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Research Review By Dr. Ceara Higgins©

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Date Posted:

May 2016

Study Title:

Leg length discrepancy and osteoarthritis in the knee, hip and lumbar spine

Authors:

Murray KJ & Azari MF

Author's Affiliations:

School of Health Sciences, RMIT University, Melbourne Australia; Health Innovations Research Institute, RMIT University, Melbourne Australia

Publication Information:

Journal of the Canadian Chiropractic Association 2015; 59(3): 226-237.

Background Information:

Chronic joint pain is highly prevalent with an estimated 22% of the Australian population (1) and 30.7% of the American population (2) affected at any given point. This problem can be expected to become more prevalent as the population in industrialized countries ages, due to the link between chronic joint pain and aging itself (1).

In the spine, it is common to associate moderate to severe OA and intervertebral disc degeneration with chronic low back pain, especially in the elderly, who are twice as likely to have chronic low back pain if they have significant disc degeneration (3). A prevalent risk factor for OA is abnormal or excessive mechanical joint loading (8). Abnormal joint loading is also believed to play a significant role in the development of degeneration in segments adjacent to surgical spinal fusions (7).

Leg length discrepancy (LLD), a condition where one femoral head is lower than the other, has been shown to involve abnormal loading of the lower extremity and lumbar spinal joints (8). LLD can be found to some degree in approximately 90% of the population, but is generally classified as mild if the side-to-side discrepancy is less than 20mm (10). However, there is still a great degree of controversy with regard to the amount of LLD required to cause or contribute to a musculoskeletal disorder.

As LLD causes abnormal joint loading and abnormal joint loading has been associated with OA, it is important to understand the association between LLD (particularly mild LLD of ≤ 20 mm) and OA in the joints of the lower extremity, lumbar facet joints, and intervertebral discs. Therefore, the purpose of this paper was to examine the methods utilized to measure LLD and outline the potential association between LLD and OA of the joints of the lumbar spine and lower extremity.

Summary:

Definition of Leg Length Discrepancy (LLD):

LLD is classified as anatomical/structural (due to bony asymmetry between the femoral head and the calcaneus), functional (due to biomechanical abnormalities of joint function in the lower limbs), or environmental (occuring in runners who run on a sloping or slightly banked surface in one direction for long periods of time) (12, 15). For this review, environmental LLD was considered as a type of functional LLD.

Anatomical LLD can be further classified as congenital or acquired. Causes of congenital anatomical LLDs include phocomelia and dysgenetic syndromes, while causes of acquired anatomical LLDs include dysplasias; Ollier’s disease; slipped epiphysis; poliomyelitis; neurofibromatosis; septic arthritis; osteomyelitis; fractures; pes planus; knee valgus/varus and dislocation; and surgically induced (16). In cases of anatomical LLD, there may be functional adaptations on the contralateral side, leading to a functional LLD (12).

Measurement/Assessment of LLD

Clinical Methods of Assessment:
A range of clinical assessment methods exist for LLD, but all of them suffer from inaccuracy and poor inter- and intra-examiner reliability (17). Clinical assessment of LLD relies on palpation of bony anatomy, which is prone to error. A variety of studies have been performed showing the inaccuracy of clinical assessment of LLD and a thorough literature review of the quick visual leg length assessment commonly used by chiropractors shows no convincing evidence of its validity (16).

Imaging Methods of Assessment:
Imaging methods for assessing LLD include teleroentgenography; computed tomography (CT); slit scanography; and orthoroentgenography, and have been shown to have higher levels of validity and reliability than clinical methods (9). Teleroentgenography uses a single anterior-posterior exposure of the entire lower limbs in a standing subject as well as a measuring instrument, such as a ruler. Limitations of this technique include the inability to account for hip and knee joint flexion contractures and possible magnification errors (20). CT has been found to be no more accurate than plain film radiography for detecting LLD, unless the patient has hip or knee joint contractures and has a higher radiation dose (20). Slit scanography uses a lead diaphragm containing a slit placed over the x-ray tube to focus the x-ray beam while the tube is moved along the long axis of the lower extremity of a supine subject. Neither CT nor slit scanography are performed while the patient is weight-bearing, which limits their ability to detect functional LLDs. Orthoroentgenography uses separate exposures of the hips, knees, and ankles. This helps to avoid magnification errors, but errors can still occur due to patient movement and joint contractures. Friberg’s variation of orthoroentgenography (11) uses a single anterior-posterior lumbo-pelvic exposure to compare the heights of the femoral heads. This method has been shown to be accurate, reproducible, and has a lower patient radiation dose (11). Friberg’s method has shown a mean error of 0.6mm and variation of 0 to 0.2mm on repeated imaging (17). Plain film radiography can also be used and has been found to be accurate to within 3mm for both functional and anatomical LLD (18). This error can be further reduced to 1.12mm by placing the feet in line with the femoral heads (13).

More recently examined methods of measuring LLD include an ultrasound method which showed error margins of less than 1mm (21) and a LASER-ultrasound method which was found to be in almost perfect agreement with the radiographic gold standard (22). These methods should be further explored due to the advantage of lower radiation doses for the patients.

Clinically Significant LLD:
The LLD needed to reach clinical significance is controversial, with opinions ranging from 3mm to 20mm depending on the context. Studies by Giles and Taylor (13, 5) found that LLD of 10mm or more was present in 18.3% of patients with chronic low back pain compared to 8% in controls and that subjects with LLD greater than 9mm showed significantly altered lumbosacral facet joint angles, when compared to subjects with LLD of less than 3mm. This could suggest that the development of facet joints might be affected by abnormal joint loading due to LLD.

LLD and OA in the Lower Extremity & Lumbar Spine:

Solomon has proposed three pathogenic groups of secondary arthritis: 1) abnormal or incongruous loads causing failure of essentially normal cartilage; 2) cartilage breaking up under normal conditions of loading due to damage or defective cartilage; 3) defective subchondral bone causing break-up of articular cartilage (4). While the cause-effect relationship for the first category is unclear, it is theorized that pelvic tilt or torsion due to LLD may place unequal stress on the joints in the lower extremity and lumbar spine during upright activity. Further, the change in center of gravity due to pelvic tilt, may lead to compensatory muscle activity and increase the magnitude of internal joint load and altered contact areas in the joints, leading to increased pressure on some areas of cartilage, ultimately leading to OA.

Studies have found associations between OA in the knee or hip and LLD. Golightly et al. (6) found a positive association between knee OA and LLD of greater than or equal to 20mm. In adjusted models for covariates, knee OA was found to be 80% higher in individuals with LLD. However, this study is flawed. While radiographs were used to assess for OA, clinical methods were used to assess LLD, the distance from the malleolus to the floor was not measured, and a 20mm threshold was used for LLD. All of these things may have distorted the results. Harvey et al. (12) used radiographic measurements of LLD and found that LLD of 5mm was associated with higher levels of symptomatic and progressive OA in the knee. Finally, a report on 100 consecutive patients immediately prior to hip arthroplasty found that hip OA was 84% more common on the side of the longer limb in patients with LLD (14).

During combined compression and bending the facet joints carry 12-16% of the total load, and this load can increase up to 70% in individuals with reduced intervertebral disc height (25). In individuals with OA-related chronic low back pain, Hicks et al. found minimal facet OA in the upper region, with a steep increase in the prevalence of facet OA in the lumbar spine, with the greatest change at L5-S1 (3). Facet OA was also found to increase from the age of 30 to 60. From this, it was surmised that both increased or abnormal loads and aging increase the likelihood of facet OA and that this provided good evidence for a link between LLD and facet tropism at L5-S1. (NOTE: No explanation of how this data was related to LLD was provided, rendering the author’s conclusion of “good” evidence existing questionable.)

LLD and Degeneration of the Lumbar Intervertebral Disc:

A study by Arun et al. (23) used MRI to study the effect of upright posture on the lumbar vertebrae. Eight participants were subjected to sustained spinal load of 50% of body weight for 4.5 hours, while in a supine position. MRI scans were done at 1.5, 3, and 4 hours into loading, as well as at 2 and 3.5 hours after the end of loading. The sustained creep due to the load was found to reduce the transport of small solutes into the centre of the intervertebral discs and it took 3 hours after the removal of the load before the transport levels reached pre-loading levels. This reduced diffusion of nutrients could potentially predispose the intervertebral discs to degeneration. This is based on earlier work by Buckwalter, showing that reduced nutrition is one of the main causes of disc degeneration, reduction of disc height, and annulus fibrosis fragmentation, especially posteriorly (24).

Rajasekaran et al. used contrast MRI to examine the effects of dynamic and static weight bearing on diffusion of nutrients into 21 intervertebral discs in 6 idiopathic scoliosis patients prior to surgery (26). Nucleus pulposis biopsy materials were also taken from the convex (where the disc was stretched) and concave (where the disc was compressed) regions of the disc. All discs and end plates were damaged by asymmetrical pressure and showed affected diffusion patterns throughout the endplate. As well, the nucleus pulposis showed a tendency to migrate to the convex side of the curve. This suggests that asymmetrical loading of the spine may be a mechanism for intervertebral disc degeneration.

Clinical Application & Conclusions:

Due to their significant limitations, clinical methods of measuring LLD should be abandoned in favour of radiographic assessment (specifically, Friberg’s method). The evidence also supports a link between LLD and knee and hip OA. Therefore, once a LLD has been radiographically identified, clinicians should consider the increased potential for the individual to develop OA of the hip or knee.

The evidence for a link between LLD and OA in the lumbar facet joints or intervertebral discs is less robust, much less compelling and requires further study. As well, the link needs to be investigated in adolescent populations, where interventions could be used to possibly prevent the development of OA in later life. Once a link is more clearly established, interventional studies on heel-lifts, shoe-lift, or orthoses should be undertaken to evaluate these relatively simple and inexpensive methods and their possible ability to reduce the burden of OA in later life.

Study Methods:

The authors performed literature searches of PubMed, Scopus, and Index to Chiropractic Literature. Studies that were deemed low quality according to standard quality criteria were excluded.

Study Strengths / Weaknesses:

The study provided no clear description of the methods used and no criteria for evaluation of the quality of included studies. Many of the conclusions drawn seemed very loosely based on the data provided, and no cause-effect relationships were established. As such, no particular strengths were noted. This concept still represents a bit of a void in the literature, with a clear need for more high quality work on this relationship.

Additional References:

  1. Brooks PM. The burden of musculoskeletal disease – a global perspective. Clin Rheumatol 2006; 25(6): 778-781.
  2. Golightly YM, Allen KD, Helmick CG, et al. Symptoms of the knee and hip in individuals with and without limb length inequality. Osteoarthr Cartilage 2009; 17(5): 596-600.
  3. Hicks GE, Morone N, Weiner DK. Degenerative lumbar disc and facet disease in older adults: prevalence and clinical correlates. Spine 2009; 34(12): 1301-1306.
  4. Solomon L. Patterns of osteoarthritis of the hip. J Bone Joint Surg (UK) 1976; 58(2): 176-183.
  5. Giles LG, Taylor JR. The effect of postural scoliosis on lumbar apophyseal joints. Scand J Rheumatol 1984; 13(3): 209-220.
  6. Golightly YM, Allen KD, Renner JB, et al. Relationship of limb length inequality with radiographic knee and hip osteoarthritis. Osteoarthr Cartilage 2007; 15(7): 824-829.
  7. Wang JC, Arnold PM, Hermsmeyer JT, et al. Do lumbar motion preserving devices reduce the risk of adjacent segment pathology compared with fusion surgery> A systematic review. Spine 2012; 37(22 Suppl): S133-S143.
  8. Lawrence D. Lateralization of weight in the presence of structural short leg: a preliminary report. J Manipulative Physiol Ther 1984; 7(2): 105-108.
  9. Gurney B. Leg length discrepancy. Gait Posture 2002; 15(2): 195-206.
  10. Knutson GA, Anatomic and functional leg-length inequality: a review and recommendation for clinical decision-making. Part I, anatomic leg-length inequality: prevalence, magnitude, effects and clinical significance. Chiropr Osteopat 2005; 13: 11.
  11. Friberg O. Clinical symptoms and biomechanics of lumbar spine and hip joint in leg length inequality. Spine 1983; 8(6): 643-651.
  12. Subotnick SI. Limb length discrepancies of the lower extremity (the short leg syndrome). J Orthop Sport Phys Ther 1981; 3(1): 11-16.
  13. Giles LG, Taylor JR. Low-back pain associated with leg length inequality. Spine 1981; 6(5): 510-521.
  14. Gofton JP, Trueman GE. Studies in osteoarthritis of the hip. II. Osteoarthritis of the hip and leg-length disparity. Can Med Assoc J 1971; 104(9): 791-799.
  15. McCaw ST, Bates BT. Biomechanical implications of mild leg length inequality. Brit J Sport Med 1991; 25(1): 10-13.
  16. Hoikka V, Paavilainen T, Lindholm TS, et al. Measurement and restoration of equality in length of the lower limbs in total hip replacement. Skel Radiol 1987; 16(6): 442-446.
  17. Friberg O, Nurminen M, Korhonen K, et al. Accuracy and precision of clinical estimation of leg length inequality and lumbar scoliosis: comparison of clinical and radiological measurements. Intern Disabil Stud 1988; 10(2): 49-53.
  18. Clarke GR. Unequal leg length: and accurate method of detection and some clinical results. Rheumatol Phys Med 1972; 11(8): 385-390.
  19. Woerman AL, Binder-Macleod SA. Leg length discrepancy assessment: accuracy and precision in five clinical methods of evaluation. J Orthop Sports Phys Ther 1984; 5(5): 230-239.
  20. Stanitski DF. Limb-length inequality: assessment and treatment options. J Acad Orthop Surg 1999; 7(3): 143-153.
  21. Krettek C, Koch T, Henzler D, et al. A new procedure for determining leg length and leg length inequality using ultrasound. II: Comparison of ultrasound, teleradiography and 2 clinical procedures in 50 patients. Der Unfallchirug 1996; 99(1): 43-51.
  22. Rannisto S, Paalanne N, Rannisto PH, et al. Measurement of leg-length discrepancy using laser-based ultrasound method. Acta Radiologica 2011; 52(10): 1143-1146.
  23. Arun R, Freeman BJ, Scammell BE, et al. 2009 ISSLS Prize Winner: What influence does sustained mechanical load have on diffusion in the human intervertebral disc?: an in vivo study using serial postcontrast magnetic resonance imaging. Spine 2009; 34(21): 2324-2337.
  24. Buckwalter JA. Aging and degeneration of the human intervertebral disc. Spine 1995; 20(11): 1307-1314.
  25. Adams MA, Hutton WC. The effect of posture on the role of the apophysial joints in resisting intervertebral compressive forces. J Bone Joint Surg (UK) 1980; 62(3): 358-362.
  26. Rajasekaran S, Vidyadhara S, Subbiah M, et al. ISSLS prize winner: a study of effects of in vivo mechanical forces on human lumbar discs with scoliotic disc as a biological model: results from serial postcontrast diffusion studies, histopathology and biomechanical analysis of twenty-one human lumbar scoliotic discs. Spine 2010; 35(21): 1930-1943.

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