Abstract
OBJECTIVE: To determine the percentage of apoptotic cells in a contusion model of osteoarthritis (OA) and to assess whether intra-articular injection of high doses of hyaluronic acid (HA) immediately after trauma reduces chondrocyte apoptosis. METHODS: Forty knees from adult rabbits were impacted thrice with a 1 kg block released through a 1 meter tall cylinder (29.4 Joules). Subsequently, 2 mL of HA was injected in one knee and 2 mL saline in the contra-lateral knee. Medication were administered twice a week for 30 days, when animals were sacrificed. Specimens were prepared for optical microscopy exam and terminal deoxynucleotidyl transferase end labeling assay (TUNEL). RESULTS: The apoptosis rate in the contusion model was 68.01% (± 19.73%), a higher rate than previously described. HA significantly reduced the rate of apoptosis to 53.52% (± 18.09) (p <0.001). CONCLUSION: Intra-articular HA administration started immediately after trauma reduces impact-induced chondrocyte apoptosis rates in rabbits. Level of Evidence I, Experimental Study.
Highlights
Articular cartilage has a limited reparative capacity.[1]
We observed that apoptosis in the knees that received hyaluronic acid (Figure 3) was lower than the control knees (p
The impacted chondrocytes die by necrosis or after, by activation of a specific metabolic cascade that triggers apoptosis;[22] this suggests the presence of a therapeutic window in which the process could be inhibited
Summary
Articular cartilage has a limited reparative capacity.[1]. Histological studies have shown the occurrence of chondrocyte death (apoptosis or necrosis) in response to trauma.[1,2,3] Apoptosis was studied in other tissues and cells, and various inducers were identified, including chemical agents, cytokines, viral and bacterial pathogens, and thermal injuries.[4,5] This programmed cell death process plays a critical role in embryonic development and homeostasis.[6]. High apoptosis rates help explain the occurrence of post-traumatic osteoarthritis, even in intra-articular fractures anatomically fixed.[12] Prevention of post-traumatic arthrosis is directly related to the prevention of apoptosis.[13] Many pharmacologic agents can block apoptosis and enhance cell survival Some of these agents include inhibitors of caspases (cysteine-dependent aspartate specific proteases), glucosamine, diacerein, hyaluronic acid, platelet rich plasma and osteogenic -1 protein (OP-1).[14,15,16,17,18,19] The intra-articular injection (IA) of glucosamine in rabbits played a chondroprotective effect, reducing the degradation of articular cartilage while suppressing synovitis.[15] In dogs, IA and intravenous (IV) injection of hyaluronic acid (HA) suppressed chondrocytes apoptosis after surgical resection of the anterior cruciate ligament (ACL),[18] as well as after cartilage damage mediated by fibronectin fragments.[20] A progressive increase in the number of apoptotic cells starting six hours after the trauma has been noticed, providing a potential therapeutic window in the first six hours after injury.[13] In rabbits, the immediate and continuous administration of diacerein for three months after injury reduced post-traumatic osteoarthritis, as well as the use of platelet-rich plasma (PRP).[16] HA can slow the degeneration of articular cartilage and inhibit the production of reactive oxygen species and prostaglandin E2; the hypothesis raised is that early administration of HA reduces apoptosis of chondrocytes after injury. The objective of this study was to evaluate whether high doses of HA may reduce or inhibit apoptosis subsequent to a postcontusional model of OA,[17] and whether the model is low, medium or high energy, since it has not been described for measuring apoptosis
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