Stabilize with Healthy Tissue and Reduce Pocket Scarring.
CanGaroo secures the implantable device with healthy tissue and reduces the risk of erosion, migration, and development of excessive scar tissue.1,2 CanGaroo is an extracellular matrix that creates a hospitable environment for host cells to migrate and initiate tissue remodeling, stabilizing the device in healthy vascularized tissue.2,3
Reduce Risk. Naturally.
A natural biologic solution to help reduce complications.
Reduce complications and risk while making patient care more predictable and manageable. CanGaroo helps orchestrate a controlled healing response, promotes device stabilization and mitigates excessive scar tissue formation—and the associated complications.1,2
“The host response to biomaterials is a critical determinant of their success or failure in tissue-repair applications.”
Dziki JL, et al. J Biomed Mater Res A. 2017;105(1):138–147.
How Aziyo Helps.
Common patients CanGaroo can help.
Patients Expected to Have Multiple Change-Outs
Patients at Higher Risk for Calcification
Patients at Risk for Migration and/or Erosion
Placing a CanGaroo Envelope provides a soft conforming layer around the device which helps anchor the can, naturally mitigating risk of migration and/or erosion.2
Patients at Risk For Pocket Pain2
ECM. How It Works.
The Body’s Reaction
When a device or foreign material is implanted in a patient, their immune response either integrates and remodels it into healthy tissue or induces prolonged inflammation that may result in the formation of fibrotic tissue. While the former is more desirable, the latter is too common.
Stephen F. Badylak, DVM, PhD, MD
Deputy Director, McGowan Institute for Regenerative Medicine, University of Pittsburgh
To minimize inflammation (and the associated complications) and achieve optimal tissue remodeling outcomes in patients CanGaroo is created using two multilaminate sheets of decellularized, non-crosslinked, lyophilized SIS. SIS ECM is associated with biologic activity such as recruitment of endogenous stem/progenitor cells and modulation of the host response to injury resulting in pro-remodeling, anti-inflammatory tissue growth.3
Healthy Tissue Growth
SIS derived ECM is a biomaterial rich in growth factors and structural proteins.3,4,5 Useful in multiple clinical applications, SIS remodels into healthy, site-specific tissue that stimulates healthy tissue growth and eliminates scarring.2,3,4,5
Phases of ECM Guided Wound Healing.
Inflammation involving M1 macrophages is an inherent component of healing. However, prolonged M1 macrophage function can cause chronic inflammation and lead to fibrosis and scarring. The presence of SIS ECM promotes a shift from M1 to a pro-remodeling, anti-inflammatory M2 phenotype.6
Concurrent with the inflammatory phase, in the proliferation phase fibroblasts populate the SIS ECM through attaching and proliferating.7 This stage is also marked by angiogenesis and epithelization which forms healthy vascularized tissue.7
As the SIS ECM is broken down and absorbed, the number of fibroblasts and macrophages in the matrix declines over time.7 Matrix turnover ultimately slows and eventually stops, ending angiogenesis.6 Scaffold remodeling is complete when metabolic activity stabilizes and the newly regenerated tissue becomes fully functional.7,8
Learn About CanGaroo.
Make patient care more predictable and manageable.
Learn how you can regulate your patients’ biologic healing response post implant, reduce inflammation, and mitigate excessive scar tissue formation and thus the associated complications with CanGaroo.
Interested in CanGaroo?
Try CanGaroo Envelope Today!
To schedule a product demo or request an in-service for a product evaluation contact us today.
1. Data on file at Aziyo Biologics, Inc.
2. Pre-clinical data on file at Aziyo Biologics, Inc. using CIEDs.
3. Dziki JL, et al. J Biomed Mater Res A. 2017;105(1):138-147.
4. Badylak SF, et al. J Surg Res. 2002 Apr;103(2):190-202.
5. Brennan EP, et al. Tissue Eng. 2006 Oct;12(10):2949-2955.
6. Londono R, et al. Ann Biomed Eng. 2015;43(3):577-92.
7. Turner MD, et al. Biochim Biophys Acta. 2014;1843(11):2563-82.
8. Tonnesen MG, et al. J Investig Dermatol Symp Proc. 2000:5(1):40-46.