Part Two: The role of constitutional factors, diet, and infectious disease in the etiology of porotic hyperostosis and periosteal reactions in prehistoric infants and children.

Abstract A model of analysis incorporating methodological improvements and epidemiological refinements has been employed to investigate the etiology of porotic hyperostosis and periosteal reactions in infants and children from the Libben Site, a Late Woodland ossuary and occupation site from Ottawa County, Ohio. Results of the age-specific intrapopulational analysis of porotic hyperostosis demonstrate that the skeletal lesion strongly fits the age-specific distribution of hypochromic microcytic iron-deficiency anemia in infants and children. The data indicate that the lesion is a response to nutritional stress. Similarly, our findings show that the age-specific distribution of periosteal reactions strongly coincides with, and appears to be a response to, infectious disease as it occurs in infants and children. More importantly, survivorship and growth data indicate that porotic hyperostosis and periosteal reactions are strongly associated with patterns of infant and child morbidity and mortality, and therefore appear to play an important role in selection and fitness at Libben. Based upon the age-specific patterns and associations observed for porotic hyperostosis and periosteal reactions in the Libben infants and children, it is suggested that: 1. the current methodological procedure of partitioning skeletal populations into broad age categories can significantly distort important age-specific pathophysiological relationships; 2. skeletal lesions should be classified according to their physical quality (i.e., remodeled and unremodeled) to provide an estimate of both the morbidity and mortality associated with the age-specific distribution of a particular skeletal lesion; 3. porotic hyperostosis may be a valuable indicator of nutritional stress which can be employed to evaluate the nutritional status of prehistoric human populations; 4. the pathogenesis of porotic hyperostosis can best be understood in terms of the synergistic interactions between constitutional factors, diet, and infectious disease.