38
Views
6
CrossRef citations to date
0
Altmetric
Review

Paget’s disease of bone

&
Pages 651-668 | Published online: 10 Jan 2014

References

  • Kanis JA. Pathophysiology and Treatment of Paget’s Disease of Bone. Martin Dunitz Ltd, London (1991).
  • Seitz S, Priemel M, Zustin J et al. Paget’s disease of bone: histologic analysis of 754 patients. J. Bone Miner. Res.24(1), 62–69 (2009).
  • Reid IR, Nicholson GC, Weinstein RS et al. Biochemical and radiologic improvement in Paget’s disease of bone treated with alendronate: a randomized, placebo-controlled trial. Am. J. Med.101(4), 341–348 (1996).
  • Renier JC, Audran M. Polyostotic Paget’s disease – a search for lesions of different durations and for new lesions. Rev. Rhum. Ed. Fr.64(4), 233–242 (1997).
  • Haddaway MJ, Davie MWJ, McCall IW, Howdle S. Effect of age and gender on the number and distribution of sites in Paget’s disease of bone. Br. J. Radiol.80, 532–536 (2007).
  • Hamadouche M, Mathieu M, Topouchian V, De Pinieux G, Courpied JP. Transfer of Paget’s disease from one part of the skeleton to another as a result of autogenous bone-grafting: a case report. J. Bone Joint Surg. Am.84A(11), 2056–2061 (2002).
  • Cundy T, Bolland M. Paget disease of bone. Trends Endocrinol. Metab.19(7), 246–253 (2008).
  • Renier JC, Leroy E, Audran M. The initial site of bone lesions in Paget’s disease – a review of two hundred cases. Rev. Rhum. Ed. Fr.63(11), 823–829 (1996).
  • Renier JC, Audran M. Progression in length and width of pagetic lesions, and estimation of age at disease onset. Rev. Rhum. Ed. Fr.64(1), 35–43 (1997).
  • Price JL. Radiology of excavated Saxon and medieval human remains from Winchester. Clin. Radiol.26(3), 363–370 (1975).
  • Wells C, Woodhouse N. Paget’s disease in an Anglo–Saxon. Med. Hist.19(4), 396–400 (1975).
  • Rogers J, Jeffrey DR, Watt I. Paget’s disease in an archeological population. J. Bone Miner. Res.17(6), 1127–1134 (2002).
  • Schmorl GC. Über ostitis deformans Paget. Virchows Arch. Pathol. Anat. Physiol. Klin. Med.283(3), 694–751 (1932).
  • Barker DJP. The epidemiology of Paget’s disease of bone. Br. Med. Bull.40(4), 396–400 (1984).
  • Detheridge FM, Guyer PB, Barker DJP. European distribution of Paget’s disease of bone. Br. Med. J.285(6347), 1005–1008 (1982).
  • Barker DJP, Chamberlain AT, Guyer PB, Gardner MJ. P aget disease of bone – the Lancashire focus. Br. Med. J.280(6222), 1105–1107 (1980).
  • Guanabens N, Garrido J, Gobbo M et al. Prevalence of Paget’s disease of bone in Spain. Bone43(6), 1006–1009 (2008).
  • Merlotti D, Gennari L, Galli B et al. Characteristics and familial aggregation of Paget’s disease of Bone in Italy. J. Bone Miner. Res.20(8), 1356–1364 (2005).
  • Gardner MJ, Guyer PB, Barker DJP. Paget’s disease of bone among British migrants to Australia. Br. Med. J.2(6149), 1436–1437 (1978).
  • Reasbeck JC, Goulding A, Campbell DR, Beale LR, Stewart RDH. Radiological prevalence of Paget’s disease in Dunedin, New Zealand. Br. Med. J.286(6382), 1937–1937 (1983).
  • Seton M, Choi HK, Hansen MF, Sebaldt RJ, Cooper C. Analysis of environmental factors in familial versus sporadic Paget’s disease of bone – the New England Registry for Paget’s disease of bone. J. Bone Miner. Res.18, 1519–1524 (2003).
  • Cody JD, Singer FR, Roodman GD, et al. Genetic linkage of Paget disease of bone to chromosome 18q. Am. J. Hum. Genet.61, 1117–1122 (1997).
  • Gomez Acotto C, Mautalen CA. European origin of patients with Paget’s disease of bone in the Buenos Aires area. Eur. J. Epidemiol.17(5), 409–411 (2001).
  • Griz L, Caldas G, Bandeira C, Assuncao V, Bandeira F. Paget’s disease of bone. Arq. Bras. Endocrinol. Metabol.50(4), 814–822 (2006).
  • Cooper C, Schafheutle K, Dennison E, Kellingray S, Guyer P, Barker D. The epidemiology of Paget’s disease in Britain: is the prevalence decreasing? J. Bone Miner. Res.14(2), 192–197 (1999).
  • Doyle T, Gunn J, Anderson G, Gill M, Cundy T. Paget’s disease in New Zealand: evidence for declining prevalence. Bone31(5), 616–619 (2002).
  • Poor G, Donath J, Fornet B, Cooper C. Epidemiology of Paget’s disease in Europe: the prevalence is decreasing. J. Bone Miner. Res.21(10), 1545–1549 (2006).
  • Cundy HR, Gamble G, Wattie D, Rutland M, Cundy T. Paget’s disease of bone in New Zealand: continued decline in disease severity. Calcif. Tissue Int.75(5), 358–364 (2004).
  • Bastin S, Bird H, Gamble GD, Cundy T. Paget’s disease of bone – becoming a rarity? Rheumatology (Oxford)48(10), 1232–1235 (2009).
  • Gardner MJ, Barker DJP. Mortality from malignant tumors of bone and Paget’s disease in United States and in England and Wales. Int. J. Epidemiol.7(2), 121–130 (1978).
  • Lopez-Abente G, Morales-Piga A, Elena-Ibanez A, Rey-Rey JS, Corres-Gonzalez J. Cattle, pets, and Paget’s disease of bone. Epidemiology8(3), 247–251 (1997).
  • Demulder A, Takahashi S, Singer FR, Hosking DJ, Roodman GD. Abnormalities in osteoclast precursors and marrow accessory cells in Paget’s disease. Endocrinology133(5), 1978–1982 (1993).
  • Kukita A, Chenu C, McManus LM, Mundy GR, Roodman GD. Atypical multinucleated cells form in long-term marrow cultures from patients with Paget’s disease. J. Clin. Invest.85(4), 1280–1286 (1990).
  • Menaa C, Barsony J, Reddy SV, Cornish J, Cundy T, Roodman GD. 1,25-dihydroxyvitamin D-3 hypersensitivity of osteoclast precursors from patients with Paget’s disease. J. Bone Miner. Res.15(2), 228–236 (2000).
  • Kurihara N, Reddy SV, Araki N et al. Role of TAF (II)-17, a VDR binding protein, in the increased osteoclast formation in Paget’s disease. J. Bone Miner. Res.19(7), 1154–1164 (2004).
  • Menaa C, Reddy SV, Kurihara N et al. Enhanced RANK ligand expression and responsivity of bone marrow cells in Paget’s disease of bone. J. Clin. Invest.105(12), 1833–1838 (2000).
  • Neale SD, Smith R, Wass JAH, Athanasou NA. Osteoclast differentiation from circulating mononuclear precursors in Paget’s disease is hypersensitive to 1,25-dihydroxyvitamin D-3 and RANKL. Bone27(3), 409–416 (2000).
  • Sun SG, Lau YS, Itonaga I, Sabokbar A, Athanasou NA. Bone stromal cells in pagetic bone and Paget’s sarcoma express RANKL and support human osteoclast formation. J. Pathol.209(1), 114–120 (2006).
  • Naot D, Bava U, Matthews B et al. Differential gene expression in cultured osteoblasts and bone marrow stromal cells from patients with Paget’s disease of bone. J. Bone Miner. Res.22(2), 298–309 (2007).
  • Alvarez L, Peris P, Guanabens N et al. Serum osteoprotegerin and its ligand in Paget’s disease of bone – relationship to disease activity and effect of treatment with bisphosphonates. Arthritis Rheum.48(3), 824–828 (2003).
  • Mossetti G, Rendina D, De Filippo G et al. Interleukin-6 and osteoprotegerin systems in Paget’s disease of bone: relationship to risedronate treatment. Bone36(3), 549–554 (2005).
  • Roodman GD, Kurihara N, Ohsaki Y et al. Interleukin 6 – a potential autocrine paracrine factor in Paget’s disease of bone. J. Clin. Invest.89(1), 46–52 (1992).
  • Hoyland JA, Freemont AJ, Sharpe PT. Interleukin-6, IL-6 receptor, and IL-6 nuclear factor gene expression in Paget’s disease. J. Bone Miner. Res.9(1), 75–80 (1994).
  • Neale SD, Schulze E, Smith R, Athanasou NA. The influence of serum cytokines and growth factors on osteoclast formation in Paget’s disease. Q. J. Med.95(4), 233–240 (2002).
  • Nagy ZB, Gergely P, Donath J, Borgulya G, Csanad M, Poor G. Gene expression profiling in Paget’s disease of bone: upregulation of interferon signaling pathways in pagetic monocytes and lymphocytes. J. Bone Miner. Res.23(2), 253–259 (2008).
  • Marshall MJ, Evans SF, Sharp CA, Powell DE, McCarthy HS, Davie MWJ. Increased circulating Dickkopf-1 in Paget’s disease of bone. Clin. Biochem.42(10–11), 965–969 (2009).
  • Tian E, Zhan FH, Walker R et al. The role of the Wnt-signaling antagonist DKK1 in the development of osteolytic lesions in multiple myeloma. N. Engl. J. Med.349(26), 2483–2494 (2003).
  • Siris ES. Epidemiological aspects of Paget’s disease: family history and relationship to other medical conditions. Semin. Arthritis Rheum.23(4), 222–225 (1994).
  • Laurin N, Brown JP, Morissette J, Raymond V. Recurrent mutation of the gene encoding sequestosome 1 (SQSTM1/p62) in Paget disease of bone. Am. J. Hum. Genet.70(6), 1582–1588 (2002).
  • Hocking LJ, Lucas GJA, Daroszewska A et al. Domain-specific mutations in sequestosome 1 (SQSTM1) cause familial and sporadic Paget’s disease. Hum. Mol. Genet.11(22), 2735–2739 (2002).
  • Johnson-Pais TL, Wisdom JH, Weldon KS et al. Three novel mutations in SQSTM1 identified in familial Paget’s disease of bone. J. Bone Miner. Res.18(10), 1748–1753 (2003).
  • Hocking LJ, Lucas GJA, Daroszewska A et al. Novel UBA domain mutations of SQSTM1 in Paget’s disease of bone: genotype phenotype correlation, functional analysis, and structural consequences. J. Bone Miner. Res.19(7), 1122–1127 (2004).
  • Eekhoff EWM, Karperien M, Houtsma D, et al. Familial Paget’s disease in The Netherlands: occurrence, identification of new mutations in the sequestosome 1 gene, and their clinical associations. Arthritis Rheum.50, 1650–1654 (2004).
  • Falchetti A, Di Stefano M, Marini F et al. Two novel mutations at exon 8 of the sequestosome 1 (SQSTM1) gene in an Italian series of patients affected by Paget’s disease of bone (PDB). J. Bone Miner. Res.19(6), 1013–1017 (2004).
  • Beyens G, Van Hul E, Van Driessche K et al. Evaluation of the role of the SQSTM1 gene in sporadic Belgian patients with Paget’s disease. Calcif. Tissue Int.75(2), 144–152 (2004).
  • Beyens G, Trujillo A, Van Hul W. Segregation of two different mutations in a Spanish family with Paget’s disease. Calcif. Tissue Int.76, 477–478 (2005).
  • Rea SL, Walsh JP, Ward L et al. A novel mutation (K378X) in the sequestosome 1 gene associated with increased NF-κB signaling and Paget’s disease of bone with a severe phenotype. J. Bone Miner. Res.21(7), 1136–1145 (2006).
  • Beyens G, Wuyts W, Cleiren E, de Freitas F, Tiegs R, Van Hul W. Identification and molecular characterization of a novel splice-site mutation (G1205C) in the SQSTM1 gene causing Paget’s disease of bone in an extended American family. Calcif. Tissue Int79(5), 281–288 (2006).
  • Collet C, Michou L, Audran M et al. Paget’s disease of bone in the French population: novel SQSTM1 mutations, functional analysis, and genotype–phenotype correlations. J. Bone Miner. Res.22(2), 310–317 (2007).
  • Rhodes EC, Johnson-Pais TL, Singer FR et al. Sequestosome 1 (SQSTM1) mutations in Paget’s disease of bone from the United States. Calcif. Tissue Int.82(4), 271–277 (2008).
  • Rios Petrakis M, Alonzo N, Selby PL, Fraser WD, Langston AL, Ralston SH. Geographic variation in type and frequency of sequestosome 1 mutations in Paget’s disease of bone. Calcif. Tissue Int.82(Suppl. 1), S146–S147 (2008).
  • Falchetti A, Di Stefano M, Marini F et al. Genetic epidemiology of Paget’s disease of bone in Italy: sequestosome1/p62 gene mutational test and haplotype analysis at 5q35 in a large representative series of sporadic and familial Italian cases of Paget’s disease of bone. Calcif. Tissue Int.84(1), 20–37 (2009).
  • Najat D, Garner T, Hagen T et al. Characterization of a non-UBA domain missense mutation of sequestosome 1 (SQSTM1) in Paget’s disease of bone. J. Bone Miner. Res.24(4), 632–642 (2009).
  • Rea SL, Walsh JP, Ward L et al. Sequestosome 1 mutations in Paget’s disease of bone in Australia: prevalence, genotype/phenotype correlation, and a novel non-UBA domain mutation (P364S) associated with increased NF-κB signaling without loss of ubiquitin binding. J. Bone Miner. Res.24(7), 1216–1223 (2009).
  • Gennari L, Gianfrancesco F, DiStefano M et al. Large collaborative study on geographic variation of SQSTM1 mutations in Paget’s disease of bone in Italy. Presented at International Symposium on Paget’s Disease. Oxford, UK, 8–9 July 2009.
  • Lucas GJA, Hocking LJ, Daroszewska A et al. Ubiquitin-associated domain mutations of SQSTM1 in Paget’s disease of bone: evidence for a founder effect in patients of British descent. J. Bone Miner. Res.20(2), 227–231 (2005).
  • Chung PYJ, Beyens G, Guañabens N et al. Founder effect in different European countries for the recurrent P392L SQSTM1 mutation in Paget’s disease of bone. Calcif. Tissue Int.83, 34–42 (2008).
  • Morissette J, Laurin N, Brown JP. Sequestosome 1: mutation frequencies, haplotypes, and phenotypes in familial Paget’s disease of bone. J. Bone Miner. Res.21(Suppl 2), P38–P44 (2006).
  • Leach RJ, Singer FR, Ench Y, Wisdom JH, Pina DS, Johnston-Pais TL. Clinical and cellular phenotypes associated with sequestosome 1 (SQSTM1) mutations. J. Bone Miner. Res.21(Suppl. 2), P45–P50 (2006).
  • Bolland MJ, Tong PC, Naot D et al. Delayed development of Paget’s disease in offspring inheriting SQSTM1 mutations. J. Bone Miner. Res.22(3), 411–415 (2007).
  • Merchant A, Smielewska M, Patel N et al. Somatic mutations in SQSTM1 detected in affected tissues from patients with sporadic Paget disease of bone. J. Bone Miner. Res.24(3), 484–494 (2009).
  • Matthews BG, Naot D, Bava U et al. Absence of somatic SQSTM1 mutations in Paget’s disease of bone. J. Clin. Endocrinol. Metab.94(2), 691–694 (2009).
  • Watts GDJ, Wymer J, Kovach MJ et al. Inclusion body myopathy associated with Paget disease of bone and frontotemporal dementia is caused by mutant valosin-containing protein. Nat. Genet.36(4), 377–381 (2004).
  • Kimonis VE, Mehta SG, Fulchiero EC et al. Clinical studies in familial VCP myopathy associated with Paget disease of bone and frontotemporal dementia. Am. J. Hum. Genet.146A, 745–757 (2008).
  • Weihl CC, Pestronk A, Kimonis VE. Valosin-containing protein disease: inclusion body myopathy with Paget’s disease of the bone and fronto–temporal dementia. Neuromuscular Disorders19(5), 308–315 (2009).
  • Lucas GJA, Mehta SG, Hocking LJ et al. Evaluation of the role of Valosin-containing protein in the pathogenesis of familial and sporadic Paget’s disease of bone. Bone38(2), 280–285 (2006).
  • Lucas GJA, Riches PL, Hocking LJ et al. Identification of a major locus for Paget disease on chromosome 10p13 in families of British descent. J. Bone Miner. Res.23(1), 58–63 (2008).
  • Albagha OME, Visconti MR, Alonso N et al. Identification of novel genetic variants that predispose to Paget’s disease of bone by genome wide association. Bone44(Suppl. 2), S224–S225 (2009).
  • Geetha T, Wooten MW. Structure and functional properties of the ubiquitin binding protein p62. FEBS Lett.512(1–3), 19–24 (2002).
  • Bjorkoy G, Lamark T, Johansen T. p62/SQSTM1 – a missing link between protein aggregates and the autophagy machinery. Autophagy2(2), 138–139 (2006).
  • Paine MG, Babu JR, Seibenhener ML, Wooten MW. Evidence for p62 aggregate formation: role in cell survival. FEBS Lett.579(22), 5029–5034 (2005).
  • Rodriguez A, Duran A, Selloum M et al. Mature-onset obesity and insulin resistance in mice deficient in the signaling adapter p62. Cell Metab.3(3), 211–222 (2006).
  • Seibenhener ML, Babu JR, Geetha T, Wong HC, Krishna NR, Wooten MW. Sequestosome 1/p62 is a polyubiquitin chain binding protein involved in ubiquitin proteasome degradation. Mol. Cell. Biol.24(18), 8055–8068 (2004).
  • Saeki Y, Kudo T, Sone T et al. Lysine 63-linked polyubiquitin chain may serve as a targeting signal for the 26S proteasome. EMBO J.28, 359–371 (2009).
  • Layfield R, Hocking LJ. SQSTM1 and Paget’s disease of bone. Calcif. Tissue Int.75(5), 347–357 (2004).
  • Babu JR, Geetha T, Wooten MW. Sequestosome 1/p62 shuttles polyubiquitinated tau for proteasomal degradation. J. Neurochem.94(1), 192–203 (2005).
  • Wang Q, Song CC, Li CCH. Molecular perspectives on p97-VCP: progress in understanding its structure and diverse biological functions. J. Struct. Biol.146(1–2), 44–57 (2004).
  • Layfield R. The molecular pathogenesis of Paget disease of bone. Expert Rev. Mol. Med.9, 1–13, (2007).
  • Yip KHM, Feng HT, Pavlos NJ, Zheng MH, Xu JK. p62 Ubiquitin binding-associated domain mediated the receptor activator of nuclear factor-κB ligand-induced osteoclast formation – A new insight into the pathogenesis of Paget’s disease of bone. Am. J. Pathol.169(2), 503–514 (2006).
  • Cavey JR, Ralston SH, Hocking LJ et al. Loss of ubiquitin-binding associated with Paget’s disease of bone p62 (SQSTM1) mutations. J. Bone Miner. Res.20(4), 619–624 (2005).
  • Cavey JR, Ralston SH, Sheppard PW et al. Loss of ubiquitin binding is a unifying mechanism by which mutations of SQSTM1 cause Paget’s disease of bone. Calcif. Tissue Int.78(5), 271–277 (2006).
  • Bjorkoy G, Lamark T, Brech A et al.p62/SQSTM1 forms protein aggregates degraded by autophagy and has a protective effect on huntingtin-induced cell death. J. Cell Biol.171(4), 603–614 (2005).
  • Pankiv S, Clausen TH, Lamark T et al. p62/SQSTM1 binds directly to Atg8/LC3 to facilitate degradation of ubiquitinated protein aggregates by autophagy. J. Biol. Chem.282(33), 24131–24145 (2007).
  • Moscat J, Diaz-Meco MT, Wooten MW. Signal integration and diversification through the p62 scaffold protein. Trends Biochem. Sci.32(2), 95–100 (2007).
  • Hiruma Y, Kurihara N, Subler MA et al. A SQSTM1/p62 mutation linked to Paget’s disease increases the osteoclastogenic potential of the bone microenvironment. Hum. Mol. Genet.17(23), 3708–3719 (2008).
  • Jin W, Chang M, Paul EM et al. Deubiquitinating enzyme CYLD negatively regulates RANK signaling and osteoclastogenesis in mice. J. Clin. Invest.118(5), 1858–1866 (2008).
  • Duran A, Serrano M, Leitges M et al. The atypical PKC-interacting protein p62 is an important mediator of RANK-activated osteoclastogenesis. Dev. Cell6(2), 303–309 (2004).
  • Babu JR, Seibenhener LM, Peng J et al. Genetic inactivation of p62 leads to accumulation of hyperphosphorylated tau and neurodegeneration. J. Neurochem.106(1), 107–120 (2008).
  • Kurihara N, Hiruma Y, Zhou H et al. Mutation of the sequestosome 1 (p62) gene increases osteoclastogenesis but does not induce Paget disease. J. Clin. Invest.117(1), 133–142 (2007).
  • Rojas JA, Daroszewska A, Layfield R, Helfrich M, Van’t Hof RJ, Ralston SH. Mice with a truncation mutation affecting the UBA domain of SQSTM1 develop several phenotypic features Paget’s including focal lytic lesions, and increased bone turnover in vivo.J. Bone Miner. Res.22(Suppl. 1), S11 (2007).
  • Daroszewska A, Rojas J, Rose L, Van’t Hof RJ, Ralston SH. Knock-in of the P392L mutation of SQSTM1 causes a phenotype similar to Paget’s disease in mice. Calcif. Tissue Int.82(Suppl. 1), S34–S35 (2008).
  • Muller JM, Deinhardt K, Rosewell I, Warren G, Shima DT. Targeted deletion of p97 (VCP/CDC48) in mouse results in early embryonic lethality. Biochem. Biophys. Res. Commun.245, 459–465 (2007).
  • Daroszewska A, Rose L, Rose K, Sedlmeier R, Van’t Hof RJ, Ralston SH. Development of a novel animal model for the syndrome of inclusion body myopathy, Paget’s disease and fronto-temporal dementia. Bone44(Suppl. 2), S247 (2009).
  • Watts GDJ, Kimonis VE, Warman ML. Mutation of the p97 gene increases osteoclastogenesis and induces Paget disease of the bone. 9th Biennial Meeting of the International Skeletal Dysplasia Society Boston, MA, USA, 16–19 July 2009 (Abstract 103).
  • Rebel A, Malkani K, Basle M. Nuclear anomalies in osteoclasts in Paget’s bone disease. Nouv. Presse Med.3(20), 1299–1301 (1974).
  • Mills BG, Singer FR. Nuclear inclusions in Paget’s disease of bone. Science,194(4261), 201–202 (1976).
  • Rebel A, Basle M, Pouplard A, Malkani K, Filmon R, Lepatezour A. Bone tissue in Paget’s disease of bone – ultrastructure and immunocytology. Arthritis Rheum.23(10), 1104–1114 (1980).
  • Reddy SV, Singer FR, Roodman GD. Bone marrow mononuclear cells from patients with Paget’s disease contain measles virus nucleocapsid messenger ribonucleic acid that has mutations in a specific region of the sequence. J. Clin. Endocrinol. Metab.80(7), 2108–2111 (1995).
  • Friedrichs WE, Reddy SV, Bruder JM et al. Sequence analysis of measles virus nucleocapsid transcripts in patients with Paget’s disease. J. Bone Miner. Res.17(1), 145–151 (2002).
  • Mee AP, Dixon JA, Hoyland JA, Davies M, Selby PL, Mawer EB. Detection of canine distemper virus in 100% of Paget’s disease samples by in situ reverse transcriptase-polymerase chain reaction. Bone23(2), 171–175 (1998).
  • Mills BG, Frausto A, Singer FR, Ohsaki Y, Demulder A, Roodman GD. Multinucleated cells formed in vitro from Pagets bone-marrow express viral-antigens. Bone15(4), 443–448 (1994).
  • Helfrich MH, Hobson RP, Grabowski PS et al. A negative search for a paramyxoviral etiology of Paget’s disease of bone: molecular, immunological, and ultrastructural studies in UK patients. J. Bone Miner. Res.15(12), 2315–2329 (2000).
  • Ooi CG, Walsh CA, Gallagher JA, Fraser WD. Absence of measles virus and canine distemper virus transcripts in long-term bone marrow cultures from patients with Paget’s disease of bone. Bone27(3), 417–421 (2000).
  • Ralston SH, Afzal MA, Helfrich MH et al. Multicenter blinded analysis of RT-PCR detection methods for paramyxoviruses in relation to Paget’s disease of bone. J. Bone Miner. Res.22(4), 569–577 (2007).
  • Matthews BG, Afzal MA, Minor PD et al. Failure to detect measles virus ribonucleic acid in bone cells from patients with Paget’s disease. J. Clin. Endocrinol. Metab.93(4), 1398–1401 (2008).
  • Kurihara N, Reddy SV, Menaa C, Anderson D, Roodman GD. Osteoclasts expressing the measles virus nucleocapsid gene display a pagetic phenotype. J. Clin. Invest.105(5), 607–614 (2000).
  • Reddy SV, Kurihara N, Menaa C et al. Osteoclasts formed by measles virus-infected osteoclast precursors from hCD46 transgenic mice express characteristics of pagetic osteoclasts. Endocrinology142(7), 2898–2905 (2001).
  • Selby PL, Davies M, Mee AP. Canine distemper virus induces human osteoclastogenesis through NF-κB and sequestosome 1/P62 activation. J. Bone Miner. Res.21(11), 1750–1756 (2006).
  • Kurihara N, Zhou H, Reddy SV et al. Expression of measles virus nucleocapsid protein in osteoclasts induces Paget’s disease-like bone lesions in mice. J. Bone Miner. Res.21(3), 446–455 (2006).
  • Weinstein RS, Roberson PK, Manolagas SC. Giant osteoclast formation and long-term oral bisphosphonate therapy. N. Engl. J. Med.360(1), 53–62 (2009).
  • Mills BG, Yabe H, Singer FR. Osteoclasts in human osteopetrosis contain viral-nucleocapsid-like nuclear inclusions. J. Bone Miner. Res.3(1), 101–106 (1988).
  • Garg RK. Subacute sclerosing panencephalitis. Postgrad. Med. J.78(916), 63–70 (2002).
  • Azzam EA, Scott DI, Gregory JS, McKinnon AD, Helfrich MH. Expression of inclusion body-associated proteins in Paget’s disease of bone. Bone44(Suppl. 2), S326–S327 (2009).
  • Ekbom A, Daszak P, Kraaz W, Wakefield AJ. Crohn’s disease after in-utero measles virus exposure. Lancet,348(9026), 515–517 (1996).
  • Afzal MA, Ozoemena LC, O’Hare A, Kidger KA, Bentley ML, Minor PD. Absence of detectable measles virus genome sequence in blood of autistic children who have had their MMR vaccination during the routine childhood immunization schedule of UK. J. Med. Virol.78(5), 623–630 (2006).
  • Rall GF. Measles virus 1998–2002: progress and controversy. Annu. Rev. Microbiol.57, 343–367 (2003).
  • Afzal MA, Armitage E, Begley J et al. Absence of detectable measles virus genome sequence in inflammatory bowel disease tissues and peripheral blood lymphocytes. J. Med. Virol.55(3), 243–249 (1998).
  • Afzal MA, Armitage E, Ghosh S, Williams LC, Minor PD. Further evidence of the absence of measles virus genome sequence in full thickness intestinal specimens from patients with Crohn’s disease. J. Med. Virol.62(3), 377–382 (2000).
  • Rima BK, Duprex WP. Morbilliviruses and human disease. J. Pathol.208, 199–214 (2006).
  • van Staa TP, Selby P, Leufkens HG, Lyles K, Sprafka JM, Cooper C. Incidence and natural history of Paget’s disease of bone in England and Wales. J. Bone Miner. Res.17(3), 465–471 (2002).
  • Nellissery MJ, Padalecki SS, Brkanac Z et al. Evidence for a novel osteosarcoma tumor-suppressor gene in the chromosome 18 region genetically linked with Paget disease of bone. Am. J. Hum. Genet.63(3), 817–824 (1998).
  • Mangham DC, Davie MW, Grimer RJ. Sarcoma arising in Paget’s disease of bone: declining incidence and increasing age at presentation Bone44(3) 431–436 (2009).
  • Haibach H, Farrell C, Dittrich FJ. Neoplasms arising in Paget’s disease of bone: a study of 82 cases. Am. J. Clin. Pathol.83(5), 594–600 (1985).
  • Wick MR, Siegal GP, Unni KK, McLeod RA, Greditzer HG 3rd. Sarcomas of bone complicating osteitis deformans (Paget’s disease): fifty years’ experience. Am. J. Surg. Pathol.5(1), 47–59 (1981).
  • Mankin HJ, Hornicek FJ. Paget’s sarcoma – a historical and outcome review. Clin. Orthop. (438), 97–102 (2005).
  • Dray MS, Miller MV. Paget’s osteosarcoma and post-radiation osteosarcoma: secondary osteosarcoma at Middlemore Hospital, New Zealand. Pathology40(6), 604–610 (2008).
  • Rendina D, Gennari L, De Filippo G et al. Evidence for increased clinical severity of familial and sporadic Paget’s disease of bone in Campania, Southern Italy. J. Bone Miner. Res.21(12), 1828–1835 (2006).
  • Jacobs TP, Michelsen J, Polay JS, Dadamo C, Canfield RE. Giant cell tumor in Paget’s disease of bone – familial and geographic clustering. Cancer44(2), 742–747 (1979).
  • Ralston SH. Juvenile Paget’s disease, familial expansile osteolysis and other genetic osteolytic disorders. Best Pract. Res. Clin. Rheumatol.22(1), 101–111 (2008).
  • Whyte MP, Obrecht SE, Finnegan PM et al. Osteoprotegerin deficiency and juvenile Paget’s disease. N. Engl. J. Med.347(3), 175–184 (2002).
  • Chong B, Hegde M, Fawkner M et al. Idiopathic hyperphosphatasia and TNFRSF11B mutations: relationships between phenotype and genotype. J. Bone Miner. Res.18(12), 2095–2104 (2003).
  • Beyens G, Daroszewska A, De Freitas F et al. Identification of sex-specific asssociations between polymorphisms of the osteoprotegerin gene, TNFRSF11B, and Paget’s disease of bone. J. Bone Miner. Res.22(7), 1062–1071 (2007).
  • Chung PYJ, Beyens G, Riches PL et al. Genetic variation in the TNRSF11A (RANK) gene contributes to the risk to develop sporadic Paget’s disease of bone. Bone44(Suppl. 2), S347–S348 (2009).
  • Reid IR, Davidson JS, Wattie D et al. Comparative responses of bone turnover markers to bisphosphonate therapy in Paget’s disease of bone. Bone35(1), 224–230 (2004).
  • Reid IR, Miller P, Lyles K et al. Comparison of a single infusion of zoledronic acid with risedronate for Paget’s disease. N. Engl. J. Med.353(9), 898–908 (2005).
  • Hosking D, Lyles K, Brown JP et al. Long-term control of bone turnover in Paget’s disease with zoledronic acid and risedronate. J. Bone Miner. Res.22(1), 142–148 (2007).
  • Douglas DL, Kanis JA, Duckworth T, Beard DJ, Paterson AD, Russell RGG. Paget’s disease: improvement of spinal cord dysfunction with diphosphonates and calcitonin. Metab. Bone Dis. Rel. Res.3(4/5) 327–336 (1981).
  • Wallace E, Wong J, Reid IR. Pamidronate treatment of the neurologic sequelae of pagetic spinal stenosis. Arch. Intern. Med.155(16), 1813–1815 (1995).
  • Langston AL, Campbell MK, Fraser WD, MacLennan GS, Selby PL, Ralston SH. Randomised trial of intensive bisphosphonate treatment versus symptomatic management in Paget’s disease of bone. J. Bone Miner. Res. (2009) (Epub ahead of print).
  • Gutteridge DH, Ward LC, Stewart GO et al. Paget’s disease: acquired resistance to one aminobisphosphonate with retained response to another. J. Bone Miner. Res.14, 79–84 (1999).
  • Papapoulos SE, Eekhoff EM, Zwinderman AH. Acquired resistance to bisphosphonates in Paget’s disease of bone. J. Bone Miner. Res.21(Suppl. 2), P88–P91 (2006).
  • Trombetti A, Arlot M, Thevenon J, Uebelhart B, Meunier PJ. Effect of multiple intravenous pamidronate courses in Paget’s disease of bone. Rev. Rhum. Engl. Ed.66(10), 467–476 (1999).
  • Ferguson DJP, Itonaga I, Maki M, McNally E, Gundle R, Athanasou NA. Heterotopic bone formation following hip arthroplasty in Paget’s disease. Bone34(6), 1078–1083 (2004).
  • Lusty PJ, Walter WL, Walter WK, Zicat B. Cementless hip arthroplasty in Paget’s disease at medium-term follow-up (average of 6.7 years). J. Arthroplasty22(5), 692–696 (2007).
  • Lewallen DG. Hip arthroplasty in patients with Paget’s disease. Clin. Orthop. (369), 243–250 (1999).
  • Lee GC, Sanchez-Sotelo J, Berry DJ. Total knee arthroplasty in patients with Paget’s disease of bone at the knee. J. Arthroplasty20(6), 689–693 (2005).
  • Song C, Xiao Z, Nagashima K et al. The heavy metal cadmium induces valosin-containing protein (VCP)-mediated aggresome formation. Toxicol. App. Pharmacol.228(3), 351–363 (2008).

Reprints and Corporate Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

To request a reprint or corporate permissions for this article, please click on the relevant link below:

Academic Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

Obtain permissions instantly via Rightslink by clicking on the button below:

If you are unable to obtain permissions via Rightslink, please complete and submit this Permissions form. For more information, please visit our Permissions help page.