Teeth and supporting tissues can be affected by many disease conditions. The size and shape of teeth can be affected by systemic diseases (e.g., infection and malnutrition) that occur during fetal, infant, and childhood dental development. Systemic diseases can also leave observable defects (hypoplasia) in the enamel. Tooth surfaces can be destroyed by bacteria, a process resulting in caries (Figure V.1.4). Caries can destroy the tooth to the point where the pulp cavity is exposed to infectious agents that can invade the bone and produce inflammation and abscess. Finally, teeth can be traumatized by gritty materials in food, by violence, and by the use of teeth as tools.
Other areas of the mouth can be affected by disease. Gums may become inflamed due to irritation from plaque or infection, resulting in periodontal disease and resorption of alveolar bone. The subsequent exposure of tooth roots with alveolar recession can result in root caries and tooth loss. Supporting bony tissues of the jaw are subject to inflammation just as bone is in other parts of the body.
In an archeological context, the dental pathologies most commonly seen are caries, periodontal disease, dental abscess, antemortem tooth loss, dental attrition, and enamel hypoplasia. Unfortunately, there are two major difficulties in extracting meaningful data from dental remains. First, like bone, teeth and their supporting tissues react to different disease conditions in similar ways, so that one may be unable to attribute an abnormal condition to a specific disease. Second, the methodology for analyzing these dental pathologies is inexact, often making comparisons among observations hazardous. For these reasons, we will examine in detail only enamel hypoplasia, a condition that has been carefully studied (e.g., Goodman, Martin, and Armelagos 1984; Molnar and Molnar 1985; Rose, Condon, and Goodman 1985; Goodman 1991). Although there is a considerable body of data on caries, methodological problems hinder interpretation. Basically, variation in caries rate appears to be attributable to two dietary factors: presence of carbohydrates and sugar, and presence of gritty food. (Gritty substances remove the crevices in the dental crown, thereby eliminating the locations for bacterial activity.)
Enamel hypoplasias can reveal a number of aspects about the health of an individual or population during childhood. If tooth surfaces have not been worn away, enamel hypoplasias can be used to estimate both the timing and severity of stress. The presence of enamel hypoplasias in the deciduous teeth indicates the occurrence of stress during the last 5 months in utero through the first year of postnatal life (Goodman et al. 1984). In the permanent incisors and canines, the teeth most commonly studied for enamel defects in adult dentitions, enamel hypoplasias reflect stress between birth and 7 years (Goodman 1991). The onset of stress can be determined in half-year intervals (Goodman 1991).
Enamel hypoplasias represent a disturbance lasting from several weeks to 2 months (Rose et al. 1985). Many sources attribute these disturbances to infection or nutritional deficiencies (y'Edynak and Fleisch 1983; Goodman et al. 1984) such as those that can occur with weaning (Rathbun 1984; Smith, Bar-Yosef, and Sillen 1984).
A general survey of the literature on enamel hypoplasia reveals several interrelated patterns. First, there seems to be a general rise in the frequency of hypoplasia from the Mesolithic to Roman period in many areas of the Old World (y'Edynak and Fleisch 1983; Rathbun 1984; Smith et al. 1984; Molnar and Molnar 1985; Formicola 1986-7; Angel and Bisel 1987). This rise seems to be related to general changes in the human environment.
P. Smith and colleagues (1984) found that in Palestine the frequency of enamel hypoplasias increased from the Natufian period (c. 10,000 to 8500 B.C.) to the Neolithic, and rose again in the later Chalco-
lithic and Bronze ages. They postulate that the slight rise in dental pathology in the Neolithic may have been due to changes in diet. However, they attribute the more definite increase in frequencies in the later periods to a marked decline in health due to chronic disease (Smith et al. 1984).
The Palestinian material also revealed interesting changes in the onset of childhood stress. In the Natufian period enamel hypoplasias indicate that a major period of stress occurred between 3 and 4 years of age and was probably associated with weaning (Smith et al. 1984). However, during the later Chalcolithic and Early Bronze Age periods, stress appears to have occurred earlier in life with deciduous teeth commonly affected. This suggests to Smith and co-workers (1984) that weaning took place earlier in life in these later time periods - a pattern that reflects a presumed decrease in birth spacing.
Angel's findings in the eastern Mediterranean also reflect changes in the human environment. He linked the increased frequency of hypoplasia in the Middle Bronze Age (c. 2000-1500 B.C.) skeletal samples of that area to the beginning of childhood epidemics. Epidemics were not a significant problem until that time period because human population sizes were not large enough to support the disease organisms (Angel and Bisel 1986).
A second pattern in enamel hypoplasia research is the often wide variation in frequencies within a specific time period. For example, in Neolithic skeletal samples from Hungary (Molnar and Molnar 1985) and Sweden (Gejvall 1974), there was no evidence of enamel hypoplasia. Enamel hypoplasia was found to be relatively rare in Neolithic samples from West Germany (Schaefer 1978), whereas Brothwell (1973) reports that enamel hypoplasia in Great Britain occurred in 37 percent of Neolithic skeletons. V. For-micola and colleagues (1987) reported the frequency to be high for one Italian sample.
Inadequacies in the samples raise questions about the results, but it does seem that variation among sites within a period can be interpreted to mean that specific local conditions such as parasite load may be more important than the general economic subsistence base.
There is other evidence that differences in rates of enamel hypoplasia may be related to specific geographic factors, although it is not always clear what these factors may be. Rathbun (1984) found that skeletal samples from Iran dated during the period from the Neolithic through the Metal Ages had a significantly higher rate of enamel hypoplasia than did analogous samples from Iraq. These differences were generally limited to male skeletons, and Rathbun (1984) suggests that the greater frequency in males supports the contention that growing males are more vulnerable to stress than are females.
Finally, there is some indication that the severity of hypoplasia in subadult populations is inversely associated with age of death. Some researchers have suggested that stress, producing hypoplasia, may be linked with the factors resulting in the death of the individual (Rathbun 1984; Goodman 1991). In contrast, Smith and colleagues (1984) suggest that hypoplasia is indicative of individuals who survive stress, unlike individuals who die before their teeth can be affected.
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