Degeneration and Inflammation



Fig. 1
Diagram of ligamentous and joint capsule attachments in the cervical spine



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Fig. 2
Diagram to demonstrate spine movement of up to 130° in the sagittal plane




Degenerative Disease


The degenerative process seems to be an inevitable consequence of ageing. The changes may be observed in the third decade and progress throughout life. The mechanisms are:


  1. 1.


    relatively poor blood supply to the intervertebral discs

     

  2. 2.


    multiple micro injuries to discs

     

  3. 3.


    cartilage wear in the joints

     

  4. 4.


    reduction in the number of chondrocytes

     

  5. 5.


    vascular ingrowth into the disc

     

  6. 6.


    marginal osteophytes on vertebral bodies and joints

     

  7. 7.


    herniation of discs

     

  8. 8.


    osteopenia and osteoporosis

     

  9. 9.


    biomechanical overload due to disease at other segments

     

There is a genetic element to the speed of progress of degeneration probably related to the proteoglycan binding of collagen fibres. More linkages mean stiffer collagen which is more brittle, fewer linkages mean softer collagen more likely to tear and displace.

The micro trauma element of degeneration is accelerated by impact and multiple minor traumatic incidents and therefore has an occupational and sporting association.


Manifestations of Degenerative Disease



Discs


Small tears within the disc lead to annular tears. A tear may be seen as a defect in the annulus, containing soft tissue material which may take on an increased water content. There is considerable debate as to whether these tears with high signal material are a cause of localised back pain [24]. Tears with scar tissue and repair produce low MRI signal. There is considerable debate over alterations in water content in the annulus, some regard this as the main cause of reduced MRI signal on all sequences but others believe that scar tissue from micro trauma is a major element. The consequence of all these changes is reduction in pliability and tension within the annulus and a tendency for disc height reduction. This in turn leads to buckling of the longitudinal ligaments. Less commonly described in imaging interpretation but probably a much more important factor in morbidity is mechanical instability due to loss of tension within the annulus and laxity of the margins of the disc. Frank herniation of disc material through tears in the annulus fibrosis (Fig. 3) may not only compress adjacent nerve roots but also releases several chemical irritants including prostaglandin, tumour necrosis factor alpha (TNFα) and interleukins [5]. These chemicals may be part of the localised pain response and are potentially toxic to the adjacent nerves.

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Fig. 3
MRI of annular tear

The loss of height in an intervertebral disc will in turn create mechanical instability and this will lead to osteophytes that may impinge on adjacent nerves [6].


Facet Joints


As for all synovial joints, articular cartilage wear and mechanical instability lead to osteoarthritis with localised pain and osteophytes. New bone formation around the joint may considerably limit movement which in turn places additional load on adjacent segments. As degeneration is inevitably widespread and extremely common it may be very difficult to determine the origin of pain as the presence of facet joint arthropathy does not predict that pain arises from this area. Synovial cysts may arise from the joint and may compress nerve roots. Haemorrhage into the cysts may increase the pressure. The fundamental problem is that facet joint disease is very common and we have no imaging technique that scans for the origin of pain. The presence of facet joint changes does not necessarily indicate an origin of pain, similarly, joints that look relatively normal may be the source of symptoms. Systems are closely interrelated and there is association between muscle atrophy and facet joint disease, it may be that spine instability is exacerbated by this connection [7] (Fig. 4).

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Fig. 4
Facet joint arthritis with a synovial cyst


End Plates


MRI is often used to assess the end plates. The changes include Schmorl’s nodes which are indentations in the end plate surface (Fig. 5) and probably represent adolescent disc protrusion through bone that is too soft to accept the loads applied. There is a genetic predisposition and severe cases affecting multiple levels may lead to progressive kyphosis probably? due to damage to growth in the anterior part of the vertebral body; this condition is termed Scheuermann’s disease or idiopathic adolescent kyphosis. This may be a factor in later facet joint arthritis and segmental instability.

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Fig. 5
Scheuermann’s disease

Stress of the end plate may lead to the changes described by Modic et al. which may be characterised by their MRI signal as, bone oedema, fatty infiltration and sclerosis. There is some evidence that end plate stress changes particularly those with oedema are linked to back pain [8, 9] but there is poor evidence to show that lumbar surgery results are related to the stage of end plate change


Spinal Stenosis


Individuals are born with spinal canals of differing dimension. Those with narrow canals need very little disc protrusion or osteophytes formation to cause pressure on the cord or cauda equina. Spinal stenosis is when the spinal canal is rendered too narrow due to disc or joint disease for normal blood supply to reach the neural structures. Patients will typically complain of back and leg pain which comes on after walking (spinal claudication), this eases after several minutes’ rest. The disease is progressive and rarely undergoes spontaneous resolution. Therefore, surgery is an important treatment method and imaging is essential in plotting the extent and severity. There is considerable literature on the efficacy of surgery but a recent Cochrane review suggested that fusion plus decompression was no better than conventional decompression alone [10] (Fig. 6).

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Fig. 6
MRI spinal stenosis


Inflammatory Disorders


The underlying pathology of target organs in spinal inflammatory disorders dictates the imaging appearances throughout the natural history of the disease processes. Although overlap exists, inflammatory disorders can predominantly affect the synovial articulations of the spine (rheumatoid disease) or primarily the enthesis of ligaments and intervertebral discs (seronegative spondyloarthropathies). The various disease states are not static but rather need to be viewed as dynamic and progressive usually resulting in complications. In rheumatoid disease it is primarily the cervical spine that is involved but it is very rare that the rheumatoid arthritis patient presents with cervical spine manifestations as the first mode of presentation. On the other hand seronegative spondyloarthropathies usually present with axial manifestations of enthesitis as the first mode of presentation which are easily overlooked.

Spondyloarthropathy may result from a wide range of inflammatory disorders. They include rheumatoid arthritis, ankylosing spondylitis, psoriatic arthropathy, reactive arthritis, Bechet’s disease, Reiter’s syndrome and SAPHO syndrome. Synovial involvement of the cervical spine in seropositive inflammatory states have a predilection for the facet joints, and in particular the C1–C2 articulations. In the seronegative spondyloarthropathy the inflammatory site is the enthesis where the collagen of the ligaments or intervertebral disc annulus enters bone directly. The cause of the inflammatory process is the generation of cytokines which results in oedema, bone erosion, disorganisation of bone and ligament structure which promotes a reactive osteitis and eventually ossification of the ligaments commencing at the enthesis interface. The seronegative spondyloarthropathies can be further categorised based on the imaging findings equated to the clinical features and laboratory findings. Although multiple modalities such as radiography, CT and scintigraphy can be employed to assess the inflammatory sites within both the axial and appendicular skeleton, it is primarily MRI which is the optimal imaging modality to assess inflammatory disorders of the spine due to its high sensitivity and specificity. Although contrast enhanced MR studies are not usually required for diagnosis, they can distinguish between active and inactive disease and also help in assessing the response to anti-inflammatory therapy.


Clinical Features


Rheumatoid arthritis very commonly affects the spine especially the cervical region and the odontoid peg [11]. Erosion of the peg may lead to severe subluxation and may be life-threatening. Imaging is important when patients are being considered for intubation anaesthesia whether they have symptoms or not. Disease modifying drugs are having a profound effect in the degree of spinal involvement by the rheumatoid process if treated early.

Ankylosing spondylitis is the prototype of the seronegative arthropathies. Associated with HLA-B27 this is a disease more common in men with an onset mean of 25 years. It usually presents with back pain and morning stiffness. Untreated the disease will progress to bony ankylosis of joints which renders the spine at risk of transverse fractures (banana fracture) with relatively minor injury. In the acute phase the pain arises from inflamed entheses (the insertion of ligaments) at the corner of the vertebral bodies (Romanus lesion or shiny corner). The disease commonly affects the sacroiliac joints and the costovertebral joints. Using MR imaging bone oedema is the hallmark but care must be taken to observe even small numbers of lesions as they may be fairly subtle and only visible on water sensitive fat suppressed sequences. Early diagnosis is key as disease modifying drugs and physical therapy should be commenced as early as possible.

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Jun 25, 2017 | Posted by in MUSCULOSKELETAL MEDICINE | Comments Off on Degeneration and Inflammation

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