Skeletal Radiol (1990) 19: 4l 1-417

Skeletal Radiology

The sclerotic p e d i c l e - how many causes are there ? T.R. Yochum, D.C., D.A.C.B.R. 1, L.T. Sellers, D.C., D.A.C.B.R. 2, D.A. Oppenheimer, M.D. 3, C.K. Peterson, R.N., D.C., D.A.C.B.R. 2, C.W. Kirton, D.C. 2, E.C. Dal Mas, D.C. 2, and A.L. Anderson, D.C., D.A.C.B.R. 2 1 Los Angeles Chiropractic College and Rocky Mountain Chiropractic Radiological Center, Denver, Colorado, USA 2 Department of Radiology, Western States Chiropractic College, Portland, Oregon, USA 3 Department of Radiology, Boulder Community Hospital, Boulder, Colorado, USA

Abstract, The sclerotic pedicle is a commonly encountered roentgen sign that may be associated with numerous conditions, both benign and malignant. The following paper discusses the c o m m o n as well as the unusual causes of this interesting phenomenon and demonstrates the radiographic presentations of the various etiologies.

Key words: Sclerotic pedicle - Hypertrophied pedicle Vertebra - Stress sclerosis

The presence of a sclerotic pedicle at any level of the vertebral column constitutes a diagnostic challenge to both the clinician and the radiologist. The numerous etiologies of this entity (Table 1) involve a broad gamut of bone diseases. Some o f the congenital etiologies are an agenetic pedicle or facet, pedicle hypoplasia with contralateral pediculate sclerosis, and spina bifida occulta. In the tumor and tumorlike categories, such disorders as a bone island, benign bone tumors, primary and secondary malignant bone tumors, Paget's disease, and fibrous dysplasia represent additional causes. A unilateral spondylolysis with reactive sclerosis of the opposite pedicle is also a possible etiology. Iatrogenic causes include spinal fusion and unilateral laminectomy which may lead to stress hypertrophy o f the opposite pedicle. Miscellaneous causes include tuberous sclerosis, sarcoidosis, infectious disorders, and Hodgkin's lymphoma. It is the purpose of this paper to provide a comprehensive differential diagnosis for the sclerotic pedicle.

Congenital Opposite an agenetic or hypoplastic pedicle

Numerous authors have noted the association between hypoplasia or aplasia of a vertebral pedicle and sclerosis Address reprint requests to: T.R. Yochum, D.C., D.A.C.B.R., Rocky Mountain Chiropractic Radiological Center, 9464 N. Federal Blvd., Denver, CO 80221, USA

and/or hypertrophy of the contralateral arch (Fig. 1, 2) [1, 2, 5, 7-9, 12, 17, 19, 20, 22, 23, 25-27, 35, 37, 40, 43, 44, 46]. Maldague and Malghem [22] feel, however, that it is the retropediculate structures, including the pars interarticularis and facet joints, which are much more influential in the development of the sclerotic pedicle. These authors were unable to find a single case of unilateral arch hypertrophy in the absence of retropediculate abnormalities, even when moderately severe pedicle hypoplasia was present. Moreover, the presence o f anatomical abnormalities in the retropediculate structures may provide specificity, in that the possibility of a pathological cause of the pediculate changes is unlikely. Conversely, destructive processes affecting the vertebral pedicle, i.e., lyric metastases, do not allow time for compensatory changes to develop. Opposite an agenetic articular facet

Less well documented is the relationship between agenesis or hypoplasia of an articular facet and sclerosis/hyTable 1. Causes of the sclerotic pedicle A. Congenital Agenetic/hypoplastic pedicle Agenetic/hypoplastic facet Asymmetric facets Spina bifida occulta B. Unilateral spondylolysis with stress sclerosis C. Tumors Benign (bone island, osteoid osteoma, osteoblastoma) Malignant (blastic metastasis, lymphoma, myeloma, Ewing's sarcoma) D. Tumorlike conditions Paget's disease, fibrous dysptasia, sarcoidosis, tuberous sclerosis E. Infection F. Iatrogenic Laminectomy G. Idiopathic 9 1990 International Skeletal Society

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T.R. Yochum et al. : Causes of the sclerotic pedicle

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Fig. 1 A-C. Agenesis of the pedicle of L4 with contralateral compensatory sclerosis of the opposite pedicle. A Plain film radiograph: observe the agenesis of the pedicle of L4 (arrows) and the sclerosis and enlargement of the contralateral pedicle of L4

(arrowheads).

B Demonstration of weight-bearing stress lines opposite an agenetic pedicle. C Normal weight-bearing stress lines through the pedicles. (Reprinted from [45] with permission of Williams & Wilkins)

Fig. 2A-C. Hypoplastic pedicle with contralateral pediculate sclerosis. A Plain film radiograph: observe the hypoplasia of the pedicle of L3 (arrow) and the contralateral pediculate hypertrophy and sclerosis (arrowhead). B Bone scan: there is an increased uptake on the side opposite the L2 pedicle defect (arrow). This stress has induced sclerosis of the L2 pedicle. C Computed tomogram of L2: observe the hypoplasia of the pedicle of L2 (arrow). Contralateral pediculate sclerosis and hypertrophy are present. (Reprinted from [45] with permission of Williams & Wilkins)

pertrophy of the contralateral pedicle [22, 30]. Maldague and Malghem [22] have found that a defect in the superior articular facet leads to sclerosis and/or hypertrophy of the contralateral pedicle at the same level, whereas a defect in the inferior facet produces sclerosis and/or hypertrophy o f the contralateral pedicle of the segment below (Fig. 3).

Asymmetrical facet joints Although asymmetry of the articular planes of the spinal facets (tropism) is a frequently encountered roentgen finding, there is little to implicate this condition as a

cause of the sclerotic pedicle. Downey et al. [8] cite one case, and we have encountered one case (Fig. 4).

Spina bifida occulta In spina bifida occulta, especially with multilevel involvement, a sclerotic pedicle or pedicles m a y occur either unilaterally or bilaterally. Two such cases with lumbar spine involvement are shown in Fig. 5. We are unable to find any published reports of this p h e n o m e n o n and believe this to be an original observation. A possible explanation for this development is that increased stress is placed u p o n the pedicles at the involved levels due to interruption of the neural arch at the midline. In this

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Fig. 3A, B. Hypoplasia of the neural arch with associated sclerotic pedicle. A Observe the hypoplasia of the inferior facet of L4 (arrow) and the hypoplasia of the pedicle of L5 (arrowhead). There is contralateral compensatory sclerosis of the opposite pedicle of L5 (curved arrow). The increased pedicle density and cortical thickness represent stress-induced compensatory changes B Observe the hypoplasia of the neural arch of L5 with associated spina bifida occulta. There is reactive sclerosis and hypertrophy of the pedicle opposite the neural arch hypoplasia and defect. (Courtesy of Tyrone Wei, Portland, Oregon) Fig. 4. Facet asymmetry with a sclerotic pedicle. There is asymmetry of the facets at the lumbosacral junction. Observe that the compensatory sclerotic pedicle (arrow) is opposite the sagittally oriented facet structures at the lumbosacral junction. With one sagittally oriented facet and one coronally oriented facet some alteration in the normal biomechanical weight-bearing at the lumbosacral junction has occurred Fig. 5 A, B. Spina bifida occulta: Multiple sclerotic pedicles. A Spina bifida occulta is identified at T12, L1, L2, L3, L4, and L5 levels. There are bilateral sclerotic pedicles seen at L1, L2, and L3, and a unilateral sclerotic pedicle seen at L4. (Courtesy of Appa L. Anderson, Portland, Oregon.) B Spina bifida occulta is noted at L2, L3, L4, and L5 segments. Observe the sclerotic pedicle seen at L2-5. The increased pedicle densities and cortical thickness represent a stress-induced compensatory change as a result of the disruption in the neural arch and altered distribution of weight-bearing. (Courtesy of Norman F. Spector, Baltimore, Maryland.) Comment: these two cases are offered as an original observation since review of the literature cites no cases of multiple spina bifida occulta with sclerotic pedicles

weight-bearing to the pedicle opposite the side o f the pars defect renders this pedicle very large and radiop a q u e as a result o f this stress (Fig. 6) [7, 13, 31]. O n occasions, the c o m p e n s a t o r y sclerotic b o n e changes m a y regress if a stress fracture develops on the same side as the dense h y p e r t r o p h i e d pedicle, resulting in bilateral spondylolysis. This m e c h a n i s m thereby equalizes weightbearing and reduces the stress at this level (Fig. 7) [20, 45].

Tumors (benign) Bone island

way, the sclerotic changes m i g h t represent a c o m p e n s a tory mechanism, such as that noted in some cases o f spondylolysis.

Unilateral spondylolysis with stress sclerosis Unilateral spondylolysis, usually affecting the m i d l u m bar spine, m a y p r o d u c e c o m p e n s a t o r y stress hypertrop h y o f the contralateral pedicle in the region o f the pars (Wilkinson s y n d r o m e ) [32, 34, 40]. The transfer o f

A b o n e island represents a solitary discrete area o f sclerosis in the skeleton; it is usually a s y m p t o m a t i c and is seen as an incidental finding. Bone islands are usually seen in the ilium, sacrum, and m o s t c o m m o n l y in the proximal femur but have also been isolated within the vertebral c o l u m n [45]. The m o s t frequent spinal location is in the vertebral bodies o f the l u m b a r spine. The thoracic and cervical spine are less frequently affected. Pedicle involvement is k n o w n to occur b u t n o t often [15, 42]. The radiological findings o f a b o n e island within

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Fig. 6. Unilateral spondylolysis with contralateral sclerotic pedicle : observe the unilateral spondylolysis of L3 (arrow)with the associated contralateral pedicular sclerosis (arrowheads). This radiographic presentation has been referred to as the Wilkinson syndrome

Fig. 7A-F. Spondylolysis and pathogenesis of the sclerotic pedicle : an 18-year-old patient followed over a 4-year period. A Initial film: a left rotatory scoliosis is visible with the second lumbar vertebra showing no pars defects or pedicle abnormalities. B Two years later: the scoliosis remains. Observe the second lumbar sclerotic

the spine are no different f r o m t h o s e in o t h e r sites. T h e y include a r o u n d o r o v o i d r a d i o p a q u e d e n s i t y w i t h a s h a r p l y d e m a r c a t e d m a r g i n (Fig. 8) [45]. N o p r o t r u s i o n f r o m the c o r t i c a l surface o f the i n v o l v e d b o n e s can be identified since these lesions are i n t r a m e d u l l a r y in location. B o n e islands c o n s t i t u t e a r a r e cause o f a sclerotic pedicle w i t h i n the spine.

T.R. Yochum et al. : Causes of the sclerotic pedicle

pedicle (arrow) and the left pars interarticularis defects (arrowhead). C Diagrammatic representation: the mechanism operating to produce the sclerotic pedicle is demonstrated. Hypertrophy is due to the additional stress of the contralateral pars defect. D, E, F Four years later: the scoliosis persists but note the resolution of the sclerotic pedicle due to the formation of bilateral pars defects (arrows). Also note the retained hypertrophy of the previously sclerotic pedicle (arrowhead). Comment: this case demonstrates the important role of stress in the production of pars defects. (Reprinted from [45] with permission of Williams & Wilkins)

Osteoid osteoma S o m e 50% o f o s t e o i d o s t e o m a s o c c u r in the f e m u r a n d t i b i a a n d a p p r o x i m a t e l y 10% in the spine. V e r t e b r a l ost e o i d o s t e o m a s m o s t c o m m o n l y involve the l u m b a r a n d cervical spine (Fig. 9) [4a, 45]. T h e r o e n t g e n findings seen in spinal o s t e o i d o s t e o m a m a y be subtle, a n d the

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Fig. 8. Bone island: observe the bone island present within the pedicle of T10 (arrow). This is an uncommon cause of a sclerotic pedicle Fig. 9. Osteoid osteoma: observe the unilateral sclerotic pedicle of L3 due to the benign tumor, osteoid osteoma. (Reprinted from [45] with permission of Williams & Wilkins) Fig. 10. Blastic metastasis: observe the radiopaque density affecting the pedicle and neural arch of L3 and L4. This represents osteoblastic metastasis in a male patient from prostate carcinoma

diagnosis can be difficult. These lesions usually involve the neural arch and may present as a sclerotic pedicle [4, 4a, 7-11, 16, 18, 20, 21, 24, 27, 29, 31, 32, 34, 39~42, 45]. Often the area of tumor nidus and reactive sclerosis occurs in association with a painful rigid scoliosis [45]. The lesion is usually found on the concave side of the curve. Pain caused by this lesion is typically worse at night and is relieved by aspirin. On tomograms, a central area of lucency, the nidus, may be seen surrounded by sclerosis. Computed tomography (CT) may help to define and localize the lesion.

Osteobtastoma Osteoblastoma is a primary benign bone neoplasm that has been referred to as a giant form o f osteoid osteoma [45]. The neural arches of the lower thoracic and upper lumbar vertebrae are the most c o m m o n locations of this tumor. Although usually expansile and radiolucent, osteoblastoma may also present as a sclerotic pedicle [7 9, 20, 26, 31, 34, 40, 42, 43, 45]. As with osteoid osteoma, osteoblastoma commonly causes a painful scoliosis; however, the pain from this lesion is not as severe as that seen in osteoid osteoma, is not typically nocturnal, and is not usually relieved by aspirin.

prostatic metastasis [7, 11] but is not limited to this disease process.

L ymphoma Lymphoma, especially Hodgkin's disease, may cause bilateral or unilateral sclerosis of the pedicles [20, 34]. Hodgkin's disease rarely involves the bones as a primary lesion. Osseous involvement is more common secondary to systemic disease, the vertebral bodies of the thoracic and lumbar spine being the most frequently involved sites [45]. Isolated involvement of the posterior elements of the vertebrae is unusual, and lymphoma as a cause of a sclerotic pedicle without any other sclerotic lesions is therefore rare.

Multiple myeloma By far the most common radiographic findings associated with this neoplasm are osteopenia and osteolytic defects. Only 3 % of patients with multiple myeloma demonstrate sclerotic lesions, the sclerotic form of myeloma being more c o m m o n in flat bones [45]. Multiple myeloma has, however, been reported as an etiology for the sclerotic pedicle [33].

Tumors (malignant)

Ewing's sarcoma Osteoblastic metastasis According to some authors osteoblastic metastasis is the most c o m m o n cause of the sclerotic pedicle [20, 34]. It may be more accurate to state that osteoblastic metastasis is the most c o m m o n malignant etiology (Fig. 10). Unilateral pedicle sclerosis more commonly results from

Ewing's sarcoma constitutes approximately 5% of primary malignant bone tumors, but it is infrequently seen in the spine [42]. When spinal involvement occurs, the lesions appear lytic and may develop pathological fractures. Rarely, Ewing's sarcoma will present with a patchy sclerosis of the vertebral bodies. Only one case

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T.R. Yochum et al. : Causes of the sclerotic pedicle Fig. 11A-C. Iatrogenic causes of the sclerotic pedicle. A Preoperative film: note the symmetrically uniform density of both pedicles of the fourth lumbar vertebra (arrows). B Film made 1 year after surgery: observe the surgically created defect within the lamina of L4 (arrows) and the contralateral sclerotic pedicle (arrowhead). (Courtesy of Tyrone Wei, Portland, Oregon. Reprinted from [45] with permission of Williams & Wilkins.) C An additional case with unilateral laminectomy (arrow) performed; stress sclerosis of the ipsilateral pedicle (arrowhead) of the transitional segment at the lumbosacral junction is observed

of Ewing's sarcoma presenting with a sclerotic pedicle has been found in the literature [42].

[45]. Sarcoidosis can, rarely, present as a solitary blastic lesion causing a sclerotic pedicle [20].

Tumorlike conditions

Tuberous sclerosis

Paget's disease

Tuberous sclerosis affecting the vertebral column has an affinity for the posterior elements where it has an osteosclerotic presentation. Multiple sclerotic pedicles are a frequent finding [11, 15, 20, 28, 36]. Sclerosis of a single pedicle has also been documented [28]. Tuberous sclerosis must be distinguished from disseminated osteoblastic metastasis, particularly when bony sclerosis is the only radiographic finding.

The spine is frequently affected in Paget's disease. The vertebral bodies may become sclerotic and enlarged, with irregular internal architecture [6]. These changes may progress to involve the posterior elements, causing sclerosis of one or both pedicles [28, 38, 45]. In rare cases pedicle involvement occurs without associated vertebral body disease [28]. In isolated pedicle involvement, the sclerotic appearance may simulate blastic metastasis. The widened interpediculate distance and enlargement of bone seen in Paget's disease may help differentiate the two entities. Expansile pagetoid bone may encroach upon the intervertebral foramina or neural canal and may produce spinal stenosis with associated neurological manifestations [28, 45].

Fibrous dysplasia Skeletal lesions in fibrous dysplasia are not present at birth but appear several years before puberty [45]. Vertebral involvement is rare and usually presents in the radiolucent polyostotic form. Although fibrous dysplasia generally affects the vertebral body rather than the neural arch, it can occasionally create a sclerotic pedicle [14, 341.

Infection Several authors include osteomyelitis in the differential diagnosis of the sclerotic pedicle [3, 7, 8, 14, 34, 42]. In the spine, osteomyelitis most commonly affects the vertebral bodies, with spread by direct extension to the pedicles occasionally occurring. Rare cases of isolated pedicle involvement have been reported [20, 34]. Sclerosis occurs with healing or chronicity [20, 28, 34]. Bell and Cockshott [3, 34] described an atypical form of spinal tuberculosis in which the pedicle was the primary focus. The disc spaces and vertebral bodies were spared relatively. With healing, considerable pedicle sclerosis occurs in most patients.

Iatrogenic

Sarcoidosis

Laminectomy

Spinal involvement is rare in sarcoidosis. Individual vertebral lesions are usually lyric with marginal sclerosis

Just as developmental defects in the neural arch may cause stress hypertrophy/sclerosis of the contralateral

T.R. Yochum et ai. : Causes of the sclerotic pedicle arch structures, so m a y a c q u i r e d defects [45]. U n i l a t e r a l l a m i n e c t o m y or facetectomy m a y cause sclerosis o f the c o n t r a l a t e r a l (or less c o m m o n l y , the ipsilateral) pedicle (Fig. 11), whereas spinal arthrodesis m a y cause sclerosis in the pedicles a b o v e or below the fusion.

Idiopathic Cases have been r e p o r t e d in w h i c h hyperplasia or sclerosis o f a pedicle occurs w i t h o u t a n associated disease process or d e v e l o p m e n t a l a n o m a l y [11, 14, 46]. These cases are t h o u g h t to be c o n g e n i t a l a n d have n o clinical significance.

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