Evaluation of the association between spondylosis deformans and clinical signs of intervertebral disk disease in dogs: 172 cases (1999–2000)

Gwendolyn J. Levine Department of Small Animal Clinical Sciences, College of Veterinary Medicine and Biomedical Sciences, Texas A&M University, College Station, TX 77843.

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Jonathan M. Levine Department of Small Animal Clinical Sciences, College of Veterinary Medicine and Biomedical Sciences, Texas A&M University, College Station, TX 77843.

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Michael A. Walker Department of Large Animal Clinical Sciences, College of Veterinary Medicine and Biomedical Sciences, Texas A&M University, College Station, TX 77843.

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Roy R. Pool Department of Veterinary Pathobiology, College of Veterinary Medicine and Biomedical Sciences, Texas A&M University, College Station, TX 77843.

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Geoffrey T. Fosgate Department of Veterinary Integrative Biosciences, College of Veterinary Medicine and Biomedical Sciences, Texas A&M University, College Station, TX 77843.

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Abstract

Objective—To evaluate the association between spondylosis deformans and clinical signs of intervertebral disk disease (IVDD) in dogs.

Design—Retrospective case series.

Animals—210 dogs.

Procedure—Records of 172 dogs with clinical signs of IVDD and 38 dogs with other neurologic disorders were reviewed. Signalment, sites of spondylosis, severity of associated osteophytosis, type of disk herniation, and duration of signs were recorded.

Results—Dogs with IVDD had significantly fewer sites of involvement and lower grades of spondylosis deformans, compared with those in the non-IVDD group. When groups were adjusted for age and weight via multivariate linear regression, there were no differences in severity of osteophytosis or number of affected sites. Dogs with type II disk disease had higher numbers of affected sites and more severe changes, compared with dogs with type I disk herniation. There was no difference between groups in the rate at which IVDD was diagnosed at sites of spondylosis, compared with the rate at which IVDD was diagnosed in unaffected disk spaces. Areas of spondylosis were closer to sites of IVDD that elicited clinical signs than to randomly chosen intervertebral spaces, and distances between sites of spondylosis and sites of IVDD had a bimodal appearance.

Conclusions and Clinical Relevance—An association may exist between radiographically apparent spondylosis and type II disk disease; type I disk disease was not associated with spondylosis. Spondylosis in radiographs of dogs with suspected type I disk disease is not clinically important. Spatial associations among sites of spondylosis and sites of IVDD may be coincidental or associated with vertebral column biomechanics.

Abstract

Objective—To evaluate the association between spondylosis deformans and clinical signs of intervertebral disk disease (IVDD) in dogs.

Design—Retrospective case series.

Animals—210 dogs.

Procedure—Records of 172 dogs with clinical signs of IVDD and 38 dogs with other neurologic disorders were reviewed. Signalment, sites of spondylosis, severity of associated osteophytosis, type of disk herniation, and duration of signs were recorded.

Results—Dogs with IVDD had significantly fewer sites of involvement and lower grades of spondylosis deformans, compared with those in the non-IVDD group. When groups were adjusted for age and weight via multivariate linear regression, there were no differences in severity of osteophytosis or number of affected sites. Dogs with type II disk disease had higher numbers of affected sites and more severe changes, compared with dogs with type I disk herniation. There was no difference between groups in the rate at which IVDD was diagnosed at sites of spondylosis, compared with the rate at which IVDD was diagnosed in unaffected disk spaces. Areas of spondylosis were closer to sites of IVDD that elicited clinical signs than to randomly chosen intervertebral spaces, and distances between sites of spondylosis and sites of IVDD had a bimodal appearance.

Conclusions and Clinical Relevance—An association may exist between radiographically apparent spondylosis and type II disk disease; type I disk disease was not associated with spondylosis. Spondylosis in radiographs of dogs with suspected type I disk disease is not clinically important. Spatial associations among sites of spondylosis and sites of IVDD may be coincidental or associated with vertebral column biomechanics.

Spondylosis deformans (eg, spinal osteophytosis and spondylosis) is a noninflammatory osteophytic reaction associated with cartilaginous joints of the vertebral column. The condition is common in dogs, reportedly1–3 affecting 17.8% to 32.8% of dogs if the diagnosis is made on the basis of radiographs alone and 61% to 75% of dogs if diagnosis is made on the basis of necropsy examination. The German Shepherd Dog, Boxer, Cocker Spaniel, and Airedale Terrier are breeds suspected of having a predisposition for developing spondylosis deformans.2,4–6

Different sites in the vertebral column are associated with different frequencies of spondylosis. Cross-sectional comparative analysis of dogs in England, Sweden, and the United States revealed that joints at L2-3 and L7-S1 were most frequently affected, with other areas of high incidence centered around the midthoracic portion of the vertebral column (ie, T4 through T6), at the T9-10 disk space, and in the midlumbar portion of the vertebral column.2 In a study7of female Beagles, the L1 through L6 disk spaces and C6-7 disk space had the highest frequency of spondylosis.

Given that development of spondylosis deformans is ubiquitous among humans and dogs, the underlying pathophysiologic features and clinical importance of the condition have been investigated in both species. Osteophyte formation is thought to be initiated by abnormalities at the site of attachment of peripheral annular fibers to the vertebral endplate.8,9 Weakened disk-to-endplate attachments lead to annular tears and result in small ventral or ventrolateral disk herniations. The combination of annular tearing and small-volume disk herniation is likely the cause of spondylosis.1,7,9,10 Although spondylosis may result in nerve root impingement and meningeal irritation when it develops on the dorsal aspect of vertebrae, the clinical importance of vertebral column osteophytes in dogs is generally regarded as small.2,7

In humans, evidence suggests that there are shared pathophysiologic associations among development of spondylosis deformans, degeneration of the nucleus pulposus, and annular hypertrophy. Endplate attachment abnormalities that drive development of spondylosis can also incite nucleus pulposus degeneration via impairment of disk nutrition and generation of stress forces.9,11,12 Annular tears responsible for inciting spondylosis deformans may also result in annular hypertrophy, a finding that has been reported1,10 in dogs. In veterinary medicine, whether an association exists between development of spondylosis deformans and clinically apparent IVDD has been questioned.2,13,14 Results of earlier studies,1,15 however, indicate that there are intrasegmental correlations between the location of sites of type II disk herniation and spondylosis deformans in dissected vertebral columns of dogs.

The purpose of the retrospective case series reported here was to investigate whether spondylosis deformans was associated with clinical signs of IVDD in dogs in which myelography had been performed. Our hypothesis was that sites of development of spondylosis would be positively associated with sites of type II IVDD (protrusion of the annulus without nuclear extrusion), which, similar to spondylosis, is thought to develop as a result of annular tearing and stress. We also hypothesized that type I IVDD (extrusion of the nucleus pulposus through an annular tear into the vertebral canal), which is linked to chondrocyte metabolic anomalies, would not be associated with spondylosis.16 Because spondylosis can alter biomechanical features of the vertebral column, we also hypothesized that associations existed among locations of spondylosis and sites of disk herniation.

Criteria for Selection of Cases

Medical records of all dogs that had myelograms at Texas A&M University from January 1999 to October 2000 were reviewed. Records were allocated to 1 of 2 groups: dogs with clinical signs of IVDD and dogs with other causes of neurologic dysfunction. Inclusion criteria for the IVDD group were complete medical records and confirmation of IVDD during surgery or necropsy examination. Records in which the Hansen type of disk herniation was not specifically recorded were excluded from portions of the analysis that relied on that data. To be included in the non-IVDD group, medical records had to be complete, including the rendering of a diagnosis made on the basis of diagnostic imaging, necropsy, or other clinical data that indicated that neurologic dysfunction was not associated with disk herniation.

Procedures

Medical records of 172 dogs with IVDD and 38 dogs without IVDD met the inclusion criteria. Age, sex, breed, weight, and duration of clinical signs (acute, ≤ 7 days; chronic, > 7 days) were recorded. The site and type (Hansen type I or II) of disk herniation had been recorded for dogs in the IVDD group.

All myelograms were examined, and sites of spondylosis deformans were recorded. The extent of osteophytosis was graded on a scale of 1 to 4 according to a described standardized method.2

Statistical analysis—The number of sites affected and grade of severity of spondylosis were compared between dogs in the IVDD and non-IVDD groups by use of the Mann-Whitney signed rank test. The analysis was repeated, stratified by duration of clinical signs (acute or chronic), breed (chondrodystrophoid or non-chondrodystrophoid), and age (< 6 years, 6 to 10 years, and > 10 years). The number of sites affected and grade of spondylosis were also compared on the basis of the duration of clinical signs (acute or chronic), breed (chondrodystrophoid or nonchondrodystrophoid), and type of disease (type I or type II).

Within the IVDD group, the rate at which disk disease was associated with spondylosis was calculated as the number of occurrences at a spondylosis site (numerator) divided by the total number of spondylosis sites in that subset of dogs (denominator). The corresponding rate at a site unaffected by spondylosis was calculated as the number of occurrences at a site without spondylosis divided by the total number of nonspondylosis sites. Each dog contributed 26 disk sites (from the C2-3 articulation to the lumbosacral space) to those calculations. Rate ratios and 95% confidence intervals were calculated with commercially available software.a A spondylosis site was randomly chosen for dogs with IVDD and spondylosis. A random disk space was also chosen from this subset of dogs. The distance from chosen spondylosis sites to the disk lesion was compared with distances from the completely random site by use of the Wilcoxon signed rank test.

Age and weight were compared between the IVDD and non-IVDD groups with Student t tests. Multiple linear regression analysis was performed to investigate differences in number of affected sites and grade of severity between the IVDD and non-IVDD groups while adjusting for the effects of age and weight. Unless otherwise noted, values of P < 0.05 were considered significant; analyses were performed with commercially available software.b

Results

The most common breed represented in the IVDD group was the Dachshund (n = 86 dogs; Miniature and Standard Dachshunds were grouped together). Other breeds in that group included mixed-breed dogs (n = 18), Cocker Spaniel (7), Miniature Poodle (6), Beagle (6), Labrador Retriever (5), Dalmatian (3), Doberman Pinscher (3), German Shepherd Dog (3), Pembroke Welsh Corgi (3), Bichon Frise (2), Chihuahua (2), Great Dane (2), Lhasa Apso (2), Pekingese (2), Pomeranian (2), Rottweiler (2), Siberian Husky (2), and 1 each of 16 other breeds. In 3 dogs, IVDD was confirmed during necropsy. Breeds in the non-IVDD group included Boxer (n = 4), German Shepherd Dog (3), Labrador Retriever (3), mixed-breed dogs (3), Cocker Spaniel (2), Lhasa Apso (2), Pomeranian (2), Rottweiler (2), and 1 each of 17 other breeds. In 3 dogs, IVDD was not detected during necropsy. Dogs with IVDD were significantly younger and had lower body weights than dogs in the non-IVDD group (age at initial examination at Texas A&M University for dogs with IVDD, 6.17 years; age for dogs with non-IVDD disease, 6.71 years; P = 0.003; weight at examination for dogs with IVDD, 12.7 kg [27.94 lb]; weight at examination for dogs with non-IVDD disease, 21.9 kg [48.18 lb]; P = 0.024) The combined group values for incidence and grade of severity were highest at T13-L1, L1-2, L2-3, and L7-S1. Disk spaces in the cervical portion of the vertebral column and in the thoracic portion of the vertebral column cranial to T11-12 had fewer affected sites and lower grades of severity, with the exception of the T4-5 and T5-6 articulations (Figure 1). Dogs with IVDD had significantly fewer sites (P = 0.015) and lesssevere changes (P = 0.014) of spondylosis deformans, compared with dogs in the non-IVDD group. When data for both groups were adjusted for age and weight by means of multivariate linear regression analysis, no differences in intensity or number of sites affected by spondylosis deformans were observed. In the group of dogs that were 6 to 10 years old, however, the number of sites with spondylosis and severity of changes were much lower in dogs with IVDD, compared with dogs with non-IVDD neurologic disease (P = 0.04).

Figure 1
Figure 1

Distribution of sites and cumulative severity scores for spondylosis deformans in the vertebral column of 210 dogs with and without IVDD. Units on the x-axis refer to segments of the vertebral column (C = Cervical; T = Thoracic; L = Lumbar; and LS = Lumbosacral).

Citation: Journal of the American Veterinary Medical Association 228, 1; 10.2460/javma.228.1.96

Duration of clinical signs and breed were not associated with the number of sites affected or severity of changes of spondylosis in the IVDD group. The dogs (n = 17) with type II disk disease had higher numbers of affected sites (P = 0.041) and higher grades of severity (P = 0.045), compared with dogs with type I disk herniation (71). Mean age and weight were higher in dogs with type II disk herniation than in dogs with type I herniation (mean age, 8.0 and 6.2 years, respectively; mean weight, 22.8 and 10.8 kg [50.2 and 23.8 lb], respectively).

The rate at which IVDD was diagnosed at sites with and without spondylosis was also investigated. There was no difference between development of IVDD at sites with spondylosis, compared with development of IVDD at sites without spondylosis (Table 1). When dogs with type I and type II disk herniation were considered separately, there was no difference between rates of development of IVDD at sites of spondylosis, compared with development at disk spaces without spondylosis.

Table 1—

Summary of rates at which IVDD was detected at sites of spondylosis in the vertebral columns of 172 dogs with IVDD and spondylosis.

VariableNo. of sites with spondylosis*No. of sites without spondylosisRR95% Confidence interval
Combined6/121166/4,351
Type I disk disease2/3569/1,811
Type II disk disease1/3816/404
Rate (combined)0.049586780.03815211.2997110.58, 2.93
Rate (type I)0.057142860.03810051.4997930.37, 6.12
Rate (type II)0.026315790.0396040.6644740.09, 5.01

Rate = Number of disk spaces with both IVDD and spondylosis divided by the number of disk spaces with spondylosis.

Rate = Number of disk spaces with IVDD but no spondylosis divided by the number of disk spaces with no spondylosis.

RR = Ratio between rate of IVDD at sites with spondylosis and rate of IVDD at sites without spondylosis.

= Not applicable.

Notice that differences in the rates of spondylosis were not significant because the 95% confidence interval included the null value of 1.0.

Randomly chosen joint spaces were farther from sites of IVDD than were regions of spondylosis. In addition, although the amount of separation between random sites and sites of disk herniation was symmetrically distributed, the distances between sites of spondylosis and sites of IVDD had a bimodal distribution (Figure 2). Dogs with spondylosis immediately adjacent to or at the site of IVDD did not differ in duration of clinical signs, type of disk herniation, or breed type, compared with other dogs with IVDD and spondylosis.

Figure 2
Figure 2

Number of vertebral articulations between a randomly chosen intervertebral disk space and a randomly chosen site of spondylosis to a site with IVDD in dogs.

Citation: Journal of the American Veterinary Medical Association 228, 1; 10.2460/javma.228.1.96

Discussion

In the veterinary literature, it is not clear whether there is an association between radiographically apparent spondylosis deformans and clinical manifestations of IVDD. Information pertaining to this subject has mostly been obtained from dogs with disk protrusion at L7-S1, suggesting that spondylosis is common in those dogs.17,18 Age- and weight-matched control populations were not used in those studies, however, making interpretation of data difficult. Results of early studies1,15 in randomly acquired disarticulated vertebral columns from dogs indicate a high incidence of spondylosis at sites of type II disk herniation in the thoracolumbar region. Questions remain regarding radiographic detection of areas of spondylosis, clinical importance of type II disk protrusion, and the possibility of confounding by age or weight.1,15,19

In our study, the number of sites affected and grades of severity of spondylosis were evaluated in dogs with surgically managed IVDD and in dogs that had myelograms but in which other forms of neurologic disease were diagnosed. The overall distribution of sites and severity of osteophytosis were similar to findings of early studies.1,7,15 When adjustments for age and weight were made, no differences in number of affected sites or grade of severity were detected between dogs with IVDD and dogs with non-IVDD neurologic disease. The validity of that finding is linked to the extent to which the multivariate linear regression model used was reliable, given that the data pertaining to the number of sites affected with spondylosis and the grades for severity at those sites were not normally distributed. The absence of differences in those variables between the groups was, however, expected. The group of dogs with IVDD was nonhomogeneous in that it was comprised of dogs with IVDD resulting from mechanical strain or annular tearing (ie, type II), similar to spondylosis, and from nuclear rupture secondary to chondrocyte senescence (ie, type I), which should be unrelated to spondylosis. We were unable to classify many dogs with IVDD into the appropriate group because in some records, surgeons only noted that disk material was removed from the vertebral canal without specifying whether there was disk protrusion or extrusion.

Dogs with type II IVDD had a higher number and greater severity of spondylosis than dogs with type I disk disease. These results should be interpreted with caution, however, because of the possibility of confounding by age and weight and by the small number of dogs in the study that had type II IVDD. The small sample size and lack of normally distributed outcome data made statistical adjustment for age and weight impossible. The finding that the rates at which type II IVDD was localized to articulations with concurrent spondylosis were not higher than rates of IVDD at unaffected intervertebral spaces may have been associated with small sample size, difficulty in detecting osteophytes radiographically, or differences in time required to develop spondylosis as opposed to disk protrusion after annular tearing. Although a higher rate of spondylosis at sites of type II IVDD has been reported,1 the diagnosis of spondylosis in that study was made via dissection of the vertebral column during necropsy. Radiographic imaging is not a sensitive modality for detecting small vertebral osteophytes, especially those that are ventrolateral or dorsal in orientation, and this may explain the low values for radiographic incidence of spondylosis in dogs and the potential for failing to detect IVDD-associated osteophytes.4,7,20 Other imaging modalities, such as magnetic resonance imaging and computed tomography, may be more sensitive for detecting subtle changes associated with disk protrusion and spondylosis.21–23 Use of such techniques may have permitted further clarification of the association between type II disk disease and spondylosis in dogs in our study. Finally, substantial lengths of time may be required to elicit the changes of spondylosis after tearing of the annulus and development of clinical IVDD.19,24 Therefore, although pathophysiologic associations exist among annular hypertrophy, intervertebral disk protrusion, and spondylosis, differences in the timing of these events may make concurrent detection in clinical cases infrequent.

Data from investigations1,15 of dissected dog vertebral columns do not support the supposition that dogs with type I disk herniation have concurrent spondylosis at sites of IVDD. Our results supported that finding in that the rate of type I IVDD detected at sites of spondylosis was the same as the rate of involvement at intervertebral spaces unaffected by spondylosis. This is consistent with the fact that spondylosis is induced by annular tearing, whereas type I disk herniation is usually a result of endogenous chondrocyte abnormalities and associated acute nuclear extrusion.25,26 The nature of nuclear degeneration associated with annular tearing is typically fibrinoid, as is observed in many cases of type II IVDD. Our results support the contention that radio-graphic evidence of spondylosis deformans in dogs with suspected type I IVDD is of little diagnostic value.

The finding that spondylosis sites were closer to sites of IVDD than were randomly chosen control sites and that distances between spondylosis sites and sites of IVDD had a bimodal appearance may have been associated with alteration in vertebral column motion or coincidence. The thoracolumbar and lumbosacral junctions are posited to be more mobile than other segments of the vertebral column in dogs,25,27 and those regions are associated with the highest incidence of disk herniation and spondylosis deformans in dogs.1,2,7,26,28–30 Because spondylosis and IVDD are common in the same regions of the vertebral column, these spatial relationships may be coincidental and not reflective of a shared etiopathogenesis. Another possibility is that, although spondylosis is not more frequent in dogs with type I IVDD and does not develop at a higher incidence at sites of disk herniation in dogs with both type I and type II herniations, it somehow alters certain biomechanical features of vertebral column movement, predisposing dogs with either type of disease to disk herniation. If sites of spondylosis represented areas of rigid stability, it could follow that adjacent vertebral motion units could be more susceptible to disk herniation. That phenomenon is most common in humans with vertebral column implants and is referred to as adjacent segment disease.31 Humans with spondylosis deformans of the cervical and lumbar portions of the vertebral column can have alterations in vertebral range of motion and in the forces of stress exerted on adjacent disk spaces.32,33 Results of a study34 in Beagles, however, suggest that spondylosis has only a minimal influence on vertebral column stability. Furthermore, spondylosis does not appear to be associated with recurrence of IVDD in dogs,35 a finding that supports the consideration that biomechanical alterations in adjacent segments are minimal.

Results of our study indicated that radiographic evidence of spondylosis of the vertebral column in dogs is not clinically important with regard to predicting sites affected by type I disk herniation. Dogs with type II disk disease may have radiographic changes associated with spondylosis that are more apparent than those in other dogs. The possibility that age and weight confounded our analyses and the small number of dogs with type II disease included in the study make the clinical importance of this finding uncertain. Possible biomechanical influences between spondylosis and development of IVDD at adjacent sites may exist.

IVDD

Intervertebral disk disease

a

Epi Info, version 6.04, CDC, Atlanta, Ga.

b

SPSS, version 11.5, SPSS Inc, Chicago, Ill.

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  • Figure 1

    Distribution of sites and cumulative severity scores for spondylosis deformans in the vertebral column of 210 dogs with and without IVDD. Units on the x-axis refer to segments of the vertebral column (C = Cervical; T = Thoracic; L = Lumbar; and LS = Lumbosacral).

  • Figure 2

    Number of vertebral articulations between a randomly chosen intervertebral disk space and a randomly chosen site of spondylosis to a site with IVDD in dogs.

  • 1

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