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G Geiler

Publications and source records attributed to G Geiler.

At least 19 recordsLinked to original sources
PubMed1996

[Pathology and progression of intra-articular inflammation in rheumatoid arthritis].

Rheumatoid arthritis (RA) is a chronic systemic inflammatory disease of the connective tissue preferentially involving joints. It is considered an autoimmune disease. Autoantibodies against immunoglobulins, so called rheumatoid factors, are detected in 80% of the patients. The etiology of the disease is unknown. An interesting association to different HLA types is observed. An overview about pathology and pathogenesis of the arthritis is given. After an initial vasculitis the synovial membrane is colonised by T and B cells. Among the more frequent T cells more CD4+ cells than CD8+ cells are found. Additionally activated cytotoxic T cells and NK cells are present. Migration of the lymphocytes is realised by adhesion molecules. By homing of lymphocytes the synovial membrane is structurally transformed an appears morphologically like a secondary immunoorgan. Enhanced pathogenic humoral and cellular immune responses are going on influenced by activated CD4+ cells associated with macrophages via MHC class II molecules. Rheumatoid factors and antibodies against type II collagen are produced, cytotoxic immune complexes are formed. Cellular interactions induce the expression of proinflammatory cytokines and growth factors, the so called pannus is formed. Aggressiveness of the pannus depends on the HLA pattern. T cell rich synovial tissue is positive for HLA-DR4 in 70% of the cases. Only 15% of B cell rich membranes show this HLA type. The T cell rich type shows a high aggressiveness. Pannus destroys articular cartilage and subchondral bone. Cells at the invasion site of the pannus are classified differently. The majority of the investigators characterizes them as macrophages others as activated fibroblasts. The latter opinion is supported by experiments done in SCID mice. RA is characterized by three pathogenic mechanisms: 1. chronic inflammation of the synovial membrane, 2. enhanced pathogenic T and B cell dependent immunoreactions including autoimmune phenomenons, 3. hyperplasia of synovial tissue. Which mechanisms is on the beginning and induces the others consecutively is an open question. Macrophages and CD4+ cells associated via MHC class II molecules play a central role in the pathogenesis of RA.

Animals↗
PubMed1994

Distribution of macrophages in rheumatoid synovial membrane and its association with basic activity.

Rheumatoid arthritis (RA) is an inflammatory disease of the synovial membrane, which results in the destruction of joints by inflammatory pannus. The synovial membrane shows proliferation and cellular infiltrates on microscopy with signs of chronic and acute inflammation. Macrophages are thought to play a central role in the pathogenesis of RA. We examined synovial membrane specimens of 21 RA patients using morphological, immunohistological and enzyme histochemical methods for number and distribution of macrophages. We were able to identify 41.5 +/- 8.8% of lining cells as macrophages, depending on the method used. In abundant diffuse lymphocellular infiltrates, 23.4 +/- 11.1% of mononuclear cells were macrophages. In addition, most cells in the region of tumorlike proliferation and a stromal population of fibroblastlike cells were detected by macrophage markers. Although cell number in synovial membrane increases drastically, we did not find correlations between the relative amount of macrophages in these regions and basic activity. Basic activity includes proliferative reaction as well as lymphoplasmacellular and mononuclear infiltration--both signs of an immunopathological process. In contrast, using enzymes or activation markers, there was a clear correlation. We consider that a constant high percentage of macrophages in RA synovial membrane is present regardless of any actual inflammatory process.

Adult↗
PubMed1987

[Pathology of primary inflammatory and primary degenerative changes in joints].

The author describes, from a general pathological viewpoint, the primary inflammatory arthropathies (arthritic diseases) and the primary degenerative arthropathies (arthroses), basing himself on a description of the joint as a complex open system consisting primarily of the highly vascularized synovial membrane, the synovial fluid and the hyaline articular cartilage. In the case of arthritis the primary lesion occurs in the synovial membrane. Different quantitative and qualitative morphological findings are obtained depending on the causes and duration of the disease and the pathomechanisms involved and, more specifically, on the involvement, or otherwise, of immunological mechanisms in the pathogenesis of arthritis. A classification of arthritic diseases following this concept is proposed. In the case of arthroses the primary lesion occurs in the non-vascularized hyaline cartilage. The latter reacts basically with metabolic disturbances which, from a morphological viewpoint, manifest themselves as degeneration and finally lead to cartilage necrosis. A distinction is made between primary arthrosis and secondary arthroses of known etiology. The close metabolic interaction of the synovial membrane and articular cartilage is the reason why, depending on the duration of the disease, arthritis develops into secondary arthrosis and the latter into secondary arthritis.

Arthritis↗
PubMed1985

[Common and contradictory aspects of inflammatory reactions and pathogenic immune reactions].

Some basic features of the reciprocal relationship between inflammation and the pathogenic immune reactions are presented. Inflammation as a non-specific defense reaction is described first followed by presentation of the fundamental mechanisms of immunity corresponding to specific defense reactions. Immune reactions may, in certain circumstances, have a pathogenic effect leading naturally to pathogenic immune reactions. The mechanisms of this process are explained in detail. Macrophages play an important connecting link between inflammation and pathogenic immune reactions. The majority of specifically triggered pathologic immune reactions produce an inflammatory picture illustrating the relationship between the two processes. Humoral reactions controlled by B-lymphocytes manifest themselves as acute inflammation; cell-mediated processes controlled by T-lymphocytes appear as chronic inflammation with granuloma formation. Granuloma formation is specific to the immune reaction rather than to a given causal agent. Inflammation and pathologic immune reactions have different origins. The process of immune reaction is initiated by a specific phase characterized by the struggle between antigen and sensitized lymphocytes. Lymphocytes and plasma cells appear in the course of prolonged inflammatory processes for reasons which are not now known.

Antibody Formation↗
PubMed1982

[Important results of experimental-theoretical pathology and etiopathogenetical research of the Institute of Pathology of Leipzig].

Since the appointment of L. Wagner to the first full professor of pathology at the University of Leipzig there are past 112 years. Based on the analysis of the scientific works during this period the author tries to characterize the whole profile of the institute among the different directors and to show the important results of the experimental-theoretical pathology and of the etiopathogenetical research. These results are concentrated upon 3 themes: inflammation, atherosclerosis and diabetes mellitus. The investigations about the inflammation by Cohnheim and Marchand and those about the allergic inflammation by Klinge are of special importance. Beside these well-known men numerous co-workers have contributed with experimental and morphological work to the scientific profile of the institute.

Arteriosclerosis↗
PubMed1980

[Immunohistochemical detection of antigammaglobulin factors in the serum (author's transl)].

Agglutination procedures for the detection of rheuma factors are inadequate concerning IgG and IgA factors and sensitivity to IgM factors, too, is generally limited. Both these disadvantages are to a great extent overcome when rheuma factors are fluorescence-marked with anti-human-gammaglobulin respectively with monospecific antiserums and when reaction steps according to Svartz and Schlossmann are applied to a microscope slide test. This test and the results of investigations of 101 cases (different joint diseases and healthy blood--donors) are described in this paper.

Agglutination Tests↗
PubMed1980

[Immunohistochemical detection of tissue-bound rheumatoid factors (author's transl)].

Different immunoglobulin classes, complement factors, complement fixation and rheumatoid-factor activity in rheumatoid synovial membranes of 16 patients were studied. After pepsin digestion of tissue sections, greatly increased numbers of plasma cells were able to bind human gamma globulin. In addition we found after the pepsin digestion more IgG and less IgM in the tissues. The results gave evidence of intracellular blocking of rheumatoid factor activity, due to IgG-IgG rheumatoid factor complexes or self associated rheumatoid factors. Additional evidence of such plasma cell complexes was obtained by observing an in vitro fixation of the complement. With the same methods we studied 3 patients whose synovial membranes had been surgically removed not later than 6 months after the onset of evident symptoms and who developed rheumatoid arthritis within an observation period of 2 years. As a result we found a small production of predominantly M and G immunoglobulins. The rheumatoid factors were also found in a small degree. Rheumatoid factor activity can be revealed only in a little number of plasma cells by pepsin digestion of tissues. In the serum we can't find more rheumatoid factor activity after pepsin digestion in the latex test. The immunofluorescence for detection of rheumatoid factors in tissues is a practicable method and important for the differential diagnosis of joint diseases.

Arthritis, Rheumatoid↗
PubMed1976

[Possibilities and limits of the morphological diagnosis of rheumatoid arthritis].

For the morphological diagnostics of rheumatoid arthritis only the judgment of the synovial membrane is of practical importance. Based on the experience gleaned on more than 2,000 synovectomy preparations the following evidence concerning the possibilities and the limits of the morphological diagnostics and the judgment of activity can be enunciated. 1. A certain histological diagnosis of the rheumatoid arthritis is possible only when rheumatoid granulomas or their equivalents are proved. 2. A probability diagnosis results from a definite combination of symptoms of proliferative and exsudative reactions of the synovial membrane. Especially the absence of proliferative signs decreases the degree of probability of the diagnostic evidence. 3. Seropositive and seronegative cases do not reveal any differences in histological respect. The possibility of the class-specific determination of rheumatoid factors by means of an immunofluorescence test and the fact the seronegative cases showed IgM and IgM rheumatoid factors, when this test was used, demands an examination of this evidence. 4. As to the synovial membranes of large joints in the same membrane so distinctive local differences of the findings may exist that thus the value of the needle biopsy is restricted. Only positive findings may be evaluated diagnostically. 5. Apart from a diagnosis the histological findings of the synovial membrane also allow a judgment of the local activity. The basis activity and the actual activity are differentiated. The basis activity is regarded as an expression of the immunological activity, the actual activity as an expression of the inflammatory activity. There are no unambiguous relations to the total clinical activity. Differences in the behaviour of the activity between seropositive and seronegative cases are not to be proved. A revision of this evidence under the aspect of the class-specific proof of the rheumatoid factor is necessary.

Arthritis, Rheumatoid↗
PubMed1975

Comparative morphological studies on adjuvant arthritis induced in the extremities of rats, mice, and golden hamsters by intracutaneous injection of Freund's complete adjuvant.

Forty rats, 60 mice, and 60 golden hamsters were administered complete Freund's adjuvant by intracutaneous injections in an attempt to produce the clinical picture of arthritis. 90% of the rats, 25% of the mice, and 40% of the golden hamsters developed swollen extremities similar to those observed in rats affected by adjuvant arthritis. 12 animals of each of the 3 species included in this investigation, which showed macroscopically visible swellings of their extremities, were used for comparative histological studies in order to find out whether the swellings of the extremities of mice and golden hamsters are real inflammations of joints and identical with rat adjuvant arthritis. The animals were killed, at 4-day intervals, between the 8th and the 44th days from administration of the adjuvant. Whereas rats showed the full clinical picture of adjuvant arthritis, mice and hamsters exhibited only inflammatory pedal edema without florid arthritis. The involvement of the joints was confined to a minor focal reaction of the synovial membranes of small individual joints. The results obtained support the view of rat adjuvant arthritis being a species-specific reaction rather than corresponding to a species-dependent, universal principle of reaction.

Animals↗