Very rapid clearance after a joint bleed in the canine knee cannot prevent adverse effects on cartilage and synovial tissue

Abstract

Blood is cleared very rapidly from the canine knee joint, but already has adverse effects on both cartilage and synovial tissue within that short time span. This rapid clearance can play a role in the discrepancy between long-term in vitro and in vivo effects of blood-induced joint damage since more than 10% v/v blood present for at least 48 h is needed to induce long-term adverse effects in vitro.

Biochemical markers of joint tissue damage increase shortly after a joint bleed; an explorative human and canine in vivo study

“…Four blood injections in the left knee were given in four successive days, because of the rapid clearance of blood from the canine joint in contrast to humans 14 . As previously shown, this results in a period of at least 4 days continuous blood exposure with at least 20% v/v blood and leads to mild progressive cartilage damage and synovitis over time mimicking HA 13,14 .…”

Ammonium–Chloride–Potassium Lysing Buffer Treatment of Fully Differentiated Cells Increases Cell Purity and Resulting Neotissue Functional Properties

“…10 Even rapid clearance of a joint bleed in a canine knee in vivo resulted in reduced proteoglycan synthesis rates in exposed cartilage. 11 It also contributed to synovial changes, which caused proteoglycan release from healthy cartilage. 11 The mechanism by which chondrocytes become apoptotic after exposure to blood is unclear.…”

“…11 It also contributed to synovial changes, which caused proteoglycan release from healthy cartilage. 11 The mechanism by which chondrocytes become apoptotic after exposure to blood is unclear. It has been suggested that hydrogen peroxide production by chondrocytes as a result of IL1b stimulation, in combination with hemoglobin-derived iron, causes an increase in free radical formation, which permanently damages chondrocytes.…”

“…7 Crucially, it has been shown that even short-term exposure of cartilage to blood induces chondrocyte apoptosis. [10][11][12] Second, in a clinical setting, autologous or allogeneic cartilage grafts are often taken from adult tissues, which exhibit matrix degradation, surface defects, and fibrillation. 13 Diseased cartilage, such as in osteoarthritis, experiences enhanced ECM degeneration and contains chondrocytes of altered phenotypes.…”

Haemophilic arthropathy

“…In the past, usual clinical practice allowed for a tacit, moderate degree of tolerance for sporadic intraarticular hemorrhages, based on the clinical observation that joints were able to tolerate an infrequent bleed with little or no harm. However, increasing knowledge on the pathophysiology of hemarthrosis in vitro and in vivo, as well as in clinical experiments, indicates that we need to move towards a more stringent policy with regards to the prevention of occasional and subclinical intraarticular hemorrhages [1][2][3].…”