The reactions of articular cartilage to experimental wounding: Role of apoptosis

Tew, Simon R.; Kwan, Alan Shu Khen; Hann, A. C.; Thomson, B.M.; Archer, Charles W.

doi:10.1002/1529-0131(200001)43:1<215::aid-anr26>3.0.co;2-x

Cited by 229 publications

(181 citation statements)

References 37 publications

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“…However, there are indications that the apoptosis accounts for the cell death after the creation of lesions in cultured fetal sternal cartilage. 34,35 Histologic analysis demonstrated that the fissures or clefts created by the Dremel tool in the treated area continued to progress to deeper levels over time as affirmed by SEM images shown in Figure 6. This finding implies that repetitive loading on the treated area after surgery degraded the articular cartilage matrix and initiated progressive cartilage degeneration and fibrillation as other investigators have reported.…”

Section: Discussionmentioning

confidence: 80%

Development of partial thickness articular cartilage injury in an ovine model

Markel

Swain

et al. 2006

Journal Orthopaedic Research

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The purpose of this study was to create a controlled partial thickness cartilage lesion in a sheep model, and to provide a foundation to study the natural history of the progression of this lesion. Twenty-eight sheep divided into four groups (1, 12, 24, and 52 weeks, n ¼ 7/group) were used in this study. In one stifle, a mechanical tool was used to create a 200 mm partial thickness lesion (1.5 Â 1.5 cm 2 ) on the medial femoral condyle via arthroscopy. Joint fluid was drawn presurgery and after euthanasia for analysis of collage II 3/4 C long (C2C). After euthanasia, the condyle was analyzed by gross appearance, confocal laser microscopy (CLM) for cell viability, scanning electronic microscopy (SEM) for surface roughness, Artscan for cartilage stiffness, and histology for cartilage morphology. The gross appearance of the treated area appeared rough, soft, and swollen compared to untreated control over time. CLM demonstrated that the depth of cell death increased to 590 mm at 52 weeks after surgery. SEM demonstrated that the treated area became more irregular over time. Stiffness of the treated area was significantly less than control by 12 weeks after surgery. Histologic analysis demonstrated that the 12, 24, and 52 week groups had significantly poorer histologic scores than the 1 week group. Joint fluid analysis demonstrated that the treatment group at 1 week had significant higher levels of C2C than the pretreatment baseline data. The results of this study demonstrated that partial thickness injury of cartilage continued to propagate and degenerate over time in this sheep model. Options for the prevention or treatment of this lesion may be tested using this model in the future. ß

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Section: Discussionmentioning

confidence: 80%

Development of partial thickness articular cartilage injury in an ovine model

Markel

Swain

et al. 2006

Journal Orthopaedic Research

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“…A mechanical injury to articular cartilage results in chondrocyte death and matrix degradation [7,19,22]. Articular cartilage heals poorly.…”

Section: Introductionmentioning

confidence: 99%

Increasing the Osmolarity of Joint Irrigation Solutions May Avoid Injury to Cartilage: A Pilot Study

Amin

Huntley

Simpson

et al. 2010

Clinical Orthopaedics &Amp; Related Research

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Saline (0.9%, 285 mOsm) and Hartmann's solution (255 mOsm) are two commonly used joint irrigation solutions that alter the extracellular osmolarity of in situ chondrocytes during articular surgery. We asked whether varying the osmolarity of these solutions influences in situ chondrocyte death in mechanically injured articular cartilage. We initially exposed osteochondral tissue harvested from the metacarpophalangeal joints of 3-year-old cows to solutions of 0.9% saline and Hartmann's solution of different osmolarity (100-600 mOsm) for 2 minutes to allow in situ chondrocytes to respond to the altered osmotic environment. The full thickness of articular cartilage then was ''injured'' with a fresh scalpel. Using confocal laser scanning microscopy, in situ chondrocyte death at the injured cartilage edge was quantified spatially as a function of osmolarity at 2.5 hours. Increasing the osmolarity of 0.9% saline and Hartmann's solution to 600 mOsm decreased in situ chondrocyte death in the superficial zone of injured cartilage. Compared with 0.9% saline, Hartmann's solution was associated with greater chondrocyte death in the superficial zone of injured cartilage, but not when the osmolarity of both solutions was increased to 600 mOsm. These experiments may have implications for the design of irrigation solutions used during arthroscopic and open articular surgery.

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“…The success rates with these treatments vary greatly. While some of these approaches show promise, many lead to formation of fibrous tissue, apoptosis, and further cartilage degeneration (1)(2)(3)(4)(5)(6). To address the need for improved therapies to promote cartilage repair or regeneration, a number of novel tissue engineering approaches have been developed for the treatment of cartilage defects or osteoarthritis.…”

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confidence: 99%

Potent induction of chondrocytic differentiation of human adipose‐derived adult stem cells by bone morphogenetic protein 6

Estes

Guilak

2006

Arthritis & Rheumatism

269

212

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Objective. Recent studies have identified an abundant source of multipotent progenitor cells in subcutaneous human adipose tissue, termed human adiposederived adult stem cells (ADAS cells). In response to specific media formulations, including transforming growth factor ␤1 (TGF␤1), these cells exhibit significant ability to differentiate into a chondrocyte-like phenotype, expressing cartilage-specific genes and proteins such as aggrecan and type II collagen. However, the influence of other growth factors on the chondrogenic differentiation of ADAS cells is not fully understood. This study was undertaken to investigate the effects of TGF␤1, TGF␤3, insulin-like growth factor 1, bone morphogenetic protein 6 (BMP-6), and dexamethasone, in various combinations, on the chondrogenic potential of ADAS cells in alginate beads.Methods. The chondrogenic response of alginateencapsulated ADAS cells was measured by quantitative polymerase chain reaction, 3 H-proline and 35 S-sulfate incorporation, and immunolabeling for specific extracellular matrix components.Results. Significant differences in chondrogenesis were observed under the different culture conditions for all outcomes measured. Most notably, BMP-6 upregulated AGC1 and COL2A1 expression by an average of 205-fold and 38-fold, respectively, over day-0 controls, while down-regulating COL10A1 expression by ϳ2-fold.Conclusion. These findings suggest that BMP-6 is a potent inducer of chondrogenesis in ADAS cells, in contrast to mesenchymal stem cells, which exhibit increased expression of type X collagen and a hypertrophic phenotype in response to BMP-6. Combinations of growth factors containing BMP-6 may provide a novel means of regulating the differentiation of ADAS cells for applications in the tissue-engineered repair or regeneration of articular cartilage.

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The reactions of articular cartilage to experimental wounding: Role of apoptosis

Cited by 229 publications

References 37 publications

Development of partial thickness articular cartilage injury in an ovine model

Development of partial thickness articular cartilage injury in an ovine model

Increasing the Osmolarity of Joint Irrigation Solutions May Avoid Injury to Cartilage: A Pilot Study

Potent induction of chondrocytic differentiation of human adipose‐derived adult stem cells by bone morphogenetic protein 6

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