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Disseminated idiopathic skeletal hyperostosis: diagnostic criteria and clinical significance Annette Wessmann Disseminated idiopathic skeletal hyperostosis (DISH) is a systemic disorder of the axial and appendicular skeleton characterised by calcification and ossification in soft tissues, including the spinal ventral longitudinal ligament and sites of attachment of tendons and capsules to bone (Resnick and Niwayama 1976). In the spine, it is classically diagnosed on survey radiographs by ossification of the ventral longitudinal ligament over several segments, causing complete bone fusion of consecutive vertebral segments (Kranenburg and others 2011). It is not a new disease process. It is commonly seen in people, and spinal hyperostosis similar to DISH has been described in dinosaurs, a saber-toothed cat and old rhesus monkeys (Kranenburg and others 2013). There is continual controversy over the diagnostic criteria for DISH. The three generally accepted diagnostic criteria, suggested by Resnick and Niwayama (1976), are solely ventral vertebral column abnormalities: (1) flowing calcification and ossification along the ventrolateral aspect of at least four contiguous vertebral bodies; (2) preservation of the intervertebral width and

Annette Wessmann, DrMedVet, DipECVN, PGCertAcPrac, FHEA, MRCVS, Pride Veterinary Centre, Riverside Road, Pride Park, Derby DE24 8HX, UK e-mail: [email protected]

630 | Veterinary Record | June 21, 2014

absence of extensive radiographic changes of degenerative intervertebral disc disease; (3) absences of articular process ankylosis, sacroiliac joint erosion, sclerosis or intraarticular osseous fusion. Since then, several reports have also identified dorsal vertebral column abnormalities in dogs with DISH. Consequently, Morgan and Stavenborn (1991) proposed diagnostic criteria that require inclusion of dorsal vertebral column changes. The more appropriate classification might be somewhere between these two extremes. A paper by De Decker and Volk (2014), summarised on p 632 of this issue of Veterinary Record, describes 10 dogs with DISH characterised by complete osseous fusion of at least four adjacent vertebral segments diagnosed by MRI or CT. Eight of the 10 dogs had changes affecting the dorsal vertebral structures. Abnormalities included articular process hypertrophy (seven dogs), periarticular new bone formation (one dog), pseudoarthrosis between spinous processes (four dogs) and thickening of the dorsal lamina (four dogs). As it can be challenging to find dorsal column abnormalities on spinal radiographs (De Decker and others 2011), this might explain why earlier publications did not include dorsal vertebral column abnormalities in the diagnosis of DISH. Nevertheless, the large variety of lesion distribution and localisation makes it difficult to appropriately define and diagnose DISH in dogs (Kranenburg and others 2013). This situation is similar in people, and has

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Research led to numerous terms for this condition (Utsinger 1985). Kranenburg and others (2011) estimated a prevalence of DISH of 3.8 per cent in clinically normal dogs. Within this study group, there was a significantly higher prevalence in older animals, males and boxer dogs. The same study showed a much higher prevalence (18 per cent) of spondylosis deformans. Spondylosis deformans is a non-inflammatory, degenerative disease of the peripheral end-plate region associated with new bone formation. Osteophytes vary from small spurs to bony bridges across the disc space leaving at least part of the ventral surface of the vertebral body unaffected. Spondylosis deformans and DISH commonly occur together and, of the dogs with DISH, 67.9 per cent also had spondylosis deformans, whereas 14 per cent of dogs with spondylosis deformans also had DISH (Kranenburg and others 2011). Overall, it is important to remember that DISH accompanied by spondylosis deformans usually appears to be a incidental radiographic finding and is only occasionally clinically significant. Milder clinical signs reported are stiffness in the back, lameness, gait changes and pain (Kranenburg and others 2013). Nevertheless, recent publications have reported clinically relevant associations between DISH formations and clinical signs, which should be considered when presented with patient with thoracolumbar myelopathy. The deficits are caused directly by the vertebral abnormalities (eg, spinal cord compression) or can occur due to changes at the adjacent vertebral segment. In people, a possible complication following vertebral fusion is the development of adjacent segment disease. Ortega and others (2012) found that this also occurred in dogs. In a group of eight dogs presented with thoracolumbar myelopathy and severe spondylosis deformans or DISH, a vertebral fusion of more than two consecutive intervertebral disc spaces was correlated with adjacent segment disease at the adjacent

unfused intervertebral disc space. De Decker and Volk (2014) investigated the clinical importance of dorsal vertebral column abnormalities occurring in dogs with DISH identified using advanced diagnostic imaging. The study concluded that six of 10 dogs had clinically relevant vertebral canal stenosis due to dorsal vertebral abnormalities and that in four dogs this was the only cause of the presenting signs. Clinical signs were consistent with cauda equina compression predominantly caused by articular facet hypertrophy. Interestingly, the extensive DISH formation included L7 vertebra but not the lumbosacral joint, and it appears that lumbosacral vertebral canal stenosis in dogs with DISH might be more common than previously considered. The aetiology of DISH remains unclear. In people, various metabolic, endocrinological and environmental factors have been proposed but none have been agreed on and sufficient evidence is lacking (Kranenburg and others 2013). The next question is whether dorsal vertebral column abnormalities present a variation of the lesion distribution of DISH or are a biomechanical consequence of DISH formation. The latter is considered more likely. Experimental studies indicate that spinal fixation and thus hypomobility results in time-dependent degenerative changes of the articular processes and these were most severe at the fused vertebral segments (Cramer and others 2004). Moreover, a human biomechanical study demonstrated increased stress and strains of articular processes at the mobile adjacent vertebral segments (Little and others 2004). It makes sense that contiguous new bone formation would cause decreased flexibility with increased stiffness of the affected vertebral segments, which then results in altered biomechanics on adjacent mobile segments and causes disease at this level (Kranenburg and others 2011). This hypothesis is supported by the clinical findings of Ortega and others (2012) and De Decker and Volk (2014), who reported degenerative changes of the remaining

mobile vertebral segment adjacent to the fused vertebral segments. Yet it remains unclear why some patients develop dorsal vertebral column changes and others do not. DISH and spondylosis deformans may be more clinically important in some dogs than previously thought. This is likely a result of changes in the biomechanics of the spine. Advanced imaging remains important in the diagnosis of other disease processes that may explain myelopathy in dogs presented with DISH or spondylosis deformans.

Reference

CRAMER, G. D., FOURNIER, J. S., HENDERSON, C. N. R. & WOLCOTT, C. H. (2004) Degenerative changes following spinal fixation in a small animal model. Journal of Manipulative and Physiological Therapeutics 27, 141-154 DE DECKER, S., GIELEN, I. M., DUCHATEAU, L., CORZO-MENÉNDEZ, N., VAN BREE, H. J., KROMHOUT, K., BOSMANS, T. & VAN HAM, L. M. (2011) Intraobserver, interobserver, and intermethod agreement for results of myelography, computed tomography-myelography, and low-field magnetic resonance imaging in dogs with disk-associated wobbler syndrome. Journal of the American Veterinary Medical Association 238, 1601-1608 DE DECKER, S. & VOLK, H. A. (2014) Dorsal vertebral column abnormalities in dogs with disseminated idiopathic skeletal hyperostosis (DISH). Veterinary Record doi:10.1136/vr.102492 KRANENBURG, H. C., HAZEWINKEL, H. A. W. & MEIJ, B. P. (2013) Spinal hyperostosis in humans and companion animals. Veterinary Quarterly 33, 30-42 KRANENBURG, H. C., VOORHOUT, G., GRINWIS, G. C. M., HAZEWINKEL, H. A. W. & MEIJ, B. P. (2011) Diffuse idiopathic skeletal hyperostosis (DISH) and spondylosis deformans in purebred dogs: a retrospective radiographic study. Veterinary Journal 190, 84-90 LITTLE, J. S., IANUZZY, A., CHIU, J. B., BAITNER, A. & KHALSA, P. S. (2004) Human lumbar facet joint capsule strains: II. Alteration of strains subsequent to anterior interbody fixation. Spine Journal 4, 153-162 MORGAN, J. P. & STAVENBORN, M. (1991) Disseminated idiopathic skeletal hyperostosis. Veterinary Radiology and Ultrasound 32, 65-70 ORTEGA, M., GONÇALVES, R., HALEY, A., WESSMANN, A. & PENDERIS, J. (2012) Spondylosis deformans and diffuse idiopathic skeletal hyperostosis (DISH) resulting in adjacent segment disease. Veterinary Radiology and Ultrasound 53, 128-134 RESNICK, D. & NIWAYAMA, G. (1976) Radiographic and pathologic features of spinal involvement in diffuse skeletal hyperostosis (DISH). Radiology 119, 559-568 UTSINGER, P. D. (1985) Diffuse skeletal hyperostosis. Clinics in Rheumatic Disease 11, 325-351

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Disseminated idiopathic skeletal hyperostosis: diagnostic criteria and clinical significance Annette Wessmann Veterinary Record 2014 174: 630-631

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Disseminated idiopathic skeletal hyperostosis: diagnostic criteria and clinical significance.

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