Lyme bacteria (B.B.) "eats" collagen? Any documented proof / studies?

Seeking any real proof to review if there is any.

Aches and pain are not proof as those can be from many other lyme and even non-lyme issues.

Somebody said...


Host metalloproteinases in Lyme arthritis

Abstract

Objective

: To assess the role of matrix metalloproteinases (MMPs) in cartilage and bone erosions in Lyme arthritis

Methods

We examined synovial fluid from 10 patients with Lyme arthritis for the presence of MMP‐2, MMP‐3, MMP‐9, and “aggrecanase” activity using gelatinolytic zymography and immunoblot analysis. We developed an in vitro model of Lyme arthritis using cartilage explants and observed changes in cartilage degradation in the presence of Borrelia burgdorferi and/or various protease inhibitors.

Results

Synovial fluid from patients with Lyme arthritis was found to contain at least 3 MMPs: gelatinase A (MMP‐2), stromelysin (MMP‐3), and gelatinase B (MMP‐9). In addition, there was evidence in 2 patients of “aggrecanase” activity not accounted for by the above enzymes. Infection of cartilage explants with B burgdorferi resulted in induction of MMP‐3, MMP‐9, and “aggrecanase” activity. Increased induction of these enzymes by B burgdorferi alone was not sufficient to cause cartilage destruction in the explants as measured by glycosaminoglycan (GAG) and hydroxyproline release. However, addition of plasminogen, which can act as an MMP activator, to cultures resulted in significant GAG and hydroxyproline release in the presence of B burgdorferi. The MMP inhibitor batimastat significantly reduced the GAG release and completely inhibited the collagen degradation.

Conclusion

MMPs are found in synovial fluids from patients with Lyme arthritis and are induced from cartilage tissue by the presence of B burgdorferi. Inhibition of MMP activity prevents B burgdorferi–induced cartilage degradation in vitro.

Somebody said...


Elevated levels of collagenase and prostaglandin e2 from synovium associated with chronic lyme arthritis

First published: May 1980 https://doi.org/10.1002/art.1780230511 Cited by: 42

Abstract
A patient with chronic Lyme arthritis and roentgenographic evidence of bony erosion underwent a synovectomy; proliferative synovium (pannus), containing aggreagates of small lymphocytes, was found adherent to eroded cartilage and bone. During 8 days in tissue culture, the synovial cells produced large amounts of collagenase and prostaglandin E2, but only low levels of both neurtral and acid proteinases. Sixty‐seven percent of the lymphocytes from the synovium were T cells; 19% were B cells. Attempts to identify agent/antigen in the synovial cells were unsuccessful. Thus, the synovium of this patient, whose disease appears to be tick‐transmitted, resembles that of rheumatoid arthritis. This finding further supports the hypothesis that many possible agents, including infectious ones, trigger a common pathway in synovium, which leads to joint destruction.

collagenase is the enzyme that breaks down collagen

With lyme, I was very ridgid and stiff. Many here mention joint issues. But wait.....

Non flexibility put tremendous strain on joints. Releasing tension in muscle and tendons (I learned how), lessened the strain on my joints. So some here might have real joint issues and some like me have tendon issues , some have both. Muscle is another topic, has its own issues (knots and adhessions), but muscle turns into tendons at the bone attachment.

Post lyme: Ive been rebuilding muscle for 2 areas. Its slow., but can do stuff in the gym that was impossible with lyme. My tendons need more help, thus my other collegian post.

Its thought that lyme runs from your immune sytem cells in your blood (negative blood tests) to the soft / clear/ white tissues that have no blood, thus no killer immune cells. Looks like they can feast there too!!! makes sense now.