Rheumatoid arthritis and prevention

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How is developing infectious nonspecific (rheumatoid) arthritis, or arthritis? The concept of "infectious" indicates that a significant role in causing the disease plays an infection. But how the infection affects the joints and is it always possible to determine its presence? To answer this question is rather difficult.
A significant part (35-40%) patients cannot neither according to the study of the development of the disease (history), nor on the results of special studies to determine whether the infection. If it was, it is not clear enough, what changes occur in the body, primarily in the joints, whether it will lead to serious changes in the tissues and can inflammatory process periodically to subside? How often gives relapses? How this process takes a progressive course and results in severe anatomic and functional disturbances?
Clinical observations suggest that the onset of rheumatoid arthritis sometimes coincides with the emergence of angina or acute exacerbation of chronic tonsillitis, sinusitis (inflammation of the paranasal cavities of the nose) or with the activation of streptococcal infections, nesting in other hotbeds - carious teeth, tonsils, biliary system, intestines, etc. But there are times when they don't match, and rheumatoid arthritis progresses. In some cases the infection is clinically once was suspected, but then no longer shown. Nevertheless, if even to give meaning to this infection, and above all beta-hemolytic Streptococcus group a, it performs as only the start mechanism in the development of inflammation, as in the future when you remove the infection atrophic process continues to progress, and do not detect infection. Endo - and exotoxins beta-hemolytic Streptococcus, getting in the internal environment of the organism, increase the sensitivity of different tissues and cells, and first of all the autonomic nervous system and joints, especially in persons with genetically weak design of the musculoskeletal system. Various negative aspects of the external environment (negative emotional impact, cold cooling, mikrotravmatizatsiya, physical strain and others) are factors of development of an Allergy, clinical manifestation and which serve as arthritis and polyarthritis.
However, this way of development of the disease is too simple. Modern methods of research shows that infection may cause sensitisation not only synovial membrane and fibrous capsule of the joints, but also, as stated above, the nerve ganglia, their fibers, especially vegetative nervous formations up to the highest vegetative lower centers. This process is quick to respond the hypothalamic-pituitary system, synthesizing and throwing in humoral environment adrenocorticotropic (ACTH) and thyroid-stimulating (TSH) hormones. As is now well known, ACTH stimulates the function of the adrenal cortex, and TSH - secretory cells of the thyroid. An overactive adrenal cortex increases the synthesis of 11-oxycorticosteroids, reduces binding capacity, interacted. This mechanism, as a physiological measure of protection against the disease contributes to the weakening of the inflammatory process, since it steroid hormones condense cell membranes, reduces the permeability tissue structures and reduce exudative component of inflammation. However, as a result of the deregulation of the function of the pituitary-adrenal axis exhausted its function and decreases over time daily balance of corticosteroids increases binding capacity, interacted and increases the inflammatory process. In this process involved thymus, and lymph nodes, which at the initial stage of the disease play a protective role, and then, as the destruction of collagen connective tissue that develop autoimmune chain reaction to those antigens that are generated.