Tissue-integrated prostheses

Causation and pathogenesis of periodontal disease.

Effect of tetracycline and/or scaling on human periodontal disease. Clinical, microbiological, and histological observations.

The pathological events leading to the destruction of the periodontium during inflammatory periodontal diseases are likely to represent complex interactions involving an imbalance in enzymic and non-enzymic degradative mechanisms. This paper aims to review the increasing body of evidence implicating reactive oxygen species (ROS), derived from many metabolic sources, in the pathogenesis of periodontal tissue destruction. ROS are generated predominantly by polymorphonuclear leukocytes (PMN) during an inflammatory response and are regarded as being highly destructive in nature. The detection of ROS oxidation products, the elevation of iron and copper ions, which catalyse the production of the most reactive radical species, and the identification of an imbalance in the oxidant/antioxidant activity within periodontal pockets, suggests a significant role for ROS in periodontal tissue destruction. In vitro studies have shown that ROS are capable of degrading a number of extracellular matrix components including proteoglycans, resulting in the modification of amino acid functional groups, leading to fragmentation of the core protein, whilst the constituent glycosaminoglycan chains undergo limited depolymerisation. The identification and characterisation of connective tissue metabolites in gingival crevicular fluid (GCF) resulting from the degradation of periodontal tissues, notably alveolar bone, provides further evidence for a role for ROS in tissue destruction associated with inflammatory periodontal diseases.

Periodontal Disease Mechanisms: Reactive oxygen species: a potential role in the pathogenesis of periodontal diseases

Background: Various cytokines have been identified at sites of chronic inflammation such as periodontitis. Cytokines are synthesized in response to bacteria and their products, inducing and maintaining an inflammatory response in the periodontium. The purpose of the present study was to investigate the involvement of interleukin-1β (IL-1β), IL-8, and IL-10 and RANTES (regulated on activation, normally T cell expressed and secreted) and the cell populations associated with the immune response in destructive periodontitis, as well as the effect of periodontal therapy on cytokine levels in gingival crevicular fluid (GCF). Methods: Data were obtained from 12 patients with moderate to advanced periodontitis and 6 healthy controls. Patients presenting at least 2 sites with ≥2mm clinical attachment loss were included in the destructive periodontitis group. After monitoring for 4 months, only 6 patients showed destructive periodontitis and GCF samples and soft tissues biopsies were collected from these patients. ...

Levels of Interleukin-1β, -8, and -10 and RANTES in Gingival Crevicular Fluid and Cell Populations in Adult Periodontitis Patients and the Effect of Periodontal Treatment

The pathologic alterations occurring in the gingival tissues of humans immediately following the beginning of plaque accumulation have not heen elucidated previously. Seven males, 22--31 years of age, free of clinical manifestations of dental and periodontal disease, and exhibiting a Plaque Index score of zero for the previous 28 days served as subjects. Plaque control measures were discontinued for 8 days and biopsies were taken from the buccal marginal gingiva of the first premolars on days 0, 2, 4, and 8. Paraffin- and Epon-embedded section, treated with a variety of histochemical stains were analyzed microscopically and cell counts were done on 1-micron Epon section. At 2 and 4 days following the beginning of plaque accumulation, the vessels subjacent to the juctional epithelium exhibited vasculitis and alterations in the perivascular collagen. There was a statistically significant increase in the number of neutrophils residing in the junctional epithelium. By the end of the 8-day period, the number of small mononuclear cells, mostly lymphocytes, in the connective tissues had increased by 3-fold and the area of collagen fiber alteration by 4-fold. In addition, the number of fibroblasts per unit area of connective tissue decreased significantly. Thus, within the period of 8 days following the beginning of plaque accumulation, an early lesion exhibiting many features characteristic of delayed hypersensitivity develops.

AlfredL. Ogilvie

Papers

Histopathologic features of the initial and early stages of experimental gingivitis in man.