Discovertebral (Andersson) lesions of the spine in ankylosing spondylitis revisited

Abstract

A well-known complication in patients with ankylosing spondylitis (AS) is the development of localised vertebral or discovertebral lesions of the spine, which was first described by Andersson in 1937. Since then, many different terms are used in literature to refer to these localised lesions of the spine, including the eponym 'Andersson lesion' (AL). The use of different terms reflects an ongoing debate on the exact aetiology of the AL. In the current study, we performed an extensive review of the literature in order to align communication on aetiology, diagnosis and management between treating physicians. AL may result from inflammation or (stress-) fractures of the complete ankylosed spine. There is no evidence for an infectious origin. Regardless of the exact aetiology, a final common pathway exists, in which mechanical stresses prevent the lesion from fusion and provoke the development of pseudarthrosis. The diagnosis of AL is established on conventional radiography, but computed tomography and magnetic resonance imaging both provide additional information. There is no indication for a diagnostic biopsy. Surgical instrumentation and fusion is considered the principle management in symptomatic AL that fails to resolve from a conservative treatment. We advise to use the term Andersson lesion for these spinal lesions in patients with AS.

Fig. 1

Schematic presentation of the development of discovertebral (Andersson) lesions; lesions may originate from inflammation combined with unfused segments (last mobile segment; a), fractures trough the ankylosed disc (b) or fractures trough the vertebral body (c). Finally, a characteristic Andersson lesion develops, with (e) or without (d) a kyphotic deformity

Fig. 2

Anteroposterior plain radiograph from an AL at the thoracolumbar junction in a 56-year-old female AS patient (a). A sagittal reconstructed CT image of the same patient shows central osteolysis surrounded by an irregular sclerotic zone (b). The lesion extends into the posterior elements and has resulted in narrowing of the spinal canal

Fig. 3

Lateral plain radiograph with a kyphotic discovertebral AL at the thoracolumbar junction in a 60-year-old male AS patient (a). Radiograph after posterior instrumentation and fusion of the symptomatic AL is also shown (b). T1- (c) and T2-weighted (d) sagittal MR images accurately reveal involvement of the surrounding structures. The lesion has resulted in a severely narrowed spinal canal, with dural compression, that clinically resulted in a postoperative partial peroneal nerve palsy of his right leg

Fig. 4

T1-weighted sagittal MRI of a 47-year-old AS patients showing an AL at the L1–L2 level with characteristically reduced signal intensity. T2-weighted images reveal a central destructive zone surrounded by an area with reduced signal intensity at both sides