Skeletal Changes in Anemia: Porotic Hyperostosis
Chronic anemia from any cause results in bone changes, which can be recognized in archaeological specimens. These changes, called porotic or symmetrical hyperostosis, result from an overgrowth of bone marrow tissue, which is apparently a compensatory process.
The cancellous zone between the cortical layers or tables of the skull is enlarged and the trabeculae become oriented perpendicular to the inner table, giving a radial pattern described as “hair standing on end.” The inner table is unchanged, but the outer table is displaced externally and may be thinned or completely atrophied and often has a spongy appearance. The process varies in location in different individuals; frontal, parietal, temporal, occipital, and maxillary bones can be affected. A similar process is also seen in the metaphysical ends of long bones and anterior superior and acetabular areas of the ilium.Today porotic hyperostosis is seen classically in X- rays of patients with congenital hemolytic anemias, as well as in children with chronic iron deficiency anemia. This is especially the case when the iron deficiency occurs in premature infants or is associated with protein malnutrition or rickets (Lanz- kowksy 1968).
Porotic hyperostosis has been observed in archaeological specimens from a variety of sites, including areas of Greece, Turkey, Peru, Mexico, the United States, and Canada. In most areas, the findings are considered evidence of iron-deficiency anemia, although thalassemia was apparently responsible in some areas. Around the shores of the Mediterranean, malaria was probably the most frequent cause of chronic anemia at certain times.
Archaeological specimens from the Near East show an incidence of anemia of only 2 percent in early hunters (15,000-8000 B.C.) who ingested a lot of animal protein and thus took in reasonable amounts of dietary iron.
By contrast, farming populations of 6500 to 2000 B.C. showed an anemia incidence of 50 percent.Many New World natives whose diet consisted primarily of corn (maize) and beans had a diet deficient in iron and protein. Moreover, when cooked in water for long periods of time, the food in the diet was also low in ascorbate and folate. Ascorbate helps convert dietary ferric to ferrous iron, which is more easily absorbed; therefore, deficiency of this vitamin increased the problem of deficient dietary iron. A high incidence of iron deficiency has been demonstrated by modern studies of infants and children in populations living on a diet consisting mostly of maize and beans (El-Najjar and Robertson 1976). It is not surprising then, in North America, that porotic hyperostosis was found in 54 percent of skeletons in the canyons of northern Arizona and northern New Mexico, among a population that ate little meat and subsisted mainly on maize. By contrast, plains dwellers in southern Arizona and southern New Mexico, who used more animal foods, had an incidence of only 14.5 percent. Absence of evidence for malaria or hemoglobinopathies in the New World before the arrival of the Europeans argues against these possible causes of porotic hyperostosis (Hart 1980).
Alfred Jay Bollet and Audrey K. Brown