Pathogenesis of RA continued
Since most autoimmune diseases are considered to be benign proliferative diseases we can assume the presence of an underlying sycotic process. In RA the proliferative process is focused on synovial lining cells, lymphoid elements, blood vessels, fibroblasts and other connective tissue cells in the synovial membrane to form the invading mass of tissue known as pannus.
A negative state of mind, and particularly the tendency to self-condemnation that is so prominent in the picture of the sycotic miasm can be considered to be a causative factor in the pathogenesis of the autoimmune activity in RA. An excess of negative mental energy that is transferred to the body via the pranic sheath may throw the immune system off balance so that it turns against the host. When one cannot mentally live in harmony with oneself, this will be reflected in the functioning of the body. The loss of someone dearly loved or other shocking emotional experiences causing grief and deep states of sadness may also trigger the same mechanism that precipitates the autoimmune mechanism.
Since there is yet no definitive explanation for the autoimmune activity, the immuno-proliferative feature of the rheumatic synovial membrane, it has been suggested that the source of these antigens may be viruses. The predisposition to make autoantibodies is part of a genetically determined response to persistent viral antigens. And we might add, such a genetically determined response and predisposition can be attributed to the sycotic miasm.
There are many examples in which acute polyarthritis is provoked by viral infection. For example, both rubella infection and immunization commonly precipitate acute polyarthritis. Others include Epstein-Barr virus, coxsackie B virus and the arbovirus Ross River virus. But chronic destructive disease of the joints is rarely a sequel to these acute exacerbations. The rubella virus has been isolated from the synovial fluid several months after the acute infection, and has been recovered from lymphocytes two years after vaccination. It has been demonstrated that rubella infection and rubella arthritis may occur in the absence of exanthema and may occur more frequently than is realized.
There are three basic ways in which the virus and RA may be related: 1. The virus could initiate the primary event in the disease owing to direct infection of the articular cavity or through the formation of immune complexes. 2. The virus could enhance the production of rheumatoid factor (RF) and potentiate or perpetrate the intra-articular inflammation. 3. The virus may not be handled well by patients with RA, resulting in an increased production of antibody directed toward virus–related antigens. However, if the characteristic destructive changes of the chronic RA are not present, there is still no tangible evidence for a viral etiology in RA.
Though retroviruses are highly suspect as etiologic agents in RA there is as yet no conclusive evidence. Retroviruses are known to precipitate neoplastic and immunodeficiency disease, yet so far there is no documented evidence of retroviral infection in RA.
. . . to be continued
Dr. Barbara Bova, HOD, Department of Homeopathy