[Critical considerations of the pathogenesis of "soft tissue rheumatism" (fibromyalgia) and its therapeutic consequences].


The term "fibrositis" for generalized tendomyopathia that can still be found in Anglo-American literature is obsolete. The term implies that the disease has inflammatory qualities and can be treated by antiphlogistic means. Using light or electron microscopy we could find no evidence for an inflammatory process in the either tendon or muscle tissues. The term fibromyalgia makes clear that two totally different tissues are affected: 1. the bradytrophic collagenous connective tissue that requires little oxygen 2. the highly active skeletal muscles, made up of muscle cells that require a high amount of oxygen. The way these two tissues react to disorders therefore is also totally different: The collagenous tendon and capsular tissue react to lack of oxygen and overstrain by excessive formation of fibroblasts and dissolution of collagen fibres. Muscle tissue reacts to nerval irritations by pathological muscle tone in extensive areas of human body. This indurative myoitis does not lead to muscle damage, because the increased demand for oxygen is compensated by an increased supply. In the case of excessive focal contracture in myogelosis the tissue-pO2 sinks below the level vital to the muscle cells. By means of electron microscopy we could detect severe damage to, even dissolution of, myofilaments. Therapy for "muscular rheumatism" thus requires normalisation of the pathological tone with the help of antitonic substances or physiotherapy.

Cite this paper

@article{Fassbender1992CriticalCO, title={[Critical considerations of the pathogenesis of "soft tissue rheumatism" (fibromyalgia) and its therapeutic consequences].}, author={Hans Georg Fassbender and K. D. Martens}, journal={Zeitschrift für Orthopädie und ihre Grenzgebiete}, year={1992}, volume={130 2}, pages={99-103} }