Porotic hyperostosis: Changing interpretations 



Patty Stuart-Macadam 



Porotic hyperostosis is a paleopathologic condition tiiat has 

 intrigued researchers forever 100 years. This time period has 

 seen a development of thought concerning both etiology and 

 interpretation of the biological significance of the lesions. In 

 the past a profusion of terminology existed, but today the 

 term porotic hyperostosis (after Angel 1966) is commonly 

 used to describe characteristic bone lesions seen in human 

 skeletal material. These lesions are usually symmetrical in 

 distribution and occur mainly on the orbits (also known as 

 cribra 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, ordiploe, 

 is often increased in thickness. A review of past and current 

 ideas on porotic hyperostosis illustrates how science pro- 

 gresses by building upon the work of earlier researchers and 

 by the development of new interpretations of data as the 

 result of changing belief structures or paradigms. 



Early researchers focused on descriptions of the lesions 

 and identification of the etiology. Although Welcker ( 1888) 

 is credited with the first good description of porotic hyper- 

 ostosis, Owen in 1859 may have been the first researcher to 

 comment on the lesions observed in skeletal material. In his 

 examinationof a collection of early 19th century crania from 

 East Asia, Owen came across some striking cases of porotic 

 hyperostosis. He noticed great thickening of the cranial vault 

 and commented that one skull in particular "is chiefly re- 

 markable as exemplifying the rare disease of hypertrophous 

 thickening of the parietal bones." Ideas about etiology prolif- 

 erated, with suggestions such as pressure from cradle boards 

 (Williams 1929), stress of carrying water jugs on the head 

 (Wood-Jones 1910), toxic disorders (Hrdlicka 1914), genetic 

 trait (Adachi 1904), or nutritional deficiencies (Williams 

 1929). 



In 1929 two researchers independently suggested that ane- 

 mia may be the causative factor (Moore 1929; Williams 

 1929). They based their opinion on the striking similarity 

 between radiographs of skulls with porotic hyperostosis and 

 those from clinical cases of various hemolytic anemias. In 

 both cases, bone changes include an increase in the diploe, 

 loss of outer compact bone integrity, and a "hair-on-end" 

 appearance of trabeculae. Initially a genetic anemia was im- 

 plicated but iron deficiency anemia became a possibility 

 36 



when it was realized that it too could produce the characteris- 

 tic skull changes. 



Angel ( 1964. 1966, 1967) popularized the idea that a genet- 

 ic anemia, particularly thalassemia, could be responsible for 

 lesions of porotic hyperostosis in earlier skeletal material . He 

 was one of the first researchers to develop a population ap- 

 proach to this issue and to have an evolutionary perspective. 

 Angel's work on Greek skeletal material suggested to him 

 that thalassemia may have occurred as an adaptation to some 

 disease such as malaria or amoebiasis. Mo.seley ( 1961 ) was 

 the first researcher to suggest that iron deficiency anemia 

 may also be a factor in porotic hyperostosis. Hengen, in 

 1971 , put forward the hypothesis that iron deficiency anemia 

 was the exclusive cause of cribra orbitalia. He had a broad 

 perspective and saw the population in terms of its interaction 

 with the environment. He considered that parasitic infesta- 

 tion and/or an iron deficient diet, consequent on local condi- 

 tions, were responsible for porotic hyperostosis. He said; 

 "Changes of the hygienic conditions and of the incidence of 

 iron deficiency anemias in former times depended without 

 doubt largely on deviations of the climate, differences of the 

 habits of daily life, procuring and preparation of fotnl, types 

 of housing, keeping of domestic animals, disposal of excre- 

 ment and so on." 



Later researchers continued to use a population approach 

 and to explore the complex interaction of factors behind the 

 occurrence of anemia. Carlson et al. (1974) speculated that 

 poor diet, parasitic infection, and weanling diarrhea con- 

 tributed to the development of iron deficiency anemia in 

 Nubian populations. Lallo et al. (1977) suggested a synergis- 

 tic relationship between microbial infection, malabsorption 

 due to weanling diarrhea, and the nutrient depletion that 

 occurs with rapid growth. Mensforth et al. (1978) also 

 stressed the multifactorial nature of the problem and illus- 

 trated that infectious diseases, represented by periosteal reac- 

 tions, can also play a role in the story. 



By the 1970s porotic hyperostosis was considered to be a 

 good stress marker for assessing the health and nutritional 

 .status of past human skeletal populations. Skeletal popula- 

 tions with porotic hyperostosis were considered to be "less 

 successful" in adapting to their environment than those with- 

 out lesions. The general feeling was that females had a great- 

 er incidence of porotic hyperostosis than males, and that this 



'/M^reb Palt'oputholojiy Symp. IVHH 



