| dc.description.abstract | Gingivitis is a widespread disease, which follows a characteristically chronic course with occasional acute exacerbations, and which frequently is slowly progressive. The aetiology and pathogenesis remains unresolved, and although there is an abundant indigenous oral microflora, a causal relationship between any specific micro-organism or group of micro-organisms and gingivitis, has not been established. The conclusion was drawn from a review of host-parasite interactions in the mouth, that whilst vitamins, hormones, nutritional state and debilitating disease may modify the host response to local irritants, little is yet known concerning their mode of action. Although a number of products have been isolated from oral bacteria with the potential to cause tissue damage, their actual ability to do so has not been demonstrated. The First Experimental Section was concerned with the effect of local irritants, in the form of trauma, histamine and various enzyme preparations, on the distribution of fluorescent labelled plasma proteins in clinically healthy and chronically inflamed dog gingivae. Whilst trauma and histamine were able to provoke an immediate inflammatory response, trypsin and testicular hyaluronidase seemed unable to do so, even when applied for prolonged periods. A minimal effect of staphylococcal hyaluronidase could not be precluded. As a result of these findings, previous investigations concerning crevicular fluid and the ability of enzymes to initiate gingivitis, should be re-evaluated. The dermo-epidermal basement membrane zone appeared to exert some control over the passage of labelled proteins from connective tissue to epithelium, and after trauma, the permeability of small vessels deep to the crevicular epithelium seemed to be increased more than those directly beneath the traumatised area. In the Second Experimental Section the distribution of plasma globulins in healthy and inflamed human gingivae was determined, using the fluorescent antibody technique. Tissue from the gingivae around 467 teeth in 127 patients was studied. The results showed a general resemblance to those obtained after intravenous tracing in the dog; the amount of globulin in connective and epithelial tissues varying with the extent and the acuteness or chronicity of the inflammation present. The basement membrane again appeared to exert some control over the passage of globulins from connective tissue to epithelium. Globulins found in the gingival or crevicular epithelium were usually intercellular in location, but in about 30 per cent of chronically inflamed tissues, foci of epithelial cells were observed with cytoplasmic, but not nuclear fluorescence. This occurrence could have been occasioned by trauma or may have been associated with an allergic reaction in the gingivae. Specific cytoplasmic fluorescence indicating the presence of immunoglobulins, was demonstrated in cells similar to haemocytoblasts, immature and mature plasma cells and Russell bodies. The Object of the Third Experimental Section was to investigate the feasibility of using fluorescent antibody procedures to detect the presence of bacterial antigens in gingival tissues, and to determine whether antibodies to these antigens are produced by gingival plasma cells. Bacterial hyaluronidase was selected for study from the multitude of possible antigens,as a number of investigators have implicated this enzyme in the initiation of gingival inflammation. The presence of neither streptococcal nor staphylococcal hyaluronidase, nor of specific antibody to these antigens, could be demonstrated in gingival tissues. Before further studies of this nature are pursued, it would seem desirable to determine which of the many oral micro-organisms are of fundamental importance to the initiation of gingivitis. Once a specific micro-organism or group of micro-organisms has been causally implicated, then such techniques as have been employed in the present investigation would seem eminently suitable to study host-parasite interactions in the mouth. | en |
