Effect of Impact Load on Articular Cartilage: Cell Metabolism and Viability, and Matrix Water Content

TLDR

Trauma from a single impact load below the threshold for subchondral bone fracture can permanently damage articular cartilage, causing surface fissures, proteoglycan loss, and cell death, yet the influence of varying impact stresses on chondrocyte biophysiology and matrix integrity remains poorly understood. The study hypothesizes that chondrocyte metabolic activity, viability, and matrix hydration respond in a stress‑dependent manner. Bovine cartilage explants were impacted at nominal stresses of 0.5–65 MPa, and proteoglycan biosynthesis, cell viability, and water content were measured immediately and 24 hours post‑impaction. Higher impact stresses reduced proteoglycan biosynthesis while increasing water content; a critical threshold of 15–20 MPa induced cell death and collagen rupture, which the authors attribute to the observed metabolic suppression and hydration changes, though the precise damaging mechanism remains unclear.

Abstract

Significant evidence exists that trauma to a joint produced by a single impact load below that which causes subchondral bone fracture can result in permanent damage to the cartilage matrix, including surface fissures, loss of proteoglycan, and cell death. Limited information exists, however, on the effect of a varying impact stress on chondrocyte biophysiology and matrix integrity. Based on our previous work, we hypothesized that a stress-dependent response exists for both the chondrocyte’s metabolic activity and viability and the matrix’s hydration. This hypothesis was tested by impacting bovine cartilage explants with nominal stresses ranging from 0.5 to 65 MPa and measuring proteoglycan biosynthesis, cell viability, and water content immediately after impaction and 24 hours later. We found that proteoglycan biosynthesis decreased and water content increased with increasing impact stress. However, there appeared to be a critical threshold stress (15–20 MPa) that caused cell death and apparent rupture of the collagen fiber matrix at the time of impaction. We concluded that the cell death and collagen rupture are responsible for the observed alterations in the tissue’s metabolism and water content, respectively, although the exact mechanism causing this damage could not be determined.