Pathology of connective tissue

Issue title: Microcirculation, Interstitium, Lymph, Pathophysiology and Disease. Proceedings of the International Symposium, Villa La Principessa, Lucca, Italy, June 19–20, 1981

Guest editors: Siegfried Witte

Article type: Research Article

Authors: Lindner, J. | Lindner, Ch.

Affiliations: Dept. of Pathology, University Hamburg, F.R. Germany

Abstract: The pathology of connective tissue is demonstrated by the most important example: the inflammation, summarizing the basic processes of pathological reactions of connective tissues on the several irritations and injuries. Comparative morphological and biochemical methods, employed on the same material as far as possible, allow a better insight into and investigation of the single stages of inflammation, which start very fast. They have been localized qualitatively and assayed quantitatively, esp. the processes occuring immediately after the start of inflammation as the several steps of the disturbed regulatory equilibrium between catabolism and anabolism in the involved connective tissue. The primary increase of the catabolism at the beginning of inflammation is followed almost immediately by an increased anabolism of all 3 components of the vascularized connective tissue, i.e. the substrate of inflammation: cells, ground substance and fibres. Thus their turnover is remarkably increased in inflammation. The single phases of inflammation are regarded in relation to each other and summarized: the cell injuries, endothelial cells included, the several stages of disturbed blood flow (prestasis, stasis and poststasis), the enhanced permeability and their consequences (swelling, dissolution, degradation etc.), exudation and emigration, sticking processes and chemotaxis, mediators and their effects, granulocytes, lymphocytes, monocytes and macrophages, their functions, the immunological responses included, but esp. the processes of pinocytosis and phagocytosis, the whole degradation and breakdown of phlogistics as well as of the components of the injured, inflamed and damaged connective tissue. Its replacement is achieved by the new formation of capillarized granulation tissue, depending on the intensity and duration of the inflammation. So, finally scars can result, with reduction of capillaries, cells and ground substance. Then the collagen content prevails. The catabolic and anabolic processes during inflammation are regarded in their feedback relations, esp. of the proteoglycans and collagen, their several heterogeneities, their interrelations, interactions and interdependencies included. They are also described as main processes of the disturbed equilibrium of connective tissues, i.e.: the basic and fundamental processes of the “pathology of Connective Tissues”. Than many degenerative lesions are the final results of some of these main and general steps of connective tissue reactions. The disturbances of these several relations and phases during inflammation by drugs are discussed finally. The influences of the most common antiphlogistic agents on inflammation intervene in the various mechanisms of these turnover alterations of the 3 main components (cell, proteoglycans and collagen), i.e. as a rule, not only in one process. Often cell proliferations, lysosomal degradations, syntheses of catabolic and/or anabolic enzymes and of the intracellular macromolecular substances (= the differentiation products of connective tissue cells) can be influenced by application of one antiphlogistic drug. Since the extent and duration of inflammations strongly depend on the extent of degradation and/or of the extent of enhanced catabolism and anabolism during the start of inflammation, it is emphasized to influence inflammations as early as possible, best by previous antiphlogistic drug administrations. This is practicable in many cases of inflammation in human medicine. So the most important basic subjects of the “Pathology of Connective Tissue” are demonstrated and discussed from the theoretical and clinical point of view.

Keywords: Connective tissue, inflammation, stasis, permeability, mediator substances, basement membrane

DOI: 10.3233/CH-1982-25-607

Journal: Clinical Hemorheology and Microcirculation, vol. 2, no. 5-6, pp. 453-495, 1982