| Abstract: |
Overview of the current thoughts on porotic hyperostosis. \uAppearance\u The lesions are usually symmetrical in distribution and occur mainly on the orbits (also known as criba orbitalia) and the skull vault, particularly the frontal, parietal and occipital bones. The normally smooth, dense outer compact bone is replaced by small holes of varying size and density. In addition, the middle layer of bone, or diploe, is often increased in thickness. Angel (1964, 1966, 1967) popularized the dieas that genetic anemia, particularly thalassemia, could be responsible for lesions of porotic hyperostosis in earlier skeletal materia. Angel thought it was an adaptation to some disease such as malaria or amoebiasis Moseley (1961) was the first to suggest iron deficiency anemia may also be a factor in porotic hyperostosis. Hengen (1971) considered parasitic infestation and/or iron deficient diet as responsible. Carlson et al (1974) suggested poor diet, parasites, and weanling diarrhea Lallo et al (1977) and Mensforth et al (1978) put forth a multifactorial approaches pg 37 Three lines of evidence supported the hypothesis that porotic hyperostosis is more likely due to iron deficiency anemia that a genetic anemia: 1) Calculations based on the highest gene frequencies for genetic anemias seen today show that the probability of finding individuals from archaeological collections with skeletal changes due to genetic anemia is quite low (Stuart-Macadam 1982). 2) There are high levels of porotic hyperostosis in skeletal groups from northern Europe and North America, areas where genetic anemias did not exist in the past. 3) The severe bone changes associated with genetic anemias, particularly postcranially, have not been substantiated for any individuals from archaeological collections. Stuart-Macadam (1987) presents an alternative viewpoint of individual with porotic hyperostosis. It has been assumed that skeletal groups with high levels of porotic hyperostosis were less "succesful" than groups with lower levels of porotoic hyperostosis. It may be that it is actually a positive response and a sign of a healthy defense system. It can be thought that iron deficiency strengthens the body's defenses against infection. These lower levels would inhibit the assimilation of iron by microbes. pg 38 From this, it is possible that portoic hyperostosis reflects a positive response on the part of the body to the total pathogen load of the environment Stuart-Macadam (1987). In areas where the load od pathogens is high, it would be expected that greater numbers of the population would cross the threshold between an iron deficiency as an adaptive repsonse, and iron deficiency anemia. greater population density means greater exposure to pathogens. By a shift in paradigm, individuals with chronic bone lesions can be seen to have have been more successful than individuals who did not live long enough to produce bony response to a pathogen. The presence of cribra orbitalia and porotic hyperostosis is suggested to present the occurrence of iron deficiency anemia in childhood. The cause of the disorder must be multifactorial and include the presence of infectious disease and parasites, as well as possible dietary factors.
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