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Introduction
Diffuse idiopathic skeletal hyperostosis (DISH) is a skeletal disease characterized by the ligamentous ossification
of the anterolateral spine that was first described by Forestier and RotesQuerol [1] more than 50 years ago. It is
often classified as a form of osteoarthritis but, although it
often coexists with osteoarthritis, there are a number of
differences between the two diseases: their prevalence
in the general population, gender distribution, anatomic
site of primary involvement, and their entity and distribution in the spine and peripheral joints. DISH is therefore a distinct clinical entity [2].
Spinal involvement
The portion of the spine that is classically involved in
DISH is the thoracic spine [7]. Its most common clinical
presentation is stiffness and a decreased range of spinal
motion, and there be mild pain if ankylosis has occurred.
The condition is recognized radiographically by the presence of flowing ossification along the anterolateral
margins of at least four contiguous vertebrae and the
absence of the changes associated with spondyloarthropathy or degenerative spondylosis [4]. Even in patients presenting with lumbar or cervical complaints, the
radiographic findings are almost always seen on the right
side of the thoracic spine. The ossification is not always
localized to the anterior longitudinal ligament, but is
sometimes more extensive [8]. DISH is frequently associated with OPLL and ossification of the ligamentum
flavum, but the distribution of the ossifications show a
clear trend: DISH in the thoracolumbar spine, OPLL in
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DISH
OPPL
OLF
Etiopathogenesis
DISH is a common disorder of unknown etiology, although genetic, metabolic, endocrinologic, anatomic, environmental, and toxic factors have all been suggested as
playing a possible pathogenetic role in the new bone
growth characterizing it (Fig. 1).
Studies of human leukocyte antigen factors have led to
conflicting results [26]. There are published reports that
the thoracic spine is more frequently involved, but the
ligament ossification requires the two preexisting components of disuse related to vertebral immobility and
rarefaction of the adjacent bone [6,27]. Furthermore,
Smith et al. [28] suggested that immobilization may increase the likelihood of dedifferentiated connective tissue being transformed into bone. Resnick and Niwayama found that thoracic abnormalities were more
frequent in the 7th to 10th thoracic vertebrae, and also
noted a lower incidence in the upper thoracic vertebrae
[6]. On the basis of anatomic comparisons of the lower
and upper thoracic vertebrae, the cartilage of the lower
five ribs does not join the sternum. Because this contributes to making the lower thoracic vertebrae freer and
more movable (especially in flexion and extension), the
theory of thoracic spine immobility as a predisposing factor for DISH seems unlikely. Furthermore, it does not
explain the involvement of DISH in the lumbar and
cervical spine or extraspinal sites.
One pathologic study found a significant increase in the
number and width of the nutrient foramina (which indicates hypervascularity of the involved ossified ligaments
and vertebrae), and a significant increase in the size
of the affected vertebrae. This suggests that a vascular
disorder may be involved in the pathogenesis of the disease [29].
Metabolic disorders such as obesity, hyperlipidemia, diabetes mellitus, and hypertension are frequent in patients
with DISH [22].
How is the process initiated and what is the link between
these metabolic disorders and new bone formation? The
ossification process starts in the innermost layer of the
anterior longitudinal ligament, at the site of its attachment to the vertebral body, and then extends to meet the
Diagnosis
DISH is recognized radiographically by the presence of
flowing ossification along the anterolateral margins of
at least four contiguous vertebrae, and the absence of the
changes characterizing spondyloarthropathy or degenerative spondylosis. Its diagnosis is based solely on the radiographic criteria defined by Resnick and Niwayama [6]
(Table 2).
The flowing paravertebral ossification is mainly located
in the region of the anterior longitudinal ligament, but
the extent of the ossification is usually wider. A lucent
cleavage between the ossification and the vertebral body
is considered to be a characteristic that helps to differentiate the ossification from osteophytes [44].
Although conventional radiography clearly confirms the
diagnosis of DISH, CT and MRI are more capable of
Table 2. Resnicks diagnostic criteria [6]
1) Presence of flowing calcification and ossification along the
anterolateral aspects of at least four contiguous vertebral bodies
with or without associated localised pointed excrescences at the
intervening vertebral body-disc junctions
2) A relative preservation of intervertebral disc height in the involved
vertebral segments and the absence of extensive radiographic
changes of degenerative disc disease, including vacuum
phenomena and vertebral body marginal sclerosis
3) Absence of apophyseal joint bony ankylosis and sacro-iliac joint
erosion, sclerosis or bony fusion.
detecting associated findings (eg, OPLL) and complications (eg, spinal cord compressive myelomalacia).
OPLL is readily demonstrated by lateral radiography [8],
but because of the presence of overlying osseous structures, CT is occasionally indicated for the purposes of
confirmation, and MRI can demonstrate a narrowing of
the spinal cord even though the ossification itself is not
clear. MRI can occasionally confirm ossification when
OPLL contains fatty bone marrow [45], and it can detect
the ligament hypertrophy that is an early change in
OPLL.
The ankylosed vertebrae seen in DISH patients are vulnerable to trauma [46], but the radiologic findings of
fractures and dislocations are often subtle, and MRI is
often indicated to confirm the level of spinal cord injury.
Scintigraphy is suitable for the early detection of abnormalities with unclear clinical symptoms, and may indicate the correct level of the cervical spine for MRI or CT
[47].
Treatment
Very little has been published concerning the pharmacologic or nonpharmacologic management of DISH patients, who often complain of pain and a limited range of
motion. Because no specific drug has yet been identified,
simple analgesics or nonsteroidal antiinflammatory drugs
are usually prescribed.
A recent paper described a patient who underwent chiropractic manipulation and drop-table adjustments, together with range-of-motion, extension, and standing
lumbar extension traction exercises. These improved
flexibility and daily living activities, and the effect was
maintained for 19 months after the end of the active
rehabilitation treatment period [48].
Mears [49] reported a case of an elderly woman whose
low back pain and Forestier disease were markedly improved by acupuncture, whereas other treatments had
been ineffective.
Price et al. [50] described the discovery of a fetuin
MGPmineral complex in the serum of rats treated with
bone-active bisphosphonate etidronate and showed that
this correlates with etidronate-induced inhibition of
bone mineralization. This finding may indicate a possible new treatment for DISH patients [51,52].
The failure of conservative care often leaves surgery as
the only option. Dysphagia is rare in Forestier disease
and hence often goes unrecognized [53]. Most dysphagic
patients are initially treated conservatively and later by
means of the excision of osteophytes through the lateral
cervical or perioraltranspharyngeal route [54].
19
20
Cassim B, Mody GM, Rubin DL: The prevalence of diffuse idiopathic skeletal
hyperostosis in African blacks. Br J Rheumatol 1990, 29:131132.
21
Weinfeld RM, Olson PN, Maki DD, et al.: The prevalence of diffuse idiopathic
skeletal hyperostosis (DISH) in two large American Midwest metropolitan
hospital populations. Skeletal Radiol 1997, 26:222225.
22
Kiss C, Szilagyi M, Paksy A, et al.: Risk factors for diffuse idiopathic skeletal
hyperostosis: a casecontrol study. Rheumatology 2002, 41:2730.
23
Troillet N, Gerster JC: Forestier disease and metabolism disorders. A prospective controlled study of 25 cases. Rev Rhum Ed Fr 1993, 60: 274279.
24
25
Dougados M, Leporho MA, Esmilaire L, et al.: Taux plasmatiques des vitamines A et E au cours de la maladie hyperostosique, la spondyloarthrite ankylosante, et la polyarthrite rheumatoide. Rev Rhum Mal Osteoartic 1988,
55:251254.
26
Denko CW, Boja B, Moskowitz RW: Growth promoting peptides in osteoarthritis and DISH. J Rheumatol 1994, 21:1725.
27
Oppenheimer A: Calcification and ossification of vertebral ligaments: roentgen study of pathogenesis and clinical significance. Radiology 1942, 38:160.
Conclusion
In conclusion, DISH is a widespread systemic condition
that is most probably related to abnormal bone
growth/activity reflecting the influence of various metabolic, environmental, genetic, and endocrinologic factors
that lead to new bone deposition. Vertebral blood supply
is a predisposing factor contributing to the onset, progression, and/or localization of DISH. MGP probably
plays a role in this hyperostosis syndrome.
Of special interest
Of outstanding interest
Forestier J, RotesQuerol J: Senile ankylosing hyperostosis of the spine. Ann
Rheum Dis 1950, 9:321330.
2
Mader R: Diffuse idiopathic skeletal hyperostosis: a distinct clinical entity. Isr
Med Assoc J 2003, 5:506508.
This article provides a clear and definitive definition of DISH as a clinical entity that
is distinct from osteoarthrosis on the basis of epidemiologic, pathogenetic, clinical,
and radiologic data.
3
Belanger TA, Rowe DE: Diffuse idiopathic skeletal hyperostosis: musculoskeletal manifestations. J Am Acad Orthop Surg 2001, 9:258267.
28
Smith CF, Pugh DG, Polley HF: Physiologic vertebral ligamentous calcification: an aging process. AJR Am J Roentgenol 1955, 74:1049.
Resnick D, Shapiro RF, Wiesner KB, et al.: Diffuse idiopathic skeletal hyperostosis (DISH): ankylosing hyperostosis of Forestier and Rots Querol. Semin Arthritis Rheum 1978, 7:153187.
29
El Miedany YM, Wassif G, El Baddini M: Diffuse idiopathic skeletal hyperostosis (DISH): is it of vascular aetiology? Clin Exp Rheumatol 2000, 18:193
200.
30
Fawcett DW: A Textbook of Histology, edn 12. Chapman & Hall 1994:224
233.
Resnick D, Niwayama G: Radiographic and pathologic features of spinal involvement in diffuse idiopathic skeletal hyperostosis (DISH). Radiology 1976,
119:559568.
31
Vetter U, Zapf J, Heit W, et al.: Human fetal and adult chondrocytes. Effects of
insulin-like growth factors I and II, insulin and growth hormone on clonal
growth. J Clin Invest 1986, 77:19031908.
Utsinger PD: Diffuse idiopathic skeletal hyperostosis Clin Rheum Dis 1985,
7:153187.
32
Denko CW, Boja B, Moskowitz RW: Growth promoting peptides in osteoarthritis and diffuse idiopathic skeletal hyperostosisinsulin, insulin-like growth
factor-I, growth hormone. J Rheumatol 1994, 21:17251730.
Ehara S, Shimamura T, Nakamura R, et al.: Paravertebral ligamentous ossification: DISH, OPLL and OLF. Eur J Radiol 1998, 27:196205.
33
34
10
11
12
13
Ebo D, Goethals L, Bracke P, et al.: Dysphagia in a patient with giant osteophytes: case presentation and review of the literature. Clin Rheumatol 2000,
19:7072.
14
Takasita M, Matsumoto H, Uchinou S, et al.: Atlantoaxial subluxation associated with ossification of posterior longitudinal ligament of the cervical spine.
Spine 2000, 25:21332136.
15
Littlejohn JO, Urowitz MB, Smythe HA, et al.: Radiographic features of the
hand in diffuse idiopathic skeletal hyperostosis (DISH). Diagn Radiol 1981,
140:623629.
Ohishi H, Furukawa KI, Iwasaki K, et al.: Role of prostaglandin GI2 in the gene
expression induced by mechanical stress in spinal ligament cells derived from
patients with ossification of the posterior longitudinal ligament. J Pharmacol
Exp Ther 2003, 305:818824.
In this study the investigators demonstrated that PGI2 synthase was more highly
expressed in OPLL cells. Uniaxial cyclic stretch further increased the PGI2 synthase that plays a key role in the progression of OPLL, at least partially by inducing
osteogenic differentiation in spinal ligament cells by means of the PGI2/cAMP system.
35
37
El-Maadawy S, Kaartinen MT, Schinke T, et al.: Cartilage formation and calcification in arteries of mice lacking matrix Gla protein. Connect Tissue Res
2003, 44:272278.
38
16
Beyeler C, Schlapbabach P, Gerber NJ, et al.: Diffuse idiopathic skeletal hyperostosis (DISH) of the shoulder. A cause of shoulder pain? Br J Rheumatol
1990, 29:349353.
39
17
40
Zebboudj AF, Shin V, Bostrom K, et al.: Matrix GLA protein and BMP-2 regulate osteoinduction in calcifying vascular cells. J Cell Biochem 2003,
90:756765.
47
Cammisa M, De Serio A, Guglielmi G: Diffuse idiopathic skeletal hyperostosis. Eur J Radiol 1998, 27(suppl 1):S7S11.
48
Troyanovich SJ, Buettner M: A structural chiropractic approach to the management of diffuse idiopathic skeletal hyperostosis. J Manipulat Physiol Ther
2003, 26:202206.
49
Mears T: Acupuncture for back pain in a patient with Forestiers disease (diffuse idiopathic skeletal hyperostosis/DISH). Acupunct Med 2002, 20:102
104.
50
Price PA, Caputo JM, Williamson MK: Bone origin of the serum complex of
calcium, phosphate, fetuin, and matrix Gla protein: biochemical evidence for
the cancellous bone-remodeling compartment. Bone Miner Res 2002,
17:11711179.
51
52
Ling TC, Parkin G, Islam J, et al.: What is the cumulative effect of long-term,
low-dose isotretinoin on the development of DISH? Br J Dermatol 2001,
144:630632.
Schurgers LJ, Dissel PE, Spronk HM, et al.: Role of vitamin K and vitamin K
dependent proteins in vascular calcification. Z Kardiol 2001, 90(suppl
3):5763.
44
45
53
46
Hendrix RW, Melany M, Miller F, et al.: Fracture of the spine in patients with
ankylosis due to diffuse skeletal hyperostosis: clinical and imaging findings.
AJR Am J Roentgenol 1994, 162:899904.
54
Uppal S, Wheatley AH: Transpharyngeal approach for the treatment of dysphagia due to Forestiers disease. J Laryngol Otol 1999, 113:366368.