Chondral injuries are common lesions of the knee joint. Variety of causes results to chondral injury, such as trauma, aging degeneration and infection. Currently, many treatments are available for chondral injury, such as physical therapy, lifestyle modification, pharmacological medications with non-steroid anti-inflammatory drugs (NSAID) or glucosamine, and intra-articular injection of Hyaluronan . The very limited capability for self repair and subsequent degeneration of injuried cartilage and other articular tissues often lead to osteoarthritis, which may eventually lead to the need for total knee arthroplasty . However, the better treatments for chondral injury should not only target the symptoms of the patient but also promote biological repair of the destructed articular cartilage tissue.
Ultrasound is a form of mechanical energy that can be transmitted into the biological tissue as high frequency acoustical pressure waves. It was used as a diagnostic and therapeutic tool. The therapeutic ultrasound achieves its biological result such as muscle pain relief and decrease of joint stiffness by increasing the temperature of the tissue, with intensities ranging from 1 to 3 W/cm2. In contrast, the intensities of diagnostic images are of much lower level (0.5 to 50 mW/cm2) without thermogenic and destructive actions. Low-intensity pulsed ultrasound (LIPUS) is a recommended therapy to treat fractures with non-union and promotes bone union clinically [3–8]. Application of high-intensity continuous ultrasound generates considerable heat in living tissues, whereas LIPUS (< 100 mW/cm2) has much lower intensity with non-thermogenic and non-destructive actions.
Previous studies presented the LIPUS enhances the endochondral ossification in the healing process of fractured bone and promote bone formation, possibly by inducing chondrocyte proliferation [4–8]. It also regulated vascular endothelial growth factor (VEGF) expression in early fracture healing phase and subsequent chondrogenesis . Furthermore, some in vitro studies demonstrated the LIPUS may potentially protect cartilage by inhibiting matrix metalloproteinase-13 (MMP-13) mRNA expression, and stimulate chondrocyte proliferation and matrix production in chondrocytes [10–12]. It also has been reported to promote the mRNA expression of type II collagen, type X collagen, aggrecan, and transforming growth factor (TGF)-ß in chondrocytes . In this context, the effect of LIPUS on articular cartilage metabolism has been characterized.
Most animal studies that analyze the histological and biochemical changes in osteoarthritis are anterior cruciate ligament (ACL) transection model in canines or partial meniscus resection model in rabbits or rats, which result to joint instability and induced cartilage degeneration gradually [14–18]. However, the studies had difficulties in controlling the consistency of the cartilage injuries among the animals.
We designed an experimental rabbit model of severe articular cartilage injury to evaluate the effect of cartilage repair. Surgically created defects of full-thickness cartilage were performed to build consistent severe cartilage injuries. The destruction of the full-thickness cartilage could be controlled, and the effect of cartilage repair could be evaluated quantitatively. Following the model, we investigated the effect of LIPUS on cartilage repair.