- Department of Neurosurgery, University of Illinois, Chicago, Illinois, USA
Department of Neurosurgery, University of Illinois, Chicago, Illinois, USA
DOI:10.4103/2152-7806.120780Copyright: © 2013 Pawl R. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
How to cite this article: Pawl R. Editorial on two chronic low back pain studies: A major change in surgical management of disc disease?. Surg Neurol Int 29-Oct-2013;4:
How to cite this URL: Pawl R. Editorial on two chronic low back pain studies: A major change in surgical management of disc disease?. Surg Neurol Int 29-Oct-2013;4:. Available from: http://sni.wpengine.com/surgicalint_articles/editorial-on-two-chronic-low-back-pain-studies-a-major-change-in-surgical-management-of-disc-disease/
In two recent publications, the authors’ hypothesis was that Modic type 1 changes seen in patients with chronic low back pain and herniated lumbar discs may be attributed to bacterial infection/inflammation. The first study showed that many herniated discs were infected with Proprionibacterium acnes, a common anaerobic skin organism, also found in sarcoidosis, and possibly, arthritic joints. In the second double-blind randomized study, 162 patients with disc herniation and Modic type 1 changes were treated with 100 days of oral Bioclavid (Amoxicillin/Clavulanic acid) vs. placebo; those treated with antibiotics improved in all dimensions (e.g., reduced chronic low back/leg pain, reduced disability). Together, the implications of these studies for spine surgeons and pain practitioners are momentous. If a few weeks of oral antibiotic treatment resolves chronic low back pain, then much currently performed spine surgery (e.g. including internal fixation/fusion), as well as chronic pain management/rehabilitation and psychological strategies may be rendered unnecessary.
Keywords: Disc disease, infection, Modic type I changes, nonsurgical, spine
Earlier this year, two papers by authors from Denmark published in the European Spine Journal might well be harbingers of change in the diagnosis and treatment of chronic low back pain.[
The second double-blind, randomized, controlled trial involved 162 patients with chronic low back pain due to herniated discs accompanied by bone edema (e.g., MC in the vertebral bodies) for over 6 months duration.[
If low grade infections are a significant cause of low back pain (and it does not take much to implicate the cervical spine as well) and a few weeks of antibiotic treatment solves much of the problem, then there will be a major reduction in internal fixation and fusion of the spine for chronic low back pain. That would be good for patients and significantly reduce medical costs, but would be bad economically for spine surgeons and some hospital services. Similarly, such patients successfully treated would not need the services of pain practitioners and pain rehabilitation services.
Further questions regarding pain management
What then are the implications for the psychological findings in patients with chronic low back pain syndromes? Are such findings reactions to the pain? What does that mean regarding somatization, converting emotional distress into bodily complaints, considered the underlying phenomenon leading to chronic pain complaints and which is a mainstay finding in chronic back pain patients? These questions will need answers as well.
1. Albert HB, Sorensen JS, Christensen BS, Claus Mannich C. Antibiotic treatment in patients with chronic low back pain and vertebral bone edema (Modic type 1 changes): A double-blind randomized clinical controlled trial of efficacy. Eur Spine J. 2013. 22: 697-707
2. Albert HB, Lambert P, Rollason J, Sorensen JS, Worthington T, Pedersen MB. Does nuclear tissue infected with bacteria following disc herniations lead to Modic changes in the adjacent vertebrae?. Eur Spine J. 2013. 22: 690-6
3. Eishi Y. Etiologic link between sarcoidosis and Propionibacterium acnes. Respir Investig. 2013. 51: 56-68
4. Levy O, Iyer S, Atoun E, Peter N, Hous N, Cash D. Propionibacterium acnes: An underestimated etiology in the pathogenesis of osteoarthritis?. J Shoulder Elbow Surg. 2013. 22: 505-11
5. Segre JA. What does it take to satisfy koch's postulates two centuries later?: Microbial genomics and propionibacteria acnes. J Invest Dermatol. 2013. p.