A Hyperosmolar Saline Solution Fortified with Anti-Inflammatory Components Mitigates Articular Cartilage Pro-Inflammatory and Degradative Responses in an Model of Knee Arthroscopy.

OBJECTIVE

To evaluate differences in pro-inflammatory and degradative mediator production from osteoarthritic knee articular cartilage explants treated with a hyperosmolar saline solution supplemented with anti-inflammatory components (l-glutamine, ascorbic acid, sodium pyruvate, epigallocatechin gallate [EGCG], and dexamethasone) or normal saline using an model for knee arthroscopy.

DESIGN

Full-thickness 6 mm articular cartilage explants ( = 12/patient) were created from femoral condyle and tibial plateau samples collected from patients who received knee arthroplasty. One explant half was treated for 3 hours with hyperosmolar saline (600 mOsm/L) supplemented with anti-inflammatory components and the corresponding half with normal saline (308 mOsm/L). Explants were cultured for 3 days and then collected for biomarker analyses. Media biomarker concentrations were normalized to the wet weight of the tissue (mg) and were analyzed by a paired test with significance set at < 0.05.

RESULTS

Cartilage was collected from 9 females and 2 males (mean age = 68 years). Concentrations of MCP-1 ( < 0.001), IL-8 ( = 0.03), GRO-α ( = 0.02), MMP-1 ( < 0.001), MMP-2 ( < 0.001), and MMP-3 ( < 0.001) were significantly lower in explant halves treated with the enhanced hyperosmolar solution. When considering only those cartilage explants in the top tercile of tissue metabolism, IL-6 ( = 0.005), IL-8 ( = 0.0001), MCP-1 ( < 0.001), GRO-α ( = 0.0003), MMP-1 ( < 0.001), MMP-2 ( < 0.001), MMP-3 ( < 0.001), and GAG expression ( = 0.0001) was significantly lower in cartilage explant halves treated with the enhanced hyperosmolar solution.

CONCLUSIONS

Treatment of cartilage explants with a hyperosmolar saline arthroscopic irrigation solution supplemented with anti-inflammatory components was associated with significant decreases in inflammatory and degradative mediator production and mitigation of proteoglycan loss.