Periodontal diseases may be classified according to the stage of the inflammation present, as acute or chronic. However what is usually meant by the term periodontitis is a chronic slowly progressive and destructive inflammatory process affecting one or more of the four components of the periodontium (Burnett & Schuster, 1978:213). With the exception of the early, acute and reversible inflammation of the investing gingiva, chronic periodontitis is essentially a connective tissue disease involving periodontal ligament, cementum and alveolar bone. Since only hard tissues are normally present in skeletal material, it is convenient to classify and describe chronic periodontitis in terms of the location and pattern of bone destruction as either generalized or localized.
Generalized periodontitis usually affects all teeth and is characterized by a horizontal reduction in alveolar bone height, the crestal margins being roughly perpendicular to the long axis of the affected teeth (Fig. 14.7). The reduction in alveolar bone and soft tissue height exposes significant root surface to the oral fluids. Though horizontal bone loss is quite common among contemporary adults its frequency in antiquity was less common (Clark et al., 1986).
Localized periodontitis, the more prevalent form in antiquity, is tooth-specific, commonly occurring interdentally, creating vertical defects between tooth root and alveolar bone. In its early stages interdental defects appear as craters in the crestal bone confined within the facial and lingual cortical walls. As inflammation advances deep angular defects are formed in the cancellous bone. The facio-lingually broad posterior teeth are especially vulnerable to this inflammatory progression.
While the periodontium is subject to traumatic, neoplastic and other forms of pathology, such as the acute necrotizing gingivitis of Vincent's spirochete and fusiform bacteria, acute infection changes are rarely preserved for pathological examination. Hence in the remainder of this section we will discuss periodontitis only as chronic infection and its long-term effects on the periodontium, limiting our efforts to localized, tooth specific, chronic periodontitis.
Periodontitis is a global problem, estimated by the World Health Organization to affect 75 % of adults to some degree. It is responsible for more antemortem tooth loss than is dental caries (Shafer et al., 1983:760). In contemporary populations it increases in frequency with every decade up to age 60. It is not gender-specific. In a normal, fully-erupted permanent dentition the mesio-distal diameters of all tooth crowns are wider through the occlusal and incisal thirds than they are at their cervical thirds, (see Fig. 14.5). As explained below, the loss of interproximal contact is the principal initiating event leading to periodontitis.
While the gingivitis that usually precedes periodontitis can begin with events such as a penetrating foreign body or major local trauma, by far the most frequent predisposing cause is loss of interproximal contact. Such contact loss may occur by a traumatic chip fracture of the enamel involving the contact area or even spontaneous lateral tooth drift following exfoliation of its neighbor. However, the cause most common in antiquity, was severe attrition. When wear on the occlusal surface has eroded beyond the contact areas of the crown, neighboring teeth are no longer in contact with each other. The enamel bridge at the former interproximal contact now no longer protects the tender gingival tissues occupying the interdental space. Lacking its protective enamel cover, food is now forced into this sulcus during mastication. With each subsequent meal the sulcus is traumatically expanded by retained organic matter, since the area has no self-cleansing method.
Chronic food retention in a protected niche provides opportunity for bacterial multiplication. A layer of such bacteria mixed with mucoid material (dental plaque) becomes attached to the tooth root at its cervical area. As food and microorganisms stagnate in the distended sulcus the transeptal fibers of the periodontal ligament are the first connective tissue elements to be victimized. Bacteria now invade, extending deeply into the periodontal ligament space and bacterial plaque begins to calcify, forming calculus.
Dental plaque, formed by bacterial colonization of the tooth pellicle (cuticle), is the single most important extrinsic factor in the development of periodontitis. Mineralized plaque is calculus. Supragingival calculus is mineralized by ions from the saliva, subgingival calculus by ions from gingival sulcular exudate. Besides differing in location and source of mineral ions, subgingival calculus differs from supragingival calculus in another basic feature: i.e. rather than being a direct etiologic agent of an inflammatory reaction it is a product of that reaction, forming at the bottom of an existing periodontal pocket (Shapiro & Stallard, 1977:77-8). It is so dense and firmly attached that it is often mistaken for osteocementum. Supragingival calculus, on the other hand, forms in large quantities, especially near the orifices of major salivary glands, is fragile and easily dislodged in dry skeletal specimens. In both types of calculus, however, the calcium is deposited as calcium phosphate in the form of hydroxyapatite.
The site of periodontal disruption gradually increases in this manner, creating vertical or angular defects in the bone alongside the root. The stripping of the periodontium from the tooth root exposes the root to the oral fluids, providing dental plaque with a site to initiate the necrotizing process of dental caries with its destructive effects (discussed in the next section). Purulent exudate collects in the lower recesses of the created periodontal defect, and the inflammatory process extends both more deeply and widely, eventually destroying the periodontal ligament and alveolar bone.
The body's defense mechanisms usually are inadequate to control the process, and in fact may at times even contribute to local tissue destruction (Williams, 1990) that has already been initiated by products of bacterial metabolism (Burnett & Schuster, 1978:227). Paleopathologists may observe evidence of such efforts at containment of the process in the form of peripheral buttressing bone or lipping on facial surfaces adjacent to osseous defects in alveolar bone (Caranza, 1984:243) (Fig. 14.8). Nevertheless, once firmly initiated the process is usually progressive and the ultimate effect is predominantly bone destruction. Eventually the process of periodontal tissue destruction extends around the tooth circumferentially, destroying its periodontal attachments sufficiently to result in tooth exfoliation. Following tooth loss the alveolar bone becomes resorbed since its only purpose was support and nourishment of the tooth (Moss-Salentijn & Klyvert, 1985:267). Such an effect is particularly obvious in generalized periodontitis in which diffuse periodontal recession results in such extensive exfoliation that the alveolar portion of the jaws may virtually disappear.
Evidence of chronic periodontal disease has been described in a three million year old hominid (Lavigne & Molto, 1995) as well as in an example of the Pleistocene Australopithecus africanus, while acute periodontitis (probably Vincent's infection) was reported in soldiers of Xenophon's Greek army about 4000 B.C. (Shafer et al., 1983:760). It is a commonly recognized condition in modern studies of ancient skeletal populations. These reports have a tendency to focus on generalized periodontitis with its diffuse, horizontal form of bone loss. Clark et al. (1986), however, noted that this form is not a common finding in ancient dry skulls. The tendency to lump the many forms and causes of periodontitis into a single category to the exclusion of multiple forms of localized periodontitis risks omission of important diagnostic information. Such localized forms are abundant and correlate strongly with attrition and caries. Cultural practices can modify the prevalence of periodontitis. Langsjoen (1996) has demonstrated that the Andean practice of coca-leaf-chewing is a powerful predictor of periodontitis leading to a high rate of antemortem tooth loss, and betel nut-chewing is similarly suspected. More commonly, food collection and preparation practices that add grit to the ingested items, can accelerate attrition enormously, leading to premature interproximal contact loss.
Clearly, the consequences of the chronic periodontal disease syndrome in antiquity were very destructive. By middle age and beyond, periodontal disease was the major contributor to edentulism, and it affected principally the posterior chewing teeth.
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