I. EPIDEMIOLOGY OF DENTAL CARIES
Dental caries is a destruction of enamel, dentin, or the cementum resulting from acid production by bacteria in dental plaque. It leads ultimately to a carious lesion in the crown or root surface.
The rate of dental caries is variable. Usually, caries progresses slowly as a chronic disease. There are arrested or remineralizing phases that alternate with more active phases, so that a carious lesion may remain stable for months or even for years. Rapidly progressive destruction, called rampant caries, is less common. It characteristically results in the loss of the most erupted crowns in the mouths of children.
There is a characteristic pattern in dental caries seen in living human populations. For all types of carious lesions, molars are most commonly affected, followed by premolars and then anterior teeth. Coronal caries are those of the crown, that portion of the tooth covered by enamel. The most frequently affected sites are the pits and fissures of cheek teeth (premolars and molars). Fewer caries are found on the proximal crown surfaces of posterior and anterior teeth. Buccal/labial and lingual lesions are uncommon.
Coronal caries is largely a disease of children. Its frequency steadily increases until 15 or so years of age, and then diminishes in early adulthood. Caries appears to be more common in girls than boys. This may be due to the earlier dental eruption (of permanent teeth) in girls.
Root caries particularly affects the proximal surfaces of cheek teeth. It is primarily a disease of older adults. The pattern of dental caries is similar in members of the same family over several generations. Inheritance of this susceptibiliy is suspected. Environmental factors such as diet, oral hygiene habits and diet have a large role.
The clearest single factor in caries epidemiology is sugar. This is demonstrated by the decrease in the rate of caries during sugar rationing in Japan, Norway, and the Island of Jersey during World War II.
Dental caries also occurs amongst the great apes. Caries is moderately common among the great apes, particularly the chimpanzees. Of the great apes, chimpanzees have a diet most similar to our own; in the wild their diet includes a lot of fruit in addition to leaves, flowers, nuts, termites, and on occasion--other primates. They are indeed omniverous: over 250 food types are eaten, in addition to some plants for medicinal purposes. (My note: field studies by Jane Goodall and others have confirmed the intentional consumption of specific plants by chimpanzees for medicinal purposes.)
Gorillas, which are primarily leaf eaters, have a much lower rate of dental caries. The orangutan in intermediate between chimpanzees and gorillas.
II. DENTAL CARIES IN A HISTORICAL PERSPECTIVE
From the Australopithecines (over a million years ago) to the Neolithic (since 10,000 years ago), carious lesions have been found in almost every population studied. Caries, however, was very uncommon amongst fossil hominids into the Paleolithic and Mesolithic.
One famous exception, however, is the often cited example of rampant caries in a middle Pleistocene skull (specimen BMNH 686) from Broken Hill mine, Zambia.
Figure one. Occlusal and frontal view of maxillary dental arch, from Broken Hill mine. Middle Pleistocene hominid with Neandertal affinities., known as 'Rhodesian man' in the older literature. Note the extensive dental caries. Adapted from Day, and from Keith.
In the most ancient hominids, the incidence of caries is less than 1%. Although many Neandertal specimens have been discovered, no carious lesions have been described except for a single root lesion in some Neandertal teeth from Mt. Carmel,Israel.
In European material, there is a gradual increase from very low rates through the Paleolithic, Neolithic, Bronze and Iron Age, to a rapid rise through Medieval and modern times.
There has been a sporadic, but generally increasing caries prevalence over the past 5,000 years. During the first 4,000 years there is a gradual increase in caries prevalence ranging from 2 to 10 carious teeth per 100 teeth, followed by a sharp rise at about the year 1000 A.D. to 24 carious teeth per 100 for 3 out of 4 populations. The year 1000 A.D. is the approximate date for the introduction of sugar cane to the Western world.
Incidentally, in recent years the rate of tooth decay among children in First World countries has been dropping, a fact asserted by practicing dentists and confirmed in recent European populations.
The evidence for trends in dental caries is especially interesting amongst North American Indians. The reliance upon maize agriculture is a clear cultural horizon. Several studies have shown an increase in caries rate associated with the change from a hunter-gatherer diet with meat and low carbohydrate to a diet heavy with starch-rich cereal.
Post-European contact groups also show higher caries rates than pre-contact groups, implying a still greater reliance on maize agriculture. Similar increases in caries rate have been associated with increased reliance on arable agriculture in studies of material from South America. Similar events are documented in other regions throughout the world. (see Price)
Historically, where starch-rich foods form a small part of the diet, the caries rate is very low indeed. The introduction of maize agriculture with its dietary starch has been linked to a rise in dental caries.
Where sugars have been introduced into the diet, fissure and proximal surface cavities, particularly in children, became dominant. With maize agriculture, the dominant pattern was root surface caries or lesions at the cemento-enamel junction initiated in adulthood.
What is the influence of tooth wear on caries incidence? In general, groups with high attrition rates often have low caries rate; however, this does not necessarily suggest a causal relationship. Occlusal attrition might remove fissure caries if the lesion developed slowly. The normal pattern at these sites is for rapid progression of lesions. Attrition cannot much affect caries at cervical sites, which is the predominant form in populations where attrition rates are the highest.
III. DENTAL CALCULUS
Calculus is mineralized plaque. It accumulates at the base of a living plaque deposit and is attached to the surface of the tooth. The mineral is ultimately derived from the saliva. The tooth surfaces closest to the ducts of the salivary glands, lingual surfaces of anterior teeth and buccal surfaces of molars, show the most deposition of calculus. Clinicians differentiate between supragingival and subgingival calculus. Dental calculus is a frequent finding in archaeological and museum specimens.
IV. PERIODONTAL DISEASE
In dry bone specimens, two patterns of bone loss are recognized: horizontal and vertical. Horizontal bone loss is the simultaneous loss in height of the four walls surrounding the tooth roots--mesial, distal, facial, and lingual. It implies that several neighboring teeth or even the whole dental arch is involved.
Vertical bone loss is localized around individual teeth or in pairs of neighboring teeth. This results in an intrabony defect surrounded by high walls of unaffected bone. It occurs with or without horizontal bone loss.
Most specimens show a clear pattern of bone loss that tends to be symmetrical. It particularly affects first and second molars; less often the premolars and canines. Teeth are eventually lost as well when all their surrounding alveolar bone in gone.
There is a clear relationship between periodontitis and age. Children are rarely affected before puberty. After this point, there is a gradual increase in the proportion of the population affected up to 40 or 50 years of age paralleled by an increase in severity. The same pattern is seen in the extent of bone loss from the jaws, in dry bone specimens representing living populations and in archaeological material.
Historically, bone loss amongst Native Americans was most marked in those with the greatest reliance on maize agriculture. Overall, the epidemiology of periodontal disease appears to be multifactorial. Environment, inheritance, diet, and hygiene all appear to be involved.
V. DENTAL HEALTH IN ANCIENT EGYPT
What do Egyptian dental patterns reveal about their lives and how to they compare to living populations today?
In ancient Egypt, the greatest single problem was attrition, specifically the wear of the occlusal and proximal surfaces. The teeth were rapidly worn down throughout life by the consumption of a course diet. This was true for both pharaohs and commoners. In time, the wear became so extensive that enamel and dentin were worn away, exposing the pulp. Painful chronic infection was the result. Dental surgeons of that time would drain the abcesses with the use of a hollow reed.
The second greatest problem was periodontal disease. Calculus deposits on the teeth were often so extensive that they have held the teeth in place for 2,000 years. The result of these extensive deposits were early bone loss, loose teeth, infection, and tooth loss.
Dental caries were far less frequently seen amongst ancient Egyptians and Nubians than in today's populations. Two reasons are cited. First, rapid wear literally wore away the sites of pit and fissure cavities. Second, was the lack of refined carbohydrates in their diet.
Some orthodontic observations are of interest here. Ancient Egyptians and Nubians rarely had the dental crowding and abnormal molar relationships that are observed throughout the world today. Many anthropologists and some orthodontists suggest that vigorous chewing encourages development of robust, full sized lower jaws and some degree of wear minimized joint pain and crowding that are prevalent today.
Some restorative work from that period can be seen. In one mummy with missing teeth, three substitute teeth were in place skillfully threaded together to the abutment teeth with fine gold wire.
Why was there so much dental wear? Sand infiltrated into their food, especially via stone ground bread. Modern experiments have shown that a single grinding of corn produces a course flour. The more desired finely ground flour is produced by adding sand to the course flour which exacerbates the wear process.
..... CJ '98
Cockburn, A. and Cockburn, E. eds. Mummies, Diseases and Ancient Cultures. New York: Cambridge University Press, 1995.
Day, M. Guide to Fossil Man. New York: World Publishing Company, 1965.
Hillson, S. Dental Anthropology New York: Cambridge University Press, 1996.
Keene, H. "History of Dental Caries in Human Populations: The First Million Years" Symposium and Workshop on Animal Models in Cariology, Sturbridge, Massachusets, 1980.
Keith, A. The Antiquity of Man. London: Williams and Norgate, Ltd., 1925.
Larsen, C. Matter, R., and Gebo, D. Human Origins The Fossil Record 2nd ed. Prospect Heights: Waveland Press, 1991.
Price, W. Nutrition and Physical Degeneration. New Canaan: Keats Publishing, Inc., 1989.
Figure Three. A patient bends over a brazier burning henbane seeds, the fumes of which were believed to cure toothache by driving out the 'worm' that consumes the teeth. This drawing is adapted from a thirteenth century illustration shown in Ring, M. Dentistry an Illustrated History. New York: Harry N. Abrams, Inc., 1985, p 101.
What is henbane? It is a course, hairy, foul smelling plant Hyoscyamus niger of the nightshade family. It is poisonous to animals, especially fowls. It is used in medicine as a narcotic. Also called hyoscyamus, it is an Old World herb that has toothed leaves and white and yellow flowers. The alkaloid phytochemical is isomeric with atropine. The dried leaves are used in medicine.