so i found some literature that suggests what i spectulated, which was hidden deep in a hand surgery book.
"Rheumatoid arthritis (RA) is the most common systemic inflammatory disease with a world-wide prevalence of approximately 1% and an incidence rate of 0.03% (
1). The majority of patients develop RA between the ages of 30 and 60 years. RA is a chronic, systemic autoimmune disease that is characterized by an immunologically caused chronic inflammatory synovitis. Probably driven by a still unknown antigen response, a cascade of immunologic and inflammatory processes are mediated, which finally lead to destruction of joints and soft tissues. Genetics seem to play an important role in the pathogenesis of RA. In monozygotic twins, there is a 30% to 50% chance of that both persons are affected, compared to a 1% rate in the general population (
2,
3). Besides the possible genetic background of the disease,
bacterial and viral infection have been speculated as trigger agents that cause RA (
4,
5). Studies suggest that osteoclasts mediate focal bone erosion. This may offer a new approach for the treatment of this disease (
6).
The onset of RA shows first an acute inflammatory reaction within the synovial membrane, which becomes congested (
7). As shown by magnetic resonance imaging (MRI), the degree of synovitis correlates with the edema formation of the periarticular bone (
8). Along with this acute inflammation, a complex cell transformation within the synovial cells starts, including cellular and humeral immunologic processes. Becoming chronic, as a process, the inflammation leads to the formation of the so-called rheumatoid pannus, which is a mass of granulation tissue that includes all cell mediators of chronic inflammation surrounded by a matrix of connective tissue (
9). This pannus plays an important role in the destruction process of the cartilage of the affected joint and may show tumorlike characteristics.