Comment on review on T cells in bone biology

M. D. Smith

Rheumatology Research Unit, Repatriation General Hospital, Adelaide, South Australia

Correspondence to: M. D. Smith. E-mail: malcolm.smith{at}rgh.sa.gov.au

SIR, A recent review on T-cell involvement was published in Rheumatology [1] and the authors are to be congratulated on their paper. We have published two papers relevant to this topic recently [2, 3]. One paper examined the expression of RANKL protein in synovial tissue from patients with rheumatoid arthritis (RA), who had both active and inactive disease, as well as patients with a seronegative spondyloarthropathy, osteoarthritis (OA) and normal subjects. We clearly demonstrated in this paper that RANKL was expressed to a similar extent in synovial membranes from patients with active RA and seronegative spondyloarthropathy, with much less RANKL expression in inactive RA and OA synovial membranes, which was similar to that seen in normal synovial tissue [2]. In addition, we demonstrated by dual immunohistochemistry that the CD45Ro-positive T lymphocyte was the major cell expressing RANKL at the protein level, with around 40% of macrophages also expressing RANKL but few if any type B lining cells (fibroblast lineage) expressing RANKL. In a companion paper [3], we demonstrated that OPG was not seen in active RA synovial tissue, unlike the extensive expression of OPG in patients with seronegative spondyloarthropathy, OA and normal synovial tissue. We also demonstrated that synovial tissue from patients with inactive RA had extensive OPG expression and that this expression was predominantly on type A lining cells (macrophage lineage) and endothelial cells. We raised the possibility that OPG expression in RA may be a major determinant of osteoclast formation and bone erosion and therefore an attractive therapeutic target in RA.

These two papers were published in December 2002 [2] and January 2003 [3], well before the review [1] was submitted for publication, so it is surprising and rather disappointing that the authors did not feel that these papers were relevant enough to be included in a review of the subject which contained 121 references.

For those readers of this journal who are interested in this subject, we have also published on RANKL and OPG expression in tissue from patients with two other bone resorbing conditions, periodontal disease [4] and peri-implant bone loss and failure [5].

The author has declared no conflicts of interest.

References

  1. O’Gradaigh D, Compston JE. T-cell involvement in osteoclast biology: implications for rheumatoid bone erosion. Rheumatology 2004;43:122–30.[Free Full Text]
  2. Crotti TN, Smith MD, Weedon H et al. Receptor activator NF-{kappa}B ligand (RANKL) expression in synovial tissue from patients with rheumatoid arthritis, spondyloarthropathy, osteoarthritis, and from normal patients: semiquantitative and quantitative analysis. Ann Rheum Dis 2002;61:1047–54.[Abstract/Free Full Text]
  3. Haynes D, Barg E, Crotti T et al. Osteoprotegerin expression in synovial tissue from patients with rheumatoid arthritis, spondyloarthropathies and osteoarthritis and normal controls. Rheumatology 2003;42:123–34.[Free Full Text]
  4. Crotti T, Smith MD, Hirsch R et al. Receptor activator NF{kappa}B ligand (RANKL) and osteoprotegerin (OPG) protein expression in periodontitis. J Periodont Res 2003;38:380–7.[ISI][Medline]
  5. Crotti TN, Smith MD, Findlay DM et al. Factors regulating osteoclast formation in human tissues adjacent to peri-implant bone loss: expression of receptor activator NF kappaB, RANK ligand and osteoprotegerin. Biomaterials 2004;25:565–73.[CrossRef][ISI][Medline]
Accepted 28 June 2004





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