The gingival tissues, periodontal ligament, alveolar bone and cementum are known as the periodontium and invest and support the tooth root. Plaque containing food debris and bacteria derived from the normal oral flora accumulate in and around the gingival crevice. When undisturbed, the deep layers of plaque become anaerobic and increasing numbers of gram negative and filamentous bacteria flourish there. An initial inflammatory response within the gingival tissues leads to swelling and a ‘false pocket’, or cuff, rising up around the cervix of the tooth that harbours more plaque. Mineralized plaque is called calculus. Subsequent destruction of crestal alveolar bone results not only from the direct effects of proliferating micro-organisms but also from a complex inflammatory and immune response; so-called ‘bystander damage’. ‘True pockets’ result when irreversible bone loss occurs subgingivally and tooth support is lost. Gingival inflammation of some degree is almost universal among modern humans but periodontal disease progresses with age. Normal alveolar crestal bone in humans approaches the tooth with a smooth thin edge that follows the contours of the teeth. This becomes thickened ‘rolled’ and irregular in periodontal disease. In great apes, however, normal healthy alveolar crestal bone often appears rolled and everted around cheek teeth. Progressive horizontal alveolar bone recession with an increasing incidence of localised vertical bone destruction is typical in humans and older great apes. Among old and senile wild-shot great apes there is a clear association between localised vertical bone destruction and loss of tight interproximal tooth contacts. Here, food packing between teeth exacerbates both caries and periodontal disease. It is impossible, however, to attribute the incidence of dentoalveolar abscesses in great apes to either advanced interproximal periodontal disease or to necrotic pulps exposed by wear, caries or trauma. Often there is a confluence of active pulpal and periodontal pathology.
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