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Caries have been a constant nuisance to humans, decaying teeth can become a major problem for those affected. It is certainly not the oldest pathology, nor the one of the greatest prevalence throughout humankind, but the information that can be extrapolate from such pathologies is great. The aim of this paper is to outline the pathology of caries and the influence that these have had on the human populations affected. Caries or caries dentium is the common name for tooth decay. It is a local disease, which is characterized by an irreversible and permanent destruction of the tooth hard tissue, enamel. Thus spreads the destruction to the rest of the tooth and, and possibly leading to tooth loss and possibly infections in other areas, more specifically through the maxillary or mandibular areas.
Also I have included some other defects that are import and not only to the observation of caries but overall pathologies and their implications for the individuals affected. In this paper I will attempt to outline the causes of this disease and some of the numerous factors that cause it, as many have a hand in the process. Also I will show how these changes were brought about and how these affected the individuals with caries. To begin I will introduce the reader he to other defects that affect the same area and should be considered when any analysis of the area is to be understood. Any disturbance, such as severe infection can disrupt enamel formation. That disruption of enamel formation will leave an enduring record as a disorientation of enamel prisms.
Because the human dental growth sequence is known, the age at which the enamel disturbance occurred can be determined from the location of the disturbance within the enamel. A standard chart for dental development can be consulted for this purpose. There is extensive literature (now in excess of 500 articles) on the epidemiology and etiology of enamel defects. Many of which have been investigations using laboratory animals There are two types of enamel developmental disturbance of interest to the paleopathologist (1) Microdefects are histological structures known as Wilson bands. These are accentuated brown striae of Retzius. The most celebrated of these is the neontal line, reported by Schour in 1936 If the disturbance is short in duration and the enamel formation resumes, that disturbance is recorded as a narrow band seen in the section of enamel under a light microscope. That evidence of enamel formation disruption and recovery is called a Wilson band. Wilson bands are thin layers of abnormally structured enamel marking the position of the active ameoloblasts at the time of insult.
Wilson bands are sometimes called'pathological brown striae' in the literature. This descriptive term is a nice way to describe the bands, which contain 'sudden changes in prism direction associated with atypical rod forms.' Wide neonatal lines are associated with traumatic births. Wilson bands appear to represent brief periods of stress lasting from one to five days. The examination of teeth for histological disturbance is destructive; therefore, this technique is not used of rare ancient hominid teeth. 2) Macrodefects are defects visible on the tooth surface. They are known as hypoplasias.
These can vary in appearance from small pits or furrows to large, deep grooves or even large areas of missing enamel. Typically these defects are horizontal grooves that are called chronological or linear (enamel hypoplasias. They seem to reflect impairment of enamel formation for weeks or months, while Wilson lines record events limited to one or a few days. If the enamel formation does not resume, the defect can be viewed macroscopically as a transverse area of depressed enamel, this is known as enamel hypoplasia, Enamel hypoplasias show a predilection for anterior teeth and for the cervical and middle thirds of tooth crowns. Investigators have shown statistical associations between enamel hypoplasias and a variety of clinical conditions of which we will only mention a few here: premature birth, malnutrition, fluorosis, high fever, localized trauma and systemic metabolic distress such as gastrointestinal disorders. Dental plaque is a mixed microbial biofilm growing on teeth and is the prime aetiological agent of the two main oral diseases, dental caries and periodontal disease. The microbial composition of plaque varies between individuals and the location on the tooth and generally reflects the complex nature of the ecology of the mouth. In common with other biofilms, the microbial composition of dental plaque is capable of change in response to changes in the environment, notably the diet. These responses are modulated by homeostatic mechanisms inherent in the plaque in ways, which are as yet poorly understood.
The major sites of plaque accumulation are in the fissures of molar teeth, in the area bounded by margin of the gum and the tooth and between adjacent the teeth. In addition, plaque can cause gingival inflammation, which may result in loss of epithelial attachment to the tooth leading to the formation of sub-gingival pockets (Frayer 1989). These pockets may also harbor dental plaque which is significantly different from supra-gingival plaque in a number of important respects in particular a much lower redox potential which selects for a variety of anaerobic bacterial species. Although dental plaque varies considerably in composition, it has been possible to piece together a sequence of events, which lead to its establishment. The consensus view of plaque development begins with a clean tooth surface covered by a conditioning film of salivary proteins and glycoproteins, called the tooth pellicle, being colonized by so-called "pioneer species"(Larson 1995). These multiply forming first a monolayer and, subsequently, palisades of cells perpendicular to the tooth surface.
During and after this outgrowth period secondary colonization by a variety of Gram positive and negative species occurs leading to a large increase in the species diversity. Foremost among the events contributing to this secondary colonization is the process known as co-aggregation whereby colonizing microbes attach to cells already part of the developing biofilm(Moore and Colbett, 1983:140). This allows species which can not attach, or can attach only poorly, to the tooth pellicle to participate in the biofilm. At 24 hours the maturing dental plaque contains a wide variety of bacteria and it is possible to detect easily identifiable inter-species associations such as the well documented"corn-cob-configurations"(Frayer, 1989), although a wide variety of other inter-species associations will be present. Further colonization and growth of established bacteria takes place as the plaque matures to form a stable, climax community. This pattern of development leading to a climax community has been termed "bacterial succession".
The resulting community consists of individual microbes and microcolonies acting in complex consortia, which can convey a range of beneficial properties. These include feeding synergies, improved antibiotic resistance and a host of cooperative mechanisms, which are the subject of much current research. As mentioned before dental plaque is a deposit on the teeth consisting of food debris together with various components derived from the saliva. Within this plaque dwell bacteria, when these bacteria metabolize carbohydrates they produce acid waste products. It is the dissolution of the dental hard tissues by these acids that cause carries. Dietary sucrose changes both the thickness and the chemical nature of plaque.
Mutans streptococci and some other plaque bacteria use the monosaccharide components (glucose and fructose) and the energy of the disaccharide bond of sucrose to assemble extracellular polysaccharides. These increase the thickness of plaque substantially, and also change the chemical nature of its extracellular space from liquid to gel. The gel limits movement of some ions. Thick gel-plaque allows the development of an acid environment against the tooth surface, protected from salivary buffering. Plaque, which has not had contact with sucrose, is both thinner and better buffered. A diet with a high proportion of sucrose therefore increases caries risk. Thicker plaque occurs in pits and fissures, just beneath the contact area and, in patients with poor oral hygiene, near the gingival margin.
The initial area of lesion in caries consists of first, a softened, which then progresses into a small hole or caries in the enamel surface. As this process continues there is a widening of this deterioration and a caries is formed. When this reaches the dento enamel surface the destruction tends to spread latterly due to a typical increase in organic material within the affected area, which is to be expected as living individuals would undoubtedly continue to consume food and thus continue to produce saliva. This process will eventually undermine the enamel crown leaving a fragile hollow cavity which can collapse due to the stresses that are present, weather they be from eating, use as a tool or any other type of trauma that would place stress upon the subject teeth (Shafer 1983:432) In this way caries may lead to a complete destruction of an enamel crown. Due to this destruction infection of the pulp may occur, either through direct exposure to the oral environment or via opened exposed dentinal tubules (Hilson 1986: 316) This infection in the pulp cavity may lead to the formation of a dental abbess at the tooth socket by way of the root canal. Thus the presence of a dental abbess on skeletal remains and the interpretation for those situations where the tooth may not be present in the burial environment there can still be some extrapolation of carious evidence. Also it is important to mention that untreated caries ca give rise to potentially lethal complications (Mays 1998:148) Advanced caries of a maxillary tooth can lead to and cause complications, including infections that can spread to vital organs, and possibly lead to death.
Each time that plaque bacteria come into contact with food or drink containing simple sugars (monosaccharides such as glucose and fructose, and disaccharides such as sucrose, lactose and maltose) they use them for their metabolic needs, making organic acids as a metabolic by-product. If these acids are not buffered by saliva they dissolve the surface of the apatite crystals of adjacent tooth structure. This is called demineralization. In thick gel-plaque the pH falls within seconds of contact with dietary sugars, and it can stay low for up to 2 hours. When the pH is neutral the same crystals can re-grow, using calcium, phosphate and fluoride from saliva. This is called remineralization. Caries begins and progresses when demineralization outweighs remineralization. Caries therefore depends on the balance between demineralization and remineralization, i.e.
on the frequency of eating (and on the microbial composition of the plaque and its chemical nature and thickness, on the local fluoride concentration and on the buffering capacity of saliva). A frequent pattern of eating therefore increases caries risk. The breakdown of enamel by the bacterial processes mentioned earlier is most commonly associated with that of carbohydrate food residue present within the mouth. Foods such as fats oils and meats including fish, are non- cariogenic (Shaw: 1954) and the protean residues responsible for caries (Becks et al. 1944; Dreizen and Spies 1948) are in some cases inhibited by a diet made up mainly of these foods. Whereas a diet consisting mainly of carbohydrates will significantly increase the incidence of dental caries.
(Pederson:1947) The most cariogenic carbohydrates are those of a low molecular weight such as sugars, these are very readily metabolized by bacteria to produce acid by-products. Thus there would be a correlation between sweet sugary foods and the incidence of dental caries, this has been shown in the archaeological record. One of the most profound changes to occur with the foraging to farming transition was the widespread decline in oral health, which was almost certainly tied to increased consumption of plant carbohydrates. Especially obvious is the remarkable increase in dental caries wherever and whenever the transition occurred. Dental caries is a disease process characterized by focal demineralization of dental hard tissues by organic acids produced by bacterial fermentation of dietary carbohydrates, especially sugars (Larsen, 1997). Dental caries are manifested as pits (or cavities) in teeth, ranging in size from barely discernible discoloration of enamel to large cavitations or substantial loss of crown matter (Figure 1). Comparisons of foragers and farmers globally reveal a consistent pattern of increase in frequency of carious lesions (Larsen, 1995). Eastern North America offers an important perspective on the impact of increased carbohydrate consumption on humans, especially because so many dental samples have been studied in this region. Figure 2 shows the comparison of prehistoric populations lacking maize (Archaic, Early Woodland), some use of maize (Middle Woodland), and dependence on maize (Late Woodland, Mississippian, Contact) for the region.
The contrast between foragers and farmers is striking. One of the important indicators of periodontal disease in skeletal remains is antemortem tooth loss (Figure 3). Periodontal disease results in a weakening of the alveolar bone supporting the dental structures, and as the bone resorbs, teeth loosen and are exfoliated. Although the evidence is not as overwhelming as dental caries, there is a pattern of increase in antemortem loss that corresponds with cariogenesis in agricultural populations from diverse settings, such as Nubia, eastern North America, western Europe, and south Asia (reviewed in Larsen, 1995). Another example, in Britain there were only small amounts or sugar cane available until large scale imports from the New World became available. But by the seventeenth century the imports from the colonies were in full swing and sugar was being imported at a fantastic rate. These imports coincided with a greater occurrence of caries where by the early years of the twentieth century, caries in England had increased three fold in since the Iron Age In Britain (Mays: 1998; 151) Also starches are a major dietary carbohydrate, which if left in a environment such as the mouth can breakdown and start to deteriorate the enamel, but still not quite as much as the high incidence as with that of high levels of a sucrose diet.
Frayer (1989) using archaeological evidence from the early upper Paleolithic to the late Mesolithic associated an increase in caries associated with a changing environment and thus a changing subsistence for those inhabitants. He proved that sites dating to the early upper Paleolithic had a supriseingly low incidence of caries, where environmental factors did not foster extensive plant grow. In contrast late upper Paleolithic sites show a marke ....
Research essay sample on Caries