The clinical feature of rheumatoid arthritis (RA) is characterized by systemic-immunological, local-inflammatory phenomena. But it is the joint destruction which gives RA its dramatic course. Through the years we evaluated joint tissues of app. 14,500 patients with defined RA and besides the conventional inflammatory processes we could prove a mechanism which is responsible for the joint destruction and which is typical for RA. Following an exudative episode, compact, homogeneous cell masses can occur in the synovial membrane which consist of macronuclear, immature, synoviogenous cells. These masses can encroach on the adjacent structures of articular cartilage and subchondral bone which consequently enzymatically will be degraded and destroyed. Since these rapidly growing cell masses are avascular in their aggressive stage, they soon will collapse. The surviving cells "modulate" to fibroblast which start collagen synthesis and thus form the well-known pannus. In the area of the compact, homogeneous cell masses of synovial origin, there are no lymphocytes and plasma cells nor PMN or macrophages. Macrophages only occur after the breakdown of the cell masses and the beginning of pannus formation, this also is the case with lymphocytes and plasma cells. Thus, the immature synoviogenous cell masses are in contrast to the initial synovitis not of inflammatory character. Their cytological and aggressive behavior rather shows oncological analogies. This also corresponds to our proof of the expression of myc and ras to a high degree in the aggressive cell masses in RA.