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How Lyme Disease Can Trigger Osteoarthritis

osteoarthritis lyme diseaseOsteoarthritis is a condition where there is chronic degeneration of the cartilage in the joints, usually occurring after middle-age and usually with a slow progression of pain and mobility restrictions. Rapid onset osteoarthritis usually refers to cases where symptoms degenerate quickly over a period of two years. The rapid onset of Lyme arthritis may take weeks or months which again offers the opportunity to differentiate it from conventional osteoarthritis. Lyme disease does cause inflammation in the body however and may promote damage to susceptible joints and those already with degeneration from osteoarthritis. Symptoms that were previously just mildly irritating may become crippling within a few days or weeks as inflammation increases.

Research by Marre (et al, 2010) looked at the role of inflammation caused by Borrelia burgdorferi and found that adrenomedullin, a protein produced in response to bacterial invasion plays an active role in antimicrobial activity and the regulation of inflammatory processes. Patients with untreated Lyme arthritis had a higher level of adrenomedullin in their synovial fluid than other patients with conventional osteoarthritis. Adrenomedullin actually dampens the hosts inflammatory response to Borrelia, thus allowing it to avoid immune system attacks. The presence of Borrelia burgdorferi appeared to increase the adrenomedullin levels, created a ore favorable environment for the spirochaetes. This effect on the immune system’s inflammatory processes may be involved in the development of chronic arthritis that occurs in some patients with Lyme disease.

Mechanisms Behind Lyme Disease Osteoarthritis

Other processes implicated in Lyme disease, osteoarthritis, rheumatoid arthritis, gout, and ankylosing spondylitis, include the effects of Toll-like receptors (TLRs) and NOD-like receptors that drive proinflammatory sytokine production in infected or injured tissues (McCormack, et al, 2009). These receptors may provide a basis for better pain management and control of inflammation in Lyme arthritis and other joint conditions.

One sign of Lyme disease arthritis rather than osteoarthritis may be the presence of inflamed lymph nodes around the site of the joint inflammation and pain. Radiographic and ultrasonographic imaging may not reveal any specific pathology that could be responsible for the patient’s pain, especially in younger patients and children. Some patients do appear to be more sensitive to the effects of Lyme disease on the joints and are more prone to developing Lyme arthritis. Furthermore, research by Christopherson (et al, 2003) observed that mice vaccinated with Borrelia burgdorferi, but who were gamma interferon-deficient, developed chronic destructive osteoarthropathy when infected with Borrelia burgdorferi. The application of anti-tumor necrosis factor alpha antibody increased the severity of their Lyme disease osteoarthritis and affected their mobility.

Lyme Disease Vaccine-Induced Osteoarthritis

Those mice who were not deficient in gamma interferon and who had been vaccinated like the other group of mice were found to show signs of inhibition of arthritis development when challenged with recombinant TNF-alpha. The same type of mice when challenged with anti-TNF-alpha showed pronounced reduction in the production of an antibody that kills Borrelia burgdorferi. These findings suggest that the levels of TNF-alpha play a role in regulating the production of Lyme disease antibody and the process of Lyme disease vaccine-induced osteoarthritis. The ramifications for patients with abnormalities of TNF-alpha production, deficiencies in gamma-interferon, and other immune system irregularities may be significant when faced with any new Lyme disease vaccines and may offer a partial explanation for the purported effects of the LYMErix vaccine briefly available. Lyme disease osteoarthritis may be considered a rare phenomenon, but it appears that there are some specific processes at work that warrant further investigation.


Sack K. Monarthritis: differential diagnosis. Am J Med. 1997 Jan 27;102(1A):30S-34S.

Marre ML, Darcy CT, Yinh J, Akira S, Uematsu S, Steere AC, Hu LT. Role of adrenomedullin in Lyme disease. Infect Immun. 2010 Dec;78(12):5307-13. Epub 2010 Oct 4.

Iliopoulou BP, Huber BT. Infectious arthritis and immune dysregulation: lessons from Lyme disease. Curr Opin Rheumatol. 2010 Jul;22(4):451-5.

Amini B, Geller MD, Mathew M, Gerard P. MRI features of Lyme arthritis of the hips. Pediatr Radiol. 2007 Nov;37(11):1163-5. Epub 2007 Aug 18.

Christopherson JA, Munson EL, England DM, Croke CL, Remington MC, Molitor ML, DeCoster DJ, Callister SM, Schell RF. Destructive arthritis in vaccinated interferon gamma-deficient mice challenged with Borrelia burgdorferi: modulation by tumor necrosis factor alpha. Clin Diagn Lab Immunol. 2003 Jan;10(1):44-52.

McCormack WJ, Parker AE, O’Neill LA. Toll-like receptors and NOD-like receptors in rheumatic diseases. Arthritis Res Ther. 2009;11(5):243. Epub 2009 Oct 14.