Advertisement for orthosearch.org.uk
Results 1 - 1 of 1
Results per page:
Applied filters
Include Proceedings
Dates
Year From

Year To
Orthopaedic Proceedings
Vol. 92-B, Issue SUPP_I | Pages 3 - 3
1 Mar 2010
White J Herzog A Bergersen E Snitzer J Decker J Vanderby R Stampfli HF Kaplan L
Full Access

Purpose: Damage to articular cartilage leads to an incomplete healing response. This has elicited interest in improving the understanding of chondrocyte biology and finding ways to stimulate a more effective repair response. Neuropeptides play a role in the proliferative and reparative processes of many tissue types, but little is known about their effects on articular cartilage. This research aimed to investigate the effect of four neuropeptides on articular chondrocytes.

Method: Bovine chondrocytes were cultivated in monolayer culture in media alone or media containing one of four neuropeptides: NPY, CGRP, SP, and VIP. Enzymatically digested chondrocytes from the articular surface of the femoral trochlea, femoral condyles, and patella of freshly slaughtered veal (n=8) were plated at 1×10^5 cells/mL in DMEM complete media with 5% FCS. Proliferation and proteoglycan assays were conducted at days 2,4,6, and 8.

Results: Substance P showed a statistically significant stimulatory effect on chondrocyte proliferation and proteoglycan production that was greatest at a concentration of 5 μg/ml. NPY and VIP showed a dose dependent suppressive effect on chondrocyte proliferation that was greatest at their highest concentrations and was significant at all time points, with the exception of VIP at day 2. CGRP showed no significant effect on proliferation or proteoglycan production.

Conclusion: Substance P showed a reliable stimulation of chondrocyte proliferation and proteoglycan production while NPY and VIP showed dose-dependent depressive effects. These findings support the idea that the peripheral nervous system, through neuropeptides, exerts direct influence on articular chondrocytes. This may provide some insight into the pathophysiology of inflammatory and degenerative arthritis and provide targets for modifying the repair response of articular cartilage.