Rheumatology Vol. 43 No. 10 © British Society for Rheumatology 2004; all rights reserved
Letter to the Editor |
Comment on review on T cells in bone biology: reply
University of Cambridge School of Clinical Medicine, Department of Medicine Bone Research Group, Cambridge, UK
Correspondence to: D. O'Gradaigh. E-mail: ogradaighd{at}sehb.ie
SIR, We have read with interest the comments from Professor Smith following the publication of our review on T-cell interactions with the osteoclast [1]. In reviewing this topic, we concentrated on describing the current state of knowledge in this field and on presenting research from areas not normally read by the rheumatologist. Unfortunately, it was not feasible to catalogue all the work that has been carried out in this area. Papers were typically cited when reporting the earliest description of a new finding, where the work resulted in the development of a new hypothesis, or where a reader might be interested to explore an unfamiliar area of research (such as that in the dental literature). Readers with an interest in this research area will of course have noted the contributions from Professor Smith's group to the field, published in leading rheumatology journals.
Their work is of interest in demonstrating that the expression of RANKL (receptor activator of NF-
B ligand) and of OPG (osteoprotegerin) varies with disease activity in rheumatoid arthritis. We did not review OPG expression in detail, concentrating instead on T-cell-derived factors. As proposed by this group, the deficiency in OPG when compared with active spondyloarthritis may be of particular relevance to the pathogenesis of joint erosion at the bone–pannus interface. It is interesting to speculate whether dendritic cell or B-cell expression of OPG [2] renders both the inflammatory disease and the erosive component inactive through inhibition of T-cell RANKL-mediated effects. However, previous studies of OPG have demonstrated little benefit on joint inflammation [3], and Mulherin et al. [4] have suggested that radiographic progression may occur when disease is apparently ‘inactive’.
Many unanswered questions remain in this exciting area of research, and we are certain the work of Professor Smith's group and others will lead to improved outcome for patients with inflammatory joint diseases in the future.
The authors have declared no conflicts of interest.
References
- O'Gradaigh D, Compston JE. T-cell involvement in osteoclast biology: implications for rheumatoid bone erosion. Rheumatol 2004;43:122–30.
[Free Full Text] - Bengtsson AK, Ryan EJ. Immune function of the decoy receptor osteprotegerin. Crit Rev Immunol 2002;22:201–15.[Web of Science][Medline]
- Kong Y-Y, Feige U, Sarosi I et al. Activated T-cells regulate bone loss and joint destruction in adjuvant arthritis through osteoprotegerin ligand. Nature 1999;402:304–8.[CrossRef][Medline]
- Mulherin D, Fitzgerald O, Bresnihan B. Clinical improvement and radiological deterioration in rheumatoid arthritis: evidence that the pathogenesis of synovial inflammation and articular erosion may differ. Br J Rheumatol 1996;35:1263–8.
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