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Disease Activity and Bone Mineral Density of MCP Joints in Patients with Rheumatoid and Psoriatic Arthritis: Is There a Correlation?—A Study in Patients Treated with Methotrexate and an Anti-TNFα Agent

DOI: 10.1155/2013/708323

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Abstract:

Background. Bone damage in rheumatoid arthritis (RA) and in psoriatic arthritis (PsA) includes an accelerated bone mineral density (BMD) reduction. The objective was to evaluate BMD variations of the metacarpophalangeal joints (MCPs) in patients starting treatment with methotrexate (MTX) or etanercept. Methods. Patients affected by RA or PsA with hand joints involvement and with moderate or high disease activity, were enrolled in this study. All patients underwent clinical examination, laboratory exams, and a DXA scan of the most affected hand, as assessed with an ultrasound examination at the baseline, at the time of enrolment and after 1, 3, 6, and 12 months. Patients non-responders to MTX received combination therapy, while patients with no previous treatment initiated MTX. Results. 22 patients were enrolled. In both RA and PsA groups, BMD increased independently of the treatment. However, in the patients affected by RA, a slight BMD decrease was observed at the last checkup. Globally, the BMD variations of the MCPs were strongly correlated with the disease activity. At the reduction of DAS28, the scores corresponded an increase of BMD. Conclusions. MCPs BMD is inversely correlated to disease activity. BMD increase seems to be correlated with the response to treatment and not with the drug itself. 1. Introduction Bone damage in rheumatoid arthritis (RA) and in psoriatic arthritis (PsA) includes joint damage and accelerated bone mineral density (BMD) reduction [1], both at a local and generalised level. Bone damage is caused by an increased osteoclast activity and decreased osteoblast activation. This is mostly mediated by tumor necrosis factor (TNF)-α, interleukin (IL)-1, IL-6, IL-17, and receptor activator of nuclear factor kappa B ligand (RANKL) [2–5]. The erosion represents the final result of this process [6, 7] and it can be considered the central feature of bone damage of both RA and PsA, although in PsA there are significant differences when compared with RA, with a pattern characterised by concurrent erosions and new bone formation [8–10]. However, bone in the proximity of inflamed joints is susceptible to BMD reduction and it precedes erosive damage on X-ray [11–16]. Dual energy X-ray absorptiometry (DEXA, DXA) is the gold standard for measuring BMD [17]. Previous clinical studies demonstrated an association between hand BMD and RA severity, including disease activity, functional impairment and joint destruction [11–16, 18–22]. However, only a little data is available on the association between hand BMD reduction and disease activity in

References

[1]  E. M. Gravallese, “Bone destruction in arthritis,” Annals of the Rheumatic Diseases, vol. 61, supplement 2, pp. ii84–ii86, 2002.
[2]  T. Hirayama, L. Danks, A. Sabokbar, and N. A. Athanasou, “Osteoclast formation and activity in the pathogenesis of osteoporosis in rheumatoid arthritis,” Rheumatology, vol. 41, no. 11, pp. 1232–1239, 2002.
[3]  N. C. Walsh, T. N. Crotti, S. R. Goldring, and E. M. Gravallese, “Rheumatic diseases: the effects of inflammation on bone,” Immunological Reviews, vol. 208, pp. 228–251, 2005.
[4]  G. Schett, “Review: immune cells and mediators of inflammatory arthritis,” Autoimmunity, vol. 41, no. 3, pp. 224–229, 2008.
[5]  S. Herman, G. Kr?nke, and G. Schett, “Molecular mechanisms of inflammatory bone damage: emerging targets for therapy,” Trends in Molecular Medicine, vol. 14, no. 6, pp. 245–253, 2008.
[6]  S. R. Goldring, “Pathogenesis of bone erosions in rheumatoid arthritis,” Current Opinion in Rheumatology, vol. 14, no. 4, pp. 406–410, 2002.
[7]  D. O'Gradaigh, D. Ireland, S. Bord, and J. E. Compston, “Joint erosion in rheumatoid arthritis: interactions between tumour necrosis factor α, interleukin 1, and receptor activator of nuclear factor κB ligand (RANKL) regulate osteoclasts,” Annals of the Rheumatic Diseases, vol. 63, no. 4, pp. 354–359, 2004.
[8]  V. Wright, “Psoriatic arthritis: a comparative radiographic study of rheumatoid arthritis and arthritis associated with psoriasis,” Annals of the Rheumatic Diseases, vol. 20, pp. 123–132, 1961.
[9]  S. Finzel, M. Englbrecht, K. Engelke, C. Stach, and G. Schett, “A comparative study of periarticular bone lesions in rheumatoid arthritis and psoriatic arthritis,” Annals of the Rheumatic Diseases, vol. 70, no. 1, pp. 122–127, 2011.
[10]  S. R. Goldring and M. B. Goldring, “Eating bone or adding it: the Wnt pathway decides,” Nature Medicine, vol. 13, no. 2, pp. 133–134, 2007.
[11]  M. Güler-Yüksel, N. B. Klarenbeek, Y. P. M. Goekoop-Ruiterman et al., “Accelerated hand bone mineral density loss is associated with progressive joint damage in hands and feet in recent-onset rheumatoid arthritis,” Arthritis Research and Therapy, vol. 12, no. 3, p. R96, 2010.
[12]  M. Hoff, G. Haugeberg, and T. K. Kvien, “Hand bone loss as an outcome measure in established rheumatoid arthritis: 2-year observational study comparing cortical and total bone loss,” Arthritis Research and Therapy, vol. 9, no. 4, article R81, 2007.
[13]  T. Jensen, M. Hansen, K. E. Jensen, J. P?denphant, T. M. Hansen, and L. Hyldstrup, “Comparison of dual X-ray absorptiometry (DXA), digital X-ray radiogrammetry (DXR), and conventional radiographs in the evaluation of osteoporosis and bone erosions in patients with rheumatoid arthritis,” Scandinavian Journal of Rheumatology, vol. 34, no. 1, pp. 27–33, 2005.
[14]  G. Hougeberg, M. C. Lodder, W. F. Lems et al., “Hand cortical bone mass and its associations with radiographic joint damage and fractures in 50–70 year old female patients with rheumatoid arthritis: cross sectional Oslo-Truro-Amsterdam (OSTRA) collaborative study,” Annals of the Rheumatic Diseases, vol. 63, no. 10, pp. 1331–1334, 2004.
[15]  T. Jensen, M. Klarlund, M. Hansen et al., “Bone loss in unclassified polyarthritis and early rheumatoid arthritis is better detected by digital x ray radiogrammetry than dual x ray absorptiometry: relationship with disease activity and radiographic outcome,” Annals of the Rheumatic Diseases, vol. 63, no. 1, pp. 15–22, 2004.
[16]  B. J. Harrison, C. E. Hutchinson, J. Adams, I. N. Bruce, and A. L. Herrick, “Assessing periarticular bone mineral density in patients with early psoriatic arthritis or rheumatoid arthritis,” Annals of the Rheumatic Diseases, vol. 61, no. 11, pp. 1007–1011, 2002.
[17]  W. Sturtridge, B. Lentle, and D. A. Hanley, “Prevention and management of osteoporosis: consensus statements from the Scientific Advisory Board of the Osteoporosis Society of Canada. 2. The use of bone density measurement in the diagnosis and management of osteoporosis,” Canadian Medical Association Journal, vol. 155, no. 7, pp. 924–929, 1996.
[18]  M. Güler-Yüksel, C. F. Allaart, Y. P. M. Goekoop-Ruiterman et al., “Changes in hand and generalised bone mineral density in patients with recent-onset rheumatoid arthritis,” Annals of the Rheumatic Diseases, vol. 68, no. 3, pp. 330–336, 2009.
[19]  G. Haugeberg, M. J. Green, M. A. Quinn et al., “Hand bone loss in early undifferentiated arthritis: Evaluating bone mineral density loss before the development of rheumatoid arthritis,” Annals of the Rheumatic Diseases, vol. 65, no. 6, pp. 736–740, 2006.
[20]  J. B?ttcher, A. Pfeil, A. Rosholm et al., “Computerized quantification of joint space narrowing and periarticular demineralization in patients with rheumatoid arthritis based on digital x-ray radiogrammetry,” Investigative Radiology, vol. 41, no. 1, pp. 36–44, 2006.
[21]  W. B. Jawaid, D. Crosbie, J. Shotton, D. M. Reid, and A. Stewart, “Use of digital x ray radiogrammetry in the assessment of joint damage in rheumatoid arthritis,” Annals of the Rheumatic Diseases, vol. 65, no. 4, pp. 459–464, 2006.
[22]  A. A. Deodhar, J. Brabyn, I. Pande, D. L. Scott, and A. D. Woolf, “Hand bone densitometry in rheumatoid arthritis, a five year longitudinal study: an outcome measure and a prognostic marker,” Annals of the Rheumatic Diseases, vol. 62, no. 8, pp. 767–770, 2003.
[23]  M. Hoff, A. Kavanaugh, and G. Haugeberg, “Hand bone loss in patients with psoriatic arthritis: posthoc analysis of IMPACT II data comparing infliximab and lacebo,” The Journal of Rheumatology, vol. 40, no. 8, pp. 1344–1348, 2013.
[24]  A. Szentpetery, M. J. McKenna, B. F. Murray, et al., “Periarticular bone gain at proximal interphalangeal joints and changes in bone turnover markers in response to tumor necrosis factor inhibitors in rheumatoid and psoriatic arthritis,” The Journal of Rheumatology, vol. 40, no. 5, pp. 653–662, 2013.
[25]  M. Hoff, T. K. Kvien, J. K?lvesten, A. Elden, A. Kavanaugh, and G. Haugeberg, “Adalimumab reduces hand bone loss in rheumatoid arthritis independent of clinical response: subanalysis of the PREMIER study,” BMC Musculoskeletal Disorders, vol. 12, article 54, 2011.
[26]  M. Vis, E. A. Havaardsholm, G. Haugeberg et al., “Evaluation of bone mineral density, bone metabolism, osteoprotegerin and receptor activator of the NFκB ligand serum levels during treatment with infliximab in patients with rheumatoid arthritis,” Annals of the Rheumatic Diseases, vol. 65, no. 11, pp. 1495–1499, 2006.
[27]  F. C. Arnett, S. M. Edworthy, D. A. Bloch et al., “The American Rheumatism Association 1987 revised criteria for the classification of rheumatoid arthritis,” Arthritis and Rheumatism, vol. 31, no. 3, pp. 315–324, 1988.
[28]  W. Taylor, D. Gladman, P. Helliwell, A. Marchesoni, P. Mease, and H. Mielants, “Classification criteria for psoriatic arthritis: development of new criteria from a large international study,” Arthritis and Rheumatism, vol. 54, no. 8, pp. 2665–2673, 2006.
[29]  R. Caporali, F. Conti, S. Alivernini, et al., “Recommendations for the use of biologic therapy in rheumatoid arthritis: update from the Italian Society for Rheumatology I. Efficacy,” Clinical and Experimental Rheumatology, vol. 29, no. 3, supplement 66, pp. S7–S14, 2011.
[30]  C. Salvarani, N. Pipitone, A. Marchesoni et al., “Recommendations for the use of biologic therapy in the treatment of psoriatic arthritis: update from the Italian Society for Rheumatology,” Clinical and Experimental Rheumatology, vol. 29, no. 3, supplement 66, pp. S28–S41, 2011.
[31]  M. Backhaus, G.-R. Burmester, T. Gerber et al., “Guidelines for musculoskeletal ultrasound in rheumatology,” Annals of the Rheumatic Diseases, vol. 60, no. 7, pp. 641–649, 2001.
[32]  A. K. Scheel, K.-G. A. Hermann, E. Kahler et al., “A novel ultrasonographic synovitis scoring system suitable for analyzing finger joint inflammation in rheumatoid arthritis,” Arthritis and Rheumatism, vol. 52, no. 3, pp. 733–743, 2005.
[33]  B. Frediani, “Effects of two administration schemes of intramuscular clodronic acid on bone mineral density: a randomized, open-label, parallel-group study,” Clinical Drug Investigation, vol. 31, no. 1, pp. 43–50, 2011.
[34]  L. Naumann, K.-G. A. Hermann, D. Huscher et al., “Quantification of periarticular demineralization and synovialitis of the hand in rheumatoid arthritis patients,” Osteoporosis International, vol. 23, no. 12, pp. 2671–2679, 2012.
[35]  J. M. Bland and D. G. Altman, “Calculating correlation coefficients with repeated observations: part I—correlation within subjects,” British Medical Journal, vol. 310, no. 6977, article 446, 1995.
[36]  D. M. Reid, N. S. J. Kennedy, J. Nicoll, M. A. Smith, P. Tothill, and G. Nuki, “Total and peripheral bone mass in patients with psoriatic arthritis and rheumatoid arthritis,” Clinical Rheumatology, vol. 5, no. 3, pp. 372–378, 1986.
[37]  C. Cooper, V. Poll, M. McLaren, S. O. Daunt, and M. I. D. Cawley, “Alterations in appendicular skeletal mass in patients with rheumatoid, psoriatic, and osteoarthropathy,” Annals of the Rheumatic Diseases, vol. 47, no. 6, pp. 481–484, 1988.
[38]  B. Frediani, A. Allegri, P. Falsetti, et al., “Juxta-articular osteoporosis in arthritis and arthrosis: fan-beam x ray densitometry,” Arthritis and Rheumatism, vol. 42, supplement, p. S355, 1999.
[39]  G. Haugeberg, A. Strand, T. K. Kvien, and J. R. Kirwan, “Reduced loss of hand bone density with prednisolone in early rheumatoid arthritis: results from a randomized placebo-controlled trial,” Archives of Internal Medicine, vol. 165, no. 11, pp. 1293–1297, 2005.
[40]  B. Seriolo, S. Paolino, A. Sulli, V. Ferretti, and M. Cutolo, “Bone metabolism changes during anti-TNF-α therapy in patients with active rheumatoid arthritis,” Annals of the New York Academy of Sciences, vol. 1069, pp. 420–427, 2006.

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