Anthony W. Gargiulo

Reactivity of Blood Group Substances of Neoplastic Oral Epithelium

Histologic sections of 15 biopsy samples of normal oral mucosa and 8 biopsy samples of malignant oral carcinoma from patients with A, B, or AB blood groups were treated with anti-A or anti-B human antiserum and then with fluorescein isothiocyanate-bound goat antihuman globulin. Normal cells fluoresced intensely. Fluorescence of malignant cells was diminished or lost.

Aging in Human Attached Gingival Epithelium

The mitotic index of human gingival epithelium is not significantly different in men 18 to 22 years of age and in men 58 to 64 years of age. There is a significant increase in the cell density of the gingival epithelium and a significant decrease in connective tissue cells in older men.

Labeling Index and Cell Density of Aging Rat Oral Tissues

Age changes were detected in oral epithelium, dental pulp, and periodontal ligament in the Simonsen rat.

Identification of C 3a, IgG, IgM in Inflamed Human Gingiva

Departments of Pathology and *Periodontology, Loyola University qJ Chicago, School of Dentistry, 2160 South First Avenue, Maywood, Illirnois 60153, USA J Dent Res 57(5-6):696, May-June 1978. The host reaction to bacterial antigens in the gingival sulcus in gingivitis suggests a combined hypersensitivity response as IgG, IgA, IgM, and IgE have been reported both in the gingiva and the sulcus fluid (SCHWARTZ & DIBLEE: J Perliodontol 46:171, 1975; BYERS, TOTO, & GARGIULO: J Periodontal 46:387, 1975; BRILL: A cta Odontol Scand 18:421, 1960). Evidence of hypersensitivity of the host to bacterial antigens in gingivitis indicates that the inflammation process is antigen-antibody induced (NISENGARD & BEUTNER: J Periodontol 41:223, 1970; SNYDERMAN: JADA 87:1020, 1973; IVANYI & LEHNER: Arch Biol 15:1089, 1970). Autoimmunity has been indicated as a pathogenetic mechanism in gingivitis (BRANDTZAEG & KRAUSE: Odont T 73:281, 1965.) Antigen-antibody complexes by IgG and IgM bind complement which liberate C 3a fragments by the direct pathway which cause the anaphylotoxic chemotactic and cytotoxic events seen in hypersensitive reactions in the host (MULLER-EBERHARD: Ann Rev Biochem 38:389, 1969). Fluorescent antibody methods have been used to identify IgG, IgM, and IgA in human gingivitis (COONS: In General Cytochemical Methods. Vol. I. J.F. DANIELLI, (ed), New York, Academic Press, 1958). This study employed goat antihuman IgG, IgM, and C 3 bound to fluoresceine isothiocyanate to identify such proteins in human inflamed gingiva. The antiserum was reacted with human erythrocyte to eliminate binding to blood group substances. Twenty-five patients with chronic periodontitis requiring gingivoplasty were used for the collection. Tissue fragments approximately 0.5 x 0.5 cm were cut, frozen on a cryostat and sections 8 to 10 tz were cut. The sections were washed with phosphate buffered saline to remove unbound globulins. Sections were incubated with the specific antisera for 45 minutes at 37 C, washed 3 times in phosphate-buffered saline and mounted in glycerine. The sections were examined with a fluorescent microscope. * The presence of green fluorescence was scored positive; blue fluores-

Immunoglobulins of Intact Epithelium

Immunoglobulins are found in human gingiva with gingivitis, probably in response to antigenic substances produced by bacteria living in the gingival sulcus (T. F. SCHNEIDER, P. D. ToTo, A. W. GARGIULO, and R. J. POLLOCK, Periodontics 4:53-57, 1966). Plasma cells are locally produced in the gingiva and alveolar bone and cause the change to the granulomatous characteristics of gingivitis and periodontitis respectively (P. D. TOTO, R. J. POLLOCK, and A. W. GARGIULO, Periodontics 2: 197-201, 1964). Such plasma cells produce gamma globulins within the gingiva. Immunoglobulins A, G, and M have been seen in gingivitis by immunofluorescent studies (M. H. DALBOW and A. BAUMHAMMERS, abstracted, IADR Program and Abstracts of Papers, No. 405, 1968). The stimulus for the production of immunoglobulins in gingiva can be accomplished by packing the gingival sulcus, causing injury to sulcus epithelium, and simultaneously introducing antigenic substances (R. R. RANNEY, abstracted, IADR Program and Abstracts of Papers, No. 407, 1968; and H. M. DICK, abstracted, IADR Program and Abstracts of Papers, No. 407, 1969). It is evident that antigenic substance must successfully pass through the epithelial barrier of the gingiva to stimulate immunoglobulin formation. The gingival epithelium serves as the first line of defense against impregnation by antigenic substances. The constant renewal and migration of epithelial cells in the gingiva serves to carry off substances when such cells are desquamatud into the oral cavity. Another suitable line of defense would be the presence of immunoglobulins in the epithelium. They could combine and inactivate antigenic substances penetrating intercellularly. Twenty-five specimens previously histologically diagnosed as chronic gingivitis were sectioned at ten micrometers and brought to water. Sections were treated with rabbit antihuman IgA, IgM, IgG, incubated one half hour at 37 C, washed with saline and again reacted with antihuman IgA, IgM, and IgG,

Gingivitis induced by gingival impaction in monkeys

Impaction of the gingival sulcus with elastic bands deforms the gingival sulcus, forming a surface for growth of bacterial plaque, compresses and causes necrosis of surface epithelium and the subjacent lamina propria. The teeth become extruded and make premature contact with their apposing teeth. During mastication, forces applied to extruded teeth probably contribute to their displacement, resulting in their mobility. An inflammatory process commences within 3 days and becomes clinically evident by 7 days. The gingival becomes red-magenta in color and is slightly hemorrhagic. Pockets 4 to 6 min. in depth form within 1 week and remain as long as the impacted substance occupies the space between the tooth and the sulcus epithelium. Removal of the impacted substance results in prompt repair, with complete restoration within 3 weeks. Such repair may be by an epithelial attachment rather than by a fibrous periodontal ligament.