One hundred forty-five synovial biopsy specimens were obtained from 30 procedures performed on the knee joints of 29 patients with rheumatoid arthritis. All patients had clinically active rheumatoid arthritis and none had received slow-acting disease-modifying drugs or intraarticular corticosteroids. Scores were assigned to each biopsy specimen for each of 6 histologic features to quantify variation within each joint. In the majority of knee joint biopsies, there was considerable clustering of scores for all histologic features. Thus, on a scale of 0-10, 82% of the scores for synoviocyte hyperplasia were within 1 point of the median score for a given joint. Similarly, between 69% and 85% of the scores for the remaining features (fibrosis, vessel proliferation, perivascular infiltrates, focal aggregates, and diffuse infiltrates of lymphocytes) were within 1 point of the median values. Multiple biopsies were obtained at arthroscopy in 8 patients. Tissue was selected from areas of apparent maximal and minimal involvement, to enhance the likelihood of regional histologic variation. Of the scores for synoviocyte hyperplasia, 91 % were within 1 point of the median values for a given joint, and of the scores for the remaining 5 features, 72-94% fell within 1 point of the median values. In addition, highly significant statistical correlations of the intensity of synovial lining layer hyperplasia, vessel proliferation, mononuclear cell infiltration, fibrosis, and clinical measurements of synovitis were observed.

The histopathology of eight cases of sporadic ileocaecal tuberculosis is described with particular reference to caecal lymphoid tissue. Adjacent to areas of ulceration in all cases there was an increase in lymphoglandular complexes (LGC) and proliferation of paravascular lymphoid aggregates deeper in the gut wall. Early and fully-developed granulomas were present in locations comparable to LGC and lymphoid aggregates. Immunocytochemical staining of paraffin sections with monoclonal antibodies UCHL1 (T-lymphocyte membrane antigen) and LN-1, LN-2 and LN-3 (B-lymphocyte and Ia antigens) showed that central cells in LGC and lymphoid aggregates stained like follicular centre B-lymphocytes. Both LGC and lymphoid aggregates had a distinct peripheral rim of cells staining as T-lymphocytes, but LN-2 and LN-3 also stained scattered peripheral cells, some of which were recognizable as interdigitating reticulum cells. Most lymphocytes within and around granulomas stained as T-lymphocytes. In lymph nodes, granulomas appeared to occur first at the periphery of, and later to efface, cortical follicles. Lymph node compartments showed the expected T- and B-zonation, and lymphocytes associated with granulomas stained as in caecal granulomas. Our observations suggest that LGC are sites of mycobacterial antigen sampling, of T-lymphocyte and macrophage activation, and of (potential) granuloma formation in ileocaecal tuberculosis. Lymphoid aggregates deeper in the gut wall probably subserve a similar function during extension of the lesion. The location of both LGC and lymphoid aggregates beside lymphatics is suited to the transfer of their cellular constituents throughout the gut and to regional lymph nodes.