Articular changes in experimentally induced patellar trauma

Triantafillopoulos, Ioannis K.; Papagelopoulos, Panayiotis J.; Politi, Panorea K; Nikiforidis, P.

doi:10.1007/s001670100248

Cited by 6 publications

(4 citation statements)

References 33 publications

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“…These alterations gradually became more slight and may be interpreted as a compensatory response. Similar data are presented by other authors [13,14]. Likewise, we observed decreased destruction of the native cartilage and development of some pannus and clusters of active chondrocytes in the cartilage after 12 weeks.…”

Section: Discussionsupporting

confidence: 92%

Can low concentrations of Papain help repair articular cartilage defects?

2007

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Abstract:In the present study, we investigate the capability of low concentrations of Papain to stimulate cartilage mesenchymal cells proliferation and transformation to chondrocytes and evaluate the healing capability of partial thickness defects in medial condyle cartilage of 30 rabbits' knee joints. Papain 0.1 mg/ml and Ringer saline l ml each were injected intra-articularly to rabbits of experimental and control groups (15 animals each). Healthy cartilage from lateral condyle and cartilage from medial condyle where the surgical defect was created were studied histologically and by TEM. The study revealed that 0.1 mg/ml Papain activates proliferation and spreading of mesenchymal stem cells to young forms of chondrocyte from perichondrium to the upper layers of healthy cartilage. In only 22.27% cases of the experimental group, surgical defects filled with cartilaginous tissue on the background of distinct destruction of collagenous matrix in the native cartilage. However, in 55.5% of the control group the defect was spontaneously healed by hyaline cartilaginous tissue completely or partially on the basis of slight destruction of collagenous matrix. The defect site was filled with activated chondrocyte-like cells from the subchondral plate (not perichondrium) in both groups, which acquired some cisterns of rough endoplasmic reticulum (RER) and produced matrix proteins. The results suggest that Papain did not ameliorate the recovery of cartilage defects acquired through surgically-induced injury of collagenous matrix in native cartilage. We observed that articular cartilage is the source of mesenchymal stem cells which have the ability to transform into young forms of chondrocytes. This transformation process depends on the level of destruction of native cartilage collagen matrix induced by the defect or by Papain.

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Section: Discussionsupporting

confidence: 92%

Can low concentrations of Papain help repair articular cartilage defects?

2007

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“…The most dramatic injuries can produce a complete loss of mechanical function and mobility [210], with the potential to affect the mechanical integrity of adjacent spinal levels [214]. In addition, nonphysiologic acute loading below that needed to induce a fracture of the facet can also lead to osteoarthritis [234,239,240] and the development of degenerative joint disease [52,55]. In fact, facet joint degeneration can be triggered or accelerated by an injury or a trauma to the facet or its surrounding tissues.…”

Section: Structural Damage Of Cartilage Alters Its Mechanicalmentioning

confidence: 99%

Spinal Facet Joint Biomechanics and Mechanotransduction in Normal, Injury and Degenerative Conditions

Jaumard¹,

Welch²,

Winkelstein³

2011

J. Biomech. Eng.

276

225

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The facet joint is a crucial anatomic region of the spine owing to its biomechanical role in facilitating articulation of the vertebrae of the spinal column. It is a diarthrodial joint with opposing articular cartilage surfaces that provide a low friction environment and a ligamentous capsule that encloses the joint space. Together with the disc, the bilateral facet joints transfer loads and guide and constrain motions in the spine due to their geometry and mechanical function. Although a great deal of research has focused on defining the biomechanics of the spine and the form and function of the disc, the facet joint has only recently become the focus of experimental, computational and clinical studies. This mechanical behavior ensures the normal health and function of the spine during physiologic loading but can also lead to its dysfunction when the tissues of the facet joint are altered either by injury, degeneration or as a result of surgical modification of the spine. The anatomical, biomechanical and physiological characteristics of the facet joints in the cervical and lumbar spines have become the focus of increased attention recently with the advent of surgical procedures of the spine, such as disc repair and replacement, which may impact facet responses. Accordingly, this review summarizes the relevant anatomy and biomechanics of the facet joint and the individual tissues that comprise it. In order to better understand the physiological implications of tissue loading in all conditions, a review of mechanotransduction pathways in the cartilage, ligament and bone is also presented ranging from the tissue-level scale to cellular modifications. With this context, experimental studies are summarized as they relate to the most common modifications that alter the biomechanics and health of the spine-injury and degeneration. In addition, many computational and finite element models have been developed that enable more-detailed and specific investigations of the facet joint and its tissues than are provided by experimental approaches and also that expand their utility for the field of biomechanics. These are also reviewed to provide a more complete summary of the current knowledge of facet joint mechanics. Overall, the goal of this review is to present a comprehensive review of the breadth and depth of knowledge regarding the mechanical and adaptive responses of the facet joint and its tissues across a variety of relevant size scales.

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“…Clinically, two different kinds of OD can be discriminated: a juvenile OD, characterised by an OD with open epiphyses and an adult form in patients with closed growth plates. While the juvenile OD affects young males from 10 to 20 years of age twice as frequently when compared to female teenagers, the adult form does not show this disequilibrium of occurrence [39,77]. Teenagers practising high impact sport activities such as running, tennis, squash or contact sports present more frequently with OD when compared to less active children or young adults [38].…”

Section: Epidemiology Of Osteochondritis Dissecansmentioning

confidence: 99%

“…Forty percent of athletes who had been diagnosed with traumatic cartilage defects in their youth showed, within 14 years, clinical signs of OA [58]. In summary, most studies indicate knee injuries to significantly increase the risk for OA [15,22,24,39,42,46,50,58,59,67,69,77].…”

Section: Course Of Spontaneous and Circumscribed Cartilage Defectsmentioning

confidence: 99%