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Erschienen in:

01.01.2021 | Spondyloarthritis (M Khan, Section Editor)

Diffuse Idiopathic Skeletal Hyperostosis (DISH) and a Possible Inflammatory Component

verfasst von: Reuven Mader, Nicola Pappone, Xenofon Baraliakos, Iris Eshed, Piercarlo Sarzi-Puttini, Fabiola Atzeni, Amir Bieber, Irina Novofastovski, David Kiefer, Jorrit-Jan Verlaan, Pasquale Ambrosino, Dan Buskila, Jacome Bruges Armas, Muhammad Asim Khan

Erschienen in: Current Rheumatology Reports | Ausgabe 1/2021

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Abstract

Purpose of Review

Diffuse Idiopathic Skeletal Hyperostosis (DISH) is considered a metabolic condition, characterized by new bone formation affecting mainly at entheseal sites. Enthesitis and enthesopathies occur not only in the axial skeleton but also at some peripheral sites, and they resemble to some extent the enthesitis that is a cardinal feature in spondyloarthritis (SpA), which is an inflammatory disease.

Recent Findings

We review the possible non-metabolic mechanism such as inflammation that may also be involved at some stage and help promote new bone formation in DISH. We discuss supporting pathogenic mechanisms for a local inflammation at sites typically affected by this disease, and that is also supported by imaging studies that report some similarities between DISH and SpA.

Summary

Local inflammation, either primary or secondary to metabolic derangements, may contribute to new bone formation in DISH. This new hypothesis is expected to stimulate further research in both the metabolic and inflammatory pathways in order to better understand the mechanisms that lead to new bone formation. This may lead to development of measures that will help in earlier detection and effective management before damage occurs.

Resnick D, Niwayama G. Radiographic and pathologic features of spinal involvement in diffuse idiopathic skeletal hyperostosis (DISH). Radiology. 1976;119:559–68.PubMed

Mader R, Buskila D, Verlaan JJ, Atzeni F, Olivieri I, Pappone N, et al. Developing new classification criteria for diffuse idiopathic skeletal hyperostosis: back to square one. Rheumatology (Oxford). 2013;52:326–30.

• Kuperus JS, Waalwijk JF, Regan EA, van der Horst-Bruinsma IE, Oner FC, de Jong PA, et al. Simultaneous occurrence of ankylosing spondylitis and diffuse idiopathic skeletal hyperostosis: a systematic review. Rheumatology (Oxford). 2018;57:2120–8 A review on this co-occurrence of AS and DISH.

Khan MA. Ankylosing spondylitis-axial spondyloarthritis, Professional Communications Inc. (PCI). West Islip; 2016. p. 1–333. ISBN: 978-1-943236-08-4

Watad A, Cuthbert RJ, Amital H, McGonagle D. Enthesitis: much more than focal insertion poin inflammation. Best Pract Res Curr Rheumatol Rep. 2018;20(7):41. https://doi.org/10.1007/s11926-018-0751-3.CrossRef

Mader R, Sarzi-Puttini P, Atzeni F, Olivieri I, Pappone N, Verlaan JJ, et al. Extraspinal manifestations of diffuse idiopathic skeletal hyperostosis. Rheumatology (Oxford). 2009;48:1478–81.

Haller J, Resnick D, Miller GW, Schils JP, Kerr R, Bielecki D, et al. Diffuse idiopathic skeletal hyperostosis: diagnostic significance of radiographic abnormalities of the pelvis. Radiology. 1989;172:835–9.PubMed

Yagan R, Khan MA. Confusion of roentgenographic differential diagnosis between ankylosing hyperostosis (Forestier’s disease) and ankylosing spondylitis. Clin Rheumatol. 1983;2:285–92.PubMed

Yagan R, Khan MA, Bellon EM. Spondylitis and posterior longitudinal ligament ossification in the cervical spine. Arthritis Rheum. 1983;26:226–30.PubMed

10.

Slonimsky E, Leibushor N, Aharoni D, Lidar M, Eshed I. Pelvic enthesopathy on CT is significantly more prevalent in patients with diffuse idiopathic skeletal hyperostosis (DISH) compared with matched control patients. Clin Rheumatol. 2016;35:1823–7.PubMed

11.

Weiss BG, Bachmann LM, Pfirrmann CWA, Kissling RO, Zubler V. Whole body magnetic resonance imaging features in diffuse idiopathic skeletal hyperostosis MRI in conjunction with clinical variables to whole body MRI and clinical variables in ankylosing spondylitis. J Rheumatol. 2016;43:335–42.PubMed

12.

• Hiyama A, Katoh H, Sakai D, Sato M, Tanaka M, Watanabe M. Prevalence of diffuse idiopathic skeletal hyperostosis (DISH) assessed with whole-spine computed tomography in 1479 subjects. BMC Musculoskelet Disord. 2018;19:178 A very large study of DISH using who spine CT.PubMedPubMedCentral

13.

• Latourte A, Charlon SE, Etcheto A, Feydy A, Allanore Y, Dougados M, et al. Imaging findings suggestive of axial spondyloarthritis in diffuse idiopathic skeletal hyperostosis. Arthritis Care Res. 2018;70:145–52 A discussion of imaging findings of axSpA and DISH.

14.

Baraliakos X, Listing J, Buschmann J, von der Recke A, Braun J. A comparison of new bone formation in patients with ankylosing spondylitis and patients with diffuse idiopathic skeletal hyperostosis. A retrospective cohort study over six years. Arthritis Rheumatol. 2012;64:1127–33.

15.

Mader R, Novofastovski I, Iervolino S, Pavlov A, Chervinsky L, Schwartz N, et al. Ultrasonography of peripheral entheses in the diagnosis and understanding of diffuse idiopathic skeletal hyperostosis (DISH). Rheumatol Int. 2015;35:493–7.PubMed

16.

• Bieber A, Masala IF, Mader R, Atzeni F. Differences between diffuse idiopathic skeletal hyperostosis and spondyloarthritis. Immunotherapy. 2020;12:749–56 This is the most current review on this subject.PubMed

17.

Beardwell A. Familial Ankylosing vertebral hyperostosis with Tylosis. Ann Rheum Dis. 1969;28:518–23.PubMedPubMedCentral

18.

Abiteboul M, Mazières B, Ménard H. À propos De Deux Nouveaux Cas Familiaux D’Hyperostose Vertébrale Ankylosante. Rev Rheumatisme. 1985;52:645–7.

19.

Gorman C, Jawad ASM, Chikanza I. A family with diffuse idiopathic skeletal hyperostosis. Ann Rheum Dis. 2005;64:1794–5.PubMedPubMedCentral

20.

Bruges Armas J, Couto AR, Timms A, Santos MR, Bettencourt BF, Peixoto MJ, et al. Ectopic calcification among families in the Azores: clinical and radiologic manifestations in families with diffuse idiopathic skeletal hyperostosis and chondrocalcinosis. Arthritis Rheum. 2006;54:1340–9.PubMed

21.

Kranenburg HC, Westerveld LA, Verlaan JJ, Oner FC, Dhert JA, Voorhout G, et al. The dog as an animal model for DISH. Eur Spine J. 2010;19:1325–9.PubMedPubMedCentral

22.

Tsukahara S, Miyazawa N, Akagawa H, Foreijtova S, Pavelka K, Tanaka T, et al. COL6A1, the candidate gene for ossification of the posterior longitudinal ligament, is associated with diffuse idiopathic skeletal hyperostosis in Japanese. Spine. 2005;30:2321–4.PubMed

23.

Jun JK, Kim SM. Association study of fibroblast growth factor 2 and fibroblast growth factor receptors gene polymorphism in Korean ossification of the posterior longitudinal ligament patients. J Korean Neurosurg Soc. 2012;52:7–13.PubMedPubMedCentral

24.

Couto AR, Parreira B, Thomson R, Soares M, Power DM, Stankovich J, et al. Combined approach for finding susceptibility genes in DISH/chondrocalcinosis families: whole-genome-wide linkage and IBS/IBD studies. Human Genome Variation. 2017;4:17041. https://doi.org/10.1038/hgv.2017.41.CrossRefPubMedPubMedCentral

25.

Parreira B, Couto AR, Rocha F, Sousa M, Faustino V, Power DM, et al. Whole exome sequencing of patients with diffuse idiopathic skeletal hyperostosis & calcium pyrophosphate crystal chondrocalcinosis. Acta Reumatol Port. 2020;45:116–26.PubMed

26.

Zhou Y, Wang T, Hamilton JL, Di Chen D. Wnt/β-catenin signaling in osteoarthritis and in other forms of arthritis. Curr Rheumatol Rep. 2017;19:53.PubMedPubMedCentral

27.

Daoussis D, Andonopoulos AP. The emerging role of Dickkopf-1 in bone biology: is it the main switch controlling bone and joint remodeling? Semin Arthritis Rheum. 2011;41:170–7.PubMed

28.

Heiland GR, Appel H, Poddubnyy D, Zwerina J, Hueber X, Haibel H, et al. High level of functional dickkopf-1 predicts protection from syndesmophyte formation in patients with ankylosing spondylitis. Ann Rheum Dis. 2012;71:572–4.PubMed

29.

Senolt L, Hulejova H, Krystufkova O, Forejtova S, Andres Cerezo L, Gatterova J, et al. Low circulating Dickkopf-1 and its link with severity of spinal involvement in diffuse idiopathic skeletal hyperostosis. Ann Rheum Dis. 2012;71:71–4.PubMed

30.

Mader R, Verlaan JJ. Exploring factors responsible for bone formation in diffuse idiopathic skeletal hyperostosis (DISH). Nat Rev Rheumatol. 2011;8:10–2.PubMed

31.

Bakirci MS, Dabague J, Eder L, McGonagle D, Aydin SZ. The role of obesity on inflammation and damage in spondyloarthritis: a systematic literature review on body mass index and imaging. Clin Exp Rheumatol. 2020;38:144–8.PubMed

32.

Despres JP, Lemieux I, Bergeron J, et al. Abdominal obesity and the metabolic syndrome: contribution to global cardiometabolic risk. Arterioscler Thromb Vasc Biol. 2008;28:1039–49.PubMed

33.

Despres JP. Body fat distribution and risk of cardiovascular disease: an update. Circulation. 2012;126:1301–13.PubMed

34.

Toussirot E, Streit G, Wendling D. The contribution of adipose tissue and adipokines to inflammation in joint diseases. Curr Med Chem. 2007;14:1095–100.PubMed

35.

Krysiak R, Handzlik-Orlik G, Okopien B. The role of adipokines in connective tissue diseases. Eur J Nutr. 2012;51:513–28.PubMedPubMedCentral

36.

Genre F, Lopez-Mejias R, Miranda-Filloy JA, et al. Adipokines, biomarkers of endothelial activation, and metabolic syndrome in patients with ankylosing spondylitis. Biomed Res Int. 2014;860651.

37.

Kvist H, Chowdhury B, Grangard U, Tylen U, Sjostrom L. Total and visceral adipose-tissue volumes derived from measurements with computed tomography in adult men and women: predictive equations. Am J Clin Nutr. 1988;48:1351–61.PubMed

38.

Amato MC, Giordano C. Visceral adiposity index: an indicator of adipose tissue dysfunction. Int J Endocrinol. 2014;730827.

39.

Dan Lantsman C, et al. Abdominal fat distribution in diffuse idiopathic skeletal hyperostosis and ankylosing spondylitis patients compared to controls. Clin Radiol. 2018;73:910.PubMed

40.

Shinoda Y, YamaguchiM ON, Akune T, Kubota N, Yamauchi T, Terauchi Y, et al. Regulation of bone formation by adiponectin through autocrine/paracrine and endocrine pathways. J Cell Biochem. 2006;99:196–208.PubMed

41.

Luo XH, Guo LJ, Xie H, Yuan LQ, Wu XP, Zhou HD, et al. Adiponectin stimulates RANKL and inhibits OPG expression in human osteoblasts through the MAPK signaling pathway. J Bone Miner Res. 2006;1:1648–56.

42.

Kanazawa I, Yamaguchi T, Yamamoto M, Yamauchi M, Yano S, Sugimoto T. Relationships between serum adiponectin levels versus bone mineral density, bone metabolic markers, and vertebral fractures in type 2 diabetes mellitus. Eur J Endocrinol. 2009;160:265–73.PubMed

43.

Mader R, Novofastovski I, Schwartz N, Rosner E. Serum adiponectin levels in patients with diffuse idiopathic skeletal hyperostosis (DISH). Clin Rheumatol. 2018;34:2839–45.

44.

Konigorski S, Janke J, Drogan D, Bergmann MM, Hierholzer J, Kaaks R, et al. Prediction of circulating adipokine levels based on body fat compartments and adipose tissue gene expression. Obes Facts. 2019;12:590–605.PubMedPubMedCentral

45.

•• Wedell-Neergaard AS, Lehrskov LL, Christensen RH, Legaard GE, Dorph E, Larsen MK, et al. Exercise-induced changes in visceral adipose tissue mass are regulated by IL-6 signaling: a randomized controlled trial. Cell Metab. 2018;29:844–55 Visceral adipose tissue is harmful to metabolic health. These authors have shown that IL-6 is required for exercise to reduce visceral adipose tissue mass.PubMed

46.

Schett G, Lories RJ, D’Agostino MA, Elewaut D, Kirkham B. SorianoER, McGonagle D.Enthesitis: from pathophysiology to treatment. Nat Rev Rheumatol. 2017;13:731–41.PubMed

47.

Tanno M, Furukawa KI, Ueyama K, Harata S, Motomurab S. Uniaxial cyclic stretch induces osteogenic differentiation and synthesis of bone morphogenetic proteins of spinal ligament cells derived from patients with ossification of the posterior longitudinal ligaments. Bone. 2003;33:475–84.PubMed

48.

Lories RJU, Luyten FR, de Vlam K. Mechanisms of new bone formation in spondyloarthritis. Arthritis Res Ther. 2009;11:221.PubMedPubMedCentral

49.

Mader R, Verlaan JJ, Buskila D. Diffuse idiopathic skeletal hyperostosis: clinical manifestations and pathogenic mechanisms. Nat Rev Rheumatol. 2013;9:741–50.PubMed

50.

Hayden MR, Tyagi SC. Vasa vasorum in plaque angiogenesis, metabolic syndrome, type 2 diabetes mellitus, and atheroscleropathy: a malignant transformation. Cardiovasc Diabetol. 2004; 3. https://doi.org/10.1186/1475-2840-3-1

51.

Davaine JM, Quillard T, Chatelais M, Guilbaud F, Brion R, Guyomarch B, et al. Bone like arterial calcification in femoral atherosclerotic lesions: prevalence and role of osteoprotegerin and pericytes. Eur J Vasc Endovasc Surg. 2016;51:259–67.PubMed

52.

Di Girolamo DJ, Mukherjee A, Fulzele K, et al. Mode of growth hormone action in osteoblasts. J Biol Chem. 2007;282:31666–74.

53.

Olivieri I, D’Angelo S, Cutro MS, Padula A, Peruz G, Montaruli M, et al. Diffuse idiopathic skeletal hyperostosis may give the typical postural abnormalities of advanced ankylosing spondylitis. Rheumatology (Oxford). 2007;46(11):1709–11.

54.

Jumshyd A, Khan MA. Ankylosing hyperostosis in American Blacks: a longitudinal study. Clin Rheumatol. 1983;2:123–6.PubMed

55.

Carroll GP, Lim A, Breidahl WH, Dewing WM, Coleman S. Successful treatment of DISH with TNF inhibitors (TNFI). Ann Rheum Dis. 2015; suppl. https://doi.org/10.1136/annrheumdis-2015-eular.5257

56.

Lim A, Breidahl WH, Song SJ, et al. An audit of clinical service delivery and outcomes in diffuse idiopathic skeletal hyperostosis – preliminary evidence for efficacy of tumour necrosis factor inhibition therapy. Tasman Med J. 2021;3(1):11–6.

Titel: Diffuse Idiopathic Skeletal Hyperostosis (DISH) and a Possible Inflammatory Component
verfasst von: Reuven Mader
Nicola Pappone
Xenofon Baraliakos
Iris Eshed
Piercarlo Sarzi-Puttini
Fabiola Atzeni
Amir Bieber
Irina Novofastovski
David Kiefer
Jorrit-Jan Verlaan
Pasquale Ambrosino
Dan Buskila
Jacome Bruges Armas
Muhammad Asim Khan
Publikationsdatum: 01.01.2021
Verlag: Springer US
Erschienen in: Current Rheumatology Reports / Ausgabe 1/2021
Print ISSN: 1523-3774
Elektronische ISSN: 1534-6307
DOI: https://doi.org/10.1007/s11926-020-00972-x

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Diffuse Idiopathic Skeletal Hyperostosis (DISH) and a Possible Inflammatory Component