Porotic hyperostosis: Changing interpretations • 37 



corresponded to modem incidences of iron deficiency ane- 

 mia. It was also believed that juveniles had a much higher 

 incidence of porotic hyperostosis, hence iron deficiency ane- 

 mia, than adults. Some researchers began to equate the pres- 

 ence of fKirolic hyperostosis with iron deficient diets. 



By the 1980s some of the assumptions behind these inter- 

 pretations began to be challenged. Researchers showed that 

 even groups who consumed diets rich in iron suffered from 

 porotic hyperostosis (Walker 1986). The belief that porotic 

 hyperostosis was more common in females was shown to be 

 not true. Statistical analysis of a number of studies revealed 

 that in almost every case there was no significant difference 

 between males and females in incidence of porotic hyper- 

 ostosis (Stuart-Macadam 1982); if porotic hyperostosis was 

 due to iron deficiency anemia, then why were there not sig- 

 nificant differences between males and females similar to 

 those that have been observed in clinical and population stud- 

 ies for as long as iron deficiency anemia has been docu- 

 mented? 



Consideration of bone marrow physiology and data on iron 

 deficiency anemia from clinical studies suggests that lesions 

 of porotic hyperostosis in adults are not representative of an 

 episode of anemia that was current or had occurred within a 

 relatively short period prior to death (Stuart-Macadam 1985). 

 In fact, porotic hyperostosis seen in adults is probably indica- 

 tive of a childhood episode of anemia, with the resultant bone 

 lesions showing incomplete remodeling. This would explain 

 the discrepancy between modem demographic patterns of 

 iron deficiency anemia and the pattern of porotic hyper- 

 ostosis in earlier human populations. In adults, marrow 

 hyperplasia can occur without putting undue stress on the 

 available marrow space and producing bony response (Stu;ul- 

 Macadam 1985). There is no evidence from clinical studies 

 to suggest that bone changes as a result of marrow hyper- 

 plasia can occur in an adult who has only recently acquired 

 iron deficiency anemia. In young children, however, the fac- 

 tors of great bone malleability and marrow space already 

 filled to capacity with red marrow are likely to lead to bone 

 change in response to increased demands for red blood cells. 



These ideas have implications for the interpretation of por- 

 otic hyperostosis seen in past human skeletal populations. If 

 iron deficiency anemia acquired in adulthood does not lead to 

 bone change then the higher incidence of porotic hyper- 

 ostosis (therefore anemia) observed in juveniles does not 

 necessarily reflect reality. Juveniles may or may not have had 

 a higher incidence of anemia than adults; it is simply not 

 possible to assess the impact that anemia may have had on 

 adults. If porotic hyperostosis in adults does reflect a child- 

 hood episode of anemia, then the search for causative factors 

 should concentrate on the juvenile sector of the population. It 

 is also important to be aware that the total number of individ- 

 uals afl'ectcd by anemia will always be undcrrcprcscnied in a 

 skeletal population. At most, 50-75% of clinical patients 

 with anemias that are associated with bone change show 

 changes which can be .seen radiographically (Stuart-Macadam 



Zagrrb Paleopalhology Symp. I98S 



1985). As a result of all these factors it may be impossible to 

 assess the true pattern of anemia in any past human skeletal 

 population. 



Stuart-Macadam (1982,1987b) expanded on the ideas of 

 some of the earlier researchers by undertaking a detailed 

 comparison of radiographs from clinical cases of anemia 

 with radiographs of skulls with porotic hyperostosis. On the 

 basis of seven criteria, it was felt that the data strongly sup- 

 ported the hypothesis that porotic hyperostosis was indeed 

 the result of an anemia. In addition, three lines of evidence 

 supported the hypothesis that porotic hyperostosis is more 

 likely due to iron deficiency anemia than a genetic anemia: 



1 . Calculations based on the highest gene frequencies for 

 genetic anemias seen today show that the probability of find- 

 ing individuals from archeologlcal 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 ane- 

 mias, particularly postcranially, have not been substantiated 

 for any individuals from archeological collections. 



Recently, Stuart-Macadam ( 1987a) has questioned the bi- 

 ological significance of porotic hyperostosis. Fomierly its 

 presence in a skeletal population has been seen as an inability 

 to adapt, a negative response on the part of the body. It has 

 been assumed that skeletal groups with high levels of porotic 

 hyperostosis were less "successful" than groups with lower 

 levels of porotic hyperostosis. It may be that it is actually a 

 positive response and a sign of a healthy defense system. 

 This view has arisen out of changing perspectives of the 

 immune system, and iron deficiency in particular. A large 

 body of data supports the concept that iron deficiency may 

 not always be detrimental, but may actually strengthen the 

 body's defenses against infection (Strauss 1978). Lowered 

 iron levels may be a natural protective respon.se which dis- 

 courages bacteria and other pathogens. Microbes are depen- 

 dent upon assimilation of iron and actually synthesize sub- 

 stances which have the ability to bind iron. In this situation 

 hypoferremia should be advantageous to the host and disad- 

 vantageous to the microbial invader. In vitro, in vivo, and 

 population studies show that this is very often the case 

 (Lukens 1975; Strauss 1978; Wadsworth 1975). 



Normally there is a balance between the role of iron in the 

 defense system and the body's requirements for iron. Iron 

 metabolism is basically a closed system, since losses are 

 normally very low and iron obtained from destruction of old 

 blood cells by the reticuloendothelial system is recycled 

 within the body. In times of extra iron requirements the intes- 

 tine absorbs a greater percentage of the iron available in the 

 diet. It is possible that only continual and repealed exposure 

 to a large number of pathogens can destroy this balance in a 

 normal individual and ultimately lead to iron deficiency ane- 

 mia. In this view it is possible that the lesions of porotic 



