Direct & in-direct cartilage repairs after biological treatment


Direct & in-direct cartilage repairs after biological treatment

July 10,2018

Macquarie Stem Cells has provided this information to educate the public based on peer reviewed, published scientific and medical documents. We don’t aim to encourage consumers to seek out such treatments prior to an assessment by a health professional to determine your suitability for treatment. This is obtained directly from NCBI Pubmed Literature. This study was funded by the University of Veterinary Medicine, Vienna. We aim to provide you with an unbiased range of treatments that are available aside from biological therapy, This is discussed in ‘other-options’  page on our website.

Biological Treatments can directly repair cartilage and they also stimulate existing cellular structures to work better.

This publication aimed to get a mechanical understanding about biological treatments, specifically investigating the function of repairs post treatment. The previous methods used to track cellular activity based on fluorescent proteins, the bacterial enzyme LacZ, firefly luciferase, and many more can be rejected by the immune system, therefore the marker readings are not entirely accurate when it comes to long term studies. This study fills in the translational gap in understanding long term cell behaviours. Using a model that will not reject the marker long term, the scientists are able to show biological treatments not only heal the cartilage by them selves, but they also stimulate the existing cellular structures within the joint to work better, more efficiently and contribute to the repair of cartilage that has suffered full-thickness wear and tear.


The publication is below, keep in mind this is a very long publication. Below is just a small snippet. We would be more than happy to provide the entire article upon request.

TITLE: “Tracking mesenchymal stem cell contributions to regeneration in an immunocompetent cartilage regeneration model.”(Zwolanek et al., 2017)

Published: 19th Oct 2017
Journal of Clinical Investigation

“Although several studies investigating cartilage regeneration using intraarticularly injected MSC reported promising results in different model systems, it is currently controversially discussed whether the positive therapeutic effects of MSC are due to a progenitor or a nonprogenitor function of injected cells. It is unclear whether MSC injected into a joint attach to cartilage lesions, divide, differentiate, and give rise to new MSC-derived chondrocytes, or whether they just orchestrate regeneration by a nonprogenitor function, e.g., by secreting factors stimulating host cells to promote regeneration. This controversy has been fueled by the lack of appropriate translational model systems that are able to unequivocally answer this key question. We have recently shown that genetically labeled MSC are able to attach to cartilage lesions via a β1 integrin–mediated mechanism in vitro, but it is generally believed that, in vivo, only few of the intraarticularly injected cells adhere to damaged cartilage and may subsequently participate in tissue regeneration.”(Zwolanek et al., 2017)

MSC attach to full-thickness cartilage defects but do not differentiate into mature chondrocytes.”(Zwolanek et al., 2017)

“We next examined the ability of this cell tracking model to answer an unresolved question in regenerative medicine, namely whether intra-articularly injected MSC augment cartilage regeneration via a progenitor- or nonprogenitor-mediated mechanism. To this end, we established a focal cartilage defect model in rats. Full-thickness cartilage defects with a diameter of 0.7 mm were generated in the patellofemoral groove of the right knee in female Tg(ALPPm) and WT rats. The left intact knee served as internal control. Two weeks after surgery, we injected 1 × 107 MSC isolated from sex-matched Tg(ALPP) donor rats or vehicle (serum) into the left and right knees. We used native rat serum for suspension of MSC to facilitate attachment to the defects. A detailed characterization of the MSC population has been reported earlier.”(Zwolanek et al., 2017)

“Histochemical analysis of ALPP activity directly after femur isolation demonstrated that ALPP-expressing MSC were able to successfully attach to the full-thickness defects in Tg(ALPPm) recipients, whereas no attachment was seen in WT recipients or in vehicle controls 1 day after injection. Seven days after injection, only few ALPP-positive cells were found in the defects of Tg(ALPPm). Interestingly, however, 28 days after injection, a significant area of the defects was covered by ALPP-positive cells in Tg(ALPPm) recipients, whereas no ALPP staining was found in transplanted WT animals or serum-injected controls.”(Zwolanek et al., 2017)

“In order to follow up the intriguing finding that ALPP-expressing MSC were absent in cartilage defects of WT recipients as early as one day after injection, we analyzed synovial ALPP staining and the amount of ALPP present in the joint capsule tissue by histochemical staining and immunoblotting, respectively, 1 day after injection of MSC from Tg(ALPP) donors. As expected, ALPP staining and ALPP protein expression was only found in the joint capsule of knees injected with ALPP-expressing MSC but not in serum-injected WT and Tg(ALPPm) controls.”(Zwolanek et al., 2017)


REF: Zwolanek, D., Satué, M., Proell, V., Godoy, J., Odörfer, K., Flicker, M., Hoffmann, S., Rülicke, T. and Erben, R. (2017). Tracking mesenchymal stem cell contributions to regeneration in an immunocompetent cartilage regeneration model. JCI Insight, 2(20).

TAGS: Macquarie Stem Cells, Possibilities of Biological Treatments, Focusing on Osteoarthritis, Macquarie Stem Cells treating osteoarthritis, Dr. Ralph Bright biological treatment, full thickness cartilage tear, cartilage loss, 


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