Influence of negative pressure wound therapy on peri‐prosthetic tissue vascularization and inflammation around porous titanium percutaneous devices

Abstract

Negative Pressure Wound Therapy (NPWT) has been shown to limit downgrowth around percutaneous devices in a guinea pig model. However, the influence of NPWT on peri‐prosthetic tissue characteristics leading to limited downgrowth is still unclear. In order to investigate this, 12 CD hairless rats were assigned into two groups, NPWT and Untreated (n = 6/group). Each animal was implanted with a porous coated titanium percutaneous device and was dressed with a gauze and semi‐occlusive base dressing. Post‐surgery, animals in the NPWT Group received a regimen of NPWT treatment (−70 to −90 mmHg). After 4 weeks, tissue was collected over the device and stained with CD31 and CD68 to quantify blood vessel density and inflammation, respectively. The device with the surrounding tissue was also collected to quantify downgrowth. NPWT treatment led to a 1.6‐fold increase in blood vessel densities compared to untreated tissues (p p = 0.19). Additionally, the results showed a trend toward increased CD68 cell densities in the NPWT Group compared to the Untreated Group (p = 0.09). These findings suggest that NPWT may influence wound healing responses in percutaneous devices by increasing blood vessel densities, limiting downgrowth and potentially increasing inflammation. Overall, NPWT may enhance tissue vascularity around percutaneous devices, especially in patients with impaired wound healing. © 2019 Wiley Periodicals, Inc. J Biomed Mater Res Part B: Appl Biomater 107B: 2091–2101, 2019.

Document Details

Document Type
Pub Defense Publication
Publication Date
Jan 10, 2019
Source ID
10.1002/jbm.b.34302

Entities

People

  • Divya R. L. Pawar
  • Kelli Hafer
  • Kent N Bachus
  • Sujee Jeyapalina

Organizations

  • United States Army Medical Research and Development Command
  • University of Utah

Tags

Fields of Study

  • Medicine

Readers

  • Trauma Surgery or Emergency Medicine.