Rheumatoid factor (RF) was detected by latex‐slide agglutination in subgingival plaque, inflamed gingival tissue, stimulated pooled saliva and serum of patients suffering from chronic moderate periodontitis. The etiology of rheumatoid factor and its possible homeostatic role in periodontal disease are discussed, in relation to the reported association of Gram‐negative bacterial endotoxin and the chronic antigenic stimulating nature of periodontal disease.

The purpose of this study was to qualitatively compare three recent techniques of Langerhans cells detection in oral epithelium and to quantitatively compare Langerhans cells in clinically normal and clinically inflamed human gingival biopsies. Eleven subjects were selected who displayed chronic periodontitis and moderate gingival inflammation. A quadrant associated with clinically inflamed tissues was not treated, while the remaining teeth were scaled and root-planed. Two gingival biopsies were taken: clinically normal, treated tissue; and clinically inflamed, untreated tissue. Langerhans cells were stained using HLD-DR, S-100 and OKT6. They were quantitated using a standard grid for OKT6-stained sections only. Approximately 5 times as many Langerhans cells were identified in the biopsy specimens of clinically inflamed human gingiva as in clinically normal gingiva of the same patient. Of the methods studied, OKT6 was qualitatively determined to be the best for visualization of these cells. An immunologic role in the host response to chronic periodontal disease is postulated for Langerhans cells.

Fifteen patients, eight males and seven females, ranging from 30 to 88 years of age with advanced periodontal disease were selected for this study. Biopsies and blood samples were taken of both normal and inflamed gingival tissues, and processed for detection of nonspecific esterase and acid phosphatase activity in monocytes and macrophages. Activated macrophages, as indicated by their intense reaction to acid phosphatase and nonspecific esterase, were found in the gingival epithelium, lamina propria, perivascular tissues and in the blood vessels in human chronic periodontitis. Blood smears of monocytes showed variability of stain intensity suggesting that their activation occurred in blood vessels where they marginate and emigrate into the perivascular tissues in chronic periodontitis. They then appear as macrophages that migrate through the connective tissue, penetrate the basement membrane and continue through the epithelium. The nonspecific esterase stain identified T‐cells, by a singular dot‐like granule, and plasma cells by multiple granules in the cyotplasm. Lymphocytes containing multiple cytoplasmic nonspecific esterase positive granules commonly were found only in the perivascular connective tissue and may represent B‐cell differentiation to plasma cells. The plasma cell predominance, the presence of T‐cells and activated macrophages indicated both humoral and cell‐mediated responses are operative in human chronic periodontitis.

Resected inflamed gingival tissue obtained from 16 periodontal patients and a pooled sample of noninflamed gingiva from five edentulous patients were assayed for immunoglobulins IgG, IgA, and IgM using low-level immunodiffusion plates. Findings based on the gingival assays include:(1) IgA and IgG are present in both inflamed and normal gingiva and although their levels are substanitally higher in the inflamed gingiva, their ratio, one to another, remains the same; (2) IgM can not be consistently demonstrated in inflamed gingiva with the assay technique employed: (3) local immune response exists in the inflamed gingiva of humans with chronic periodontal disease; and (4) there is an unknown homeostatic mechanism which regulates the globulin levels in states of health and inflammation. Further study is needed to correlate clinical impressions with histological and quantitative measure of immunoglobulin levels in the inflamed gingiva and to investigate the role of delayed hypersensitivity in the disease process. Work must also be directed toward the detection of specific antigens responsible for elicting the immune response in the gingival tissue of the periodontal patient.