cartilage injury and degeneration are leading causes of disability. Animal studies are critically important to developing effective treatments for cartilage injuries. This review focuses on the use of animal models for the study of the repair and regeneration of focal cartilage defects. Animals commonly used in cartilage repair studies include murine, lapine, canine, caprine, porcine, and equine models. There are advantages and disadvantages to each model. Small animal rodent and lapine models are cost effective, easy to house, and useful for pilot and proof-of-concept studies. The availability of transgenic and knockout mice provide opportunities for mechanistic in vivo study. Athymic mice and rats are additionally useful for evaluating the cartilage repair potential of human cells and tissues. Their small joint size, thin cartilage, and greater potential for intrinsic healing than humans, however, limit the translational value of small animal models. Large animal models with thicker articular cartilage permit study of both partial thickness and full thickness chondral repair, as well as osteochondral repair. Joint size and cartilage thickness for canine, caprine, and mini-pig models remain significantly smaller than that of humans. The repair and regeneration of chondral and osteochondral defects of size and volume comparable to that of clinically significant human lesions can be reliably studied primarily in equine models. While larger animals may more closely approximate the human clinical situation, they carry greater logistical, financial, and ethical considerations. A multifactorial analysis of each animal model should be carried out when planning in vivo studies. Ultimately, the scientific goals of the study will be critical in determining the appropriate animal model.

Transtibial single bundle anterior cruciate ligament (ACL) reconstruction has been the gold standard for several years. This technique often fails to restore native ACL femoral origin and tibial insertion anatomy of the ACL. Recently, there is a strong trend towards a more anatomical approach in single and double bundle ACL reconstruction. Using the anatomic double bundle structure of the ACL as a principle, the entirety of both tibial insertion and femoral origin of both bundles, the posterolateral and anteromedial, may be restored. Reflected by recent publications over the past two years, there is an increasing interest in the anatomy of the ACL. In the current study, a PubMed literature search was performed looking for measurements of the ACL femoral origin and tibial insertion. These studies show a large variability in the size and the anatomy of the femoral origin and tibial ACL insertion using different methods and specimens. The diversity of reported measurements makes clinical application of these data difficult at best. Thus, it is of paramount importance to understand the individual variations in size and shape of the ACL femoral origin and tibial ACL insertion. This study is a systematic review of the morphology of the ACL femoral origin and tibial insertion as reported in the literature.

There is a large variation in size of the anterior cruciate ligament insertion sites and the AM and PL bundles. Additionally, there are significant but weak correlations between the size of the insertions and height, weight, and body mass index of the individual patient.

This in vivo study showing reduced chondrocyte density without cartilage tissue loss six months after a single intra-articular injection of 0.5% bupivacaine suggests bupivacaine toxicity. The effects of bupivacaine were milder than those of an injection of 0.6% monoiodoacetate, which resulted in chondrolysis over the same time period.

Background Impact injury to articular cartilage can lead to posttraumatic osteoarthritis. Hypotheses This study tests the hypotheses that (1) chondrocyte injury occurs after impact at energies insufficient to fracture the cartilage surface, and that (2) cartilage injury patterns vary with impact energy, time after injury, and cartilage thickness. Study Design Controlled laboratory study. Methods Fresh bovine osteochondral cores were randomly divided into 5 groups: (1) control, (2) 0.35 J, (3) 0.71 J, (4) 1.07 J, and (5) 1.43 J impact energies. Cores were subjected to computer-controlled impact loading and full-thickness sections were then prepared and incubated in Dulbecco's Modified Eagle's Medium/F12 at 37°C. Adjacent sections were harvested 1 and 4 days after impact for viability staining and fluorescent imaging. The area of dead and living chondrocytes was quantified using custom image analysis software and reported as a percentage of total cartilage area. Results The highest impact energy fractured the cartilage in all cores (1.43 J, n = 17). Seventy-three percent and 64% of the osteochondral cores remained intact after lower energy impacts of 0.71 J and 1.07 J, respectively. At lower energy levels, fractured cores were thinner (P < .01) than those remaining intact. In cores remaining intact after impact injury, chondrocyte death increased with increasing impact energy (P < .05) and with greater time after impact (P < .05). A progressive increase in dead cells near the bone/cartilage interface and at the articular surface was observed. Conclusion These data showing progressive chondrocyte death after impact injury at energies insufficient to fracture the cartilage surface demonstrate a potential need for early chondroprotective therapy. Clinical Relevance These data show that efforts to reduce chondrocyte morbidity after joint injury may be a useful strategy to delay or prevent the onset of posttraumatic osteoarthritis.