the transformations and vulnerability of growing bone introduce greater complexity into the morphogenesis of rickets. Since bones mature at different times, the two diseases may co-exist in a skeleton.

There is still controversy about the respective role of vitamin D, calcium and phophorus in the aetiology of rickets. The basic question is where vitamin D prevents rickets solely by increasing blood calcium or whether it also changes the matrix (osteoid or cartilage) so it can accept mineral. The fact that uncomplicated calcium deficiency does not produce rickets is inconclusive because only in the terminal stages of this deficiency does severe hypocalcaemia occur, at which time growth slows, obviating the development of rickets.

Enlargement of joints is a typical sign of rickets. It involves long bones and is usually accompanied by lateral or medial deviation. The enlargement is partly due to the flaring of the metaphysis and partly to retarded longitudinal growth of the epiphysis and its flattening by weight bearing. Normally, the growth of bone at the physis is followed by subperiosteal resorption at the metaphysis. In rickets, osteoid (and unmineralised cartilage) persists in the metaphysis and modelling of the shaft fails because the osteoid is resistant to resorption. This results in the club-like thickening in the metaphyseal region known as rachitic metaphysis; it is most prominent at the costochondral junctions where the row of beaded metaphyses is called the rachitic rosary.

In humans, the squat bow-legged figure is not so familiar in European countries as they were 100 years ago. Evidence has been found in Neolithic skeletons from Denmark and Norway, and more plentiful evidence comes from Hungary in the Roman period. However, rhe rarity of this disease in the past is attested by the few cases described even in exhaustive studies of human remains prior to the Medieval period. Urbanisation and the later industrial revolution in cities with their crowded housing and industrial smoke created this ‘disease of civilisation’. Rickets was a common disease in England in the 17th and 18th centuries (’The English Disease’) and Madonna and Child paintings produced in the Netherlands in the 15th and 16th centuries show characteristic deformities in the form of bowed legs and deformed chests. It was described in 17th century England as a new disease, which does support the lack of evidence before that time in the British archaeological record. Today it may be seen in Asian women in western countries where clothing covers most of their skin (and they may not consume enough vitamin D), but anybody who is housebound and not exposing their skin to the sun is susceptible.

References:

Jubb, K. V. F., Kennedy, P. C., and Palmer, N. 1993. Pathology of Domestic Animals. 4th Edition. Volumes 1, 2 and 3. London: Academic Press.

Roberts, C. and Manchester, K. 2005. The Archaeology of Disease. 3rd Edition. Stroud: Alan Sutton Publishing Ltd.

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