When planning therapy for rheumatoid arthritis (RA) in the wrist joint, knowing the pattern of joint destruction is important. There were a few studies using the Larsen and modified Larsen method to evaluate RA wrist joint destruction. However, these methods are inadequate for thoroughly assessing the severity of joint destruction because joint bone erosion and joint space narrowing could not be evaluated individually in these methods. To clarify the pattern of RA wrist joint destruction in the different zones of the wrist, we conducted a large-scale radiographic study. We modified the van der Heijde/Sharp method to assess radiographic images. Subjects were 191 RA patients (22 men and 169 women; mean age 57.0 years) who were examined at our center between 2001 and 2003 and underwent plain X-ray of both wrist joints (n = 382). Using X-ray images of the wrist joint, classification was performed based on the severity of wrist joint surface bone erosion and joint space narrowing at different zones, and the results were statistically analyzed. The results showed that joint space narrowing in the midcarpal joint (MCJ) advanced faster than in the radiocarpal joint (RCJ). Conversely, bone erosion in the RCJ advanced faster than in the MCJ. In X-ray diagnosis of RA wrist joint disorders, knowing the pattern of destruction is useful for assessing the presence or absence of early joint destruction and in planning therapy.
[Show abstract][Hide abstract] ABSTRACT: Bone destruction is a frequent and clinically serious event in patients with rheumatoid arthritis (RA). Local joint destruction can cause joint instability and often necessitates reconstructive or replacement surgery. Moreover, inflammation-induced systemic bone loss is associated with an increased fracture risk. Bone resorption is a well-controlled process that is dependent on the differentiation of monocytes to bone-resorbing osteoclasts. Infiltrating as well as resident synovial cells, such as T cells, monocytes and synovial fibroblasts, have been identified as sources of osteoclast differentiation signals in RA patients. Pro-inflammatory cytokines are amongst the most important mechanisms driving this process. In particular, macrophage colony-stimulating factor, RANKL, TNF, IL-1 and IL-17 may play dominant roles in the pathogenesis of arthritis-associated bone loss. These cytokines activate different intracellular pathways to initiate osteoclast differentiation. Thus, over the past years several promising targets for the treatment of arthritic bone destruction have been defined.
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