Cellular Responses of Embryonic Hyaline Cartilage to Experimental Wounding In Vitro

Walker, Elizabeth A.; Verner, A.; Flannery, Carl R.; Archer, Charles W.

doi:10.2106/00004623-200005000-00035

Cited by 13 publications

(19 citation statements)

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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%

“…Unfortunately, based on this study design we can not differentiate the effects of the arthroscope approach from the cartilage lesion that was created. Second, no cartilage metabolic analysis such as MTT conversion and proteoglycan 35 S incorporation was performed in this study because the size of the PARC lesion was not large enough for these analyses. Third, this study was designed to evaluate a PARC lesion that did not lead to global OA in the joint; therefore it was different from studies utilizing ACL transaction or thermal treatment to induce joint instability as a trigger for development of OA.…”

Section: Discussionmentioning

confidence: 99%

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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%

Section: Discussionmentioning

confidence: 99%

Development of partial thickness articular cartilage injury in an ovine model

Markel

Swain

et al. 2006

Journal Orthopaedic Research

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“…It has advantages compared with other animal models: (1) when similar diameters are used, the effect of cartilage repair techniques can be monitored without the confounding effects of other potential causes of cartilage degeneration; (2) the operation is relatively simple and creates circumscribed cartilage lesions; (3) repair of these chronic partial-thickness articular cartilage lesions occurs with surrounding degeneration, which resembles the clinical situation [9,12,17,23,29,32]; and (4) cartilage lesions are created on the medial femoral condyle, which is the most commonly affected zone of articular cartilage damage observed with arthroscopies in humans [6,10,11]. Existing animal models intended to replicate human OA fail to resemble the clinical situation of a focal cartilage lesion, whereas the permanent trigger for degeneration will interfere with attempts of cartilage repair or regeneration [15,31].…”

Section: Discussionmentioning

confidence: 99%

Development of Partial-thickness Articular Cartilage Injury in a Rabbit Model

Jansen

Emans

Rhijn

et al. 2008

Clinical Orthopaedics &Amp; Related Research

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In humans, partial-thickness cartilage lesions frequently result in premature osteoarthritis. While rabbits often are used as a model for partial-thickness cartilage lesions, the natural course of cartilage surrounding such a lesion is largely unknown. We developed a rabbit model of a chronic partial-thickness cartilage defect and asked whether these defects led to (1) deterioration of surrounding cartilage macroscopically and microscopically (increased Mankin score) and (2) disturbances in proteoglycan metabolism. In 55 rabbits, we created a 4-mmdiameter partial-thickness cartilage defect on one medial femoral condyle. The surrounding cartilage was characterized during the course of 26 weeks. Contralateral knees were sham-operated. In experimental knees, we found cartilage softening and fibrillation at 13 and 26 weeks.High Mankin scores observed at 1 week were partially restored at 13 weeks but worsened later and were most pronounced at 26 weeks. Mankin scores in the experimental groups were worse at 1 and 26 weeks when compared with the sham groups. Mankin scores at 26 weeks improved compared with 1 week in the sham groups. Disturbances in proteoglycan metabolism were less evident. In this rabbit model, a partial-thickness cartilage lesion resulted in early markers of degenerative changes resembling the human situation.

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“…Trauma due to repetitive impact and sudden movements such as twisting of the joint, as seen in high impact sports, can cause damage to the joint, normally resulting in swelling and pain (Buckwalter, 2002). Due to the inability o f cartilage to effectively repair itself, these injuries can in a number o f cases A number of studies looking at the events subsequent to wounding have been performed in cartilage from both bovine (Tew et al, 2000) and chick cartilage (Walker et al, 2000). The initial events which appear to follow wounding are a zone of cell death adjacent to the wound edge, termed the 'zone o f necrosis' (Stockwell, 1979) This response occurs later than the initiation of cell death and the reason for this increase in proliferation is not known.…”

Section: Articular Cartilage Injuriesmentioning

confidence: 99%

“…The initial events which appear to follow wounding are a zone of cell death adjacent to the wound edge, termed the 'zone o f necrosis' (Stockwell, 1979) This response occurs later than the initiation of cell death and the reason for this increase in proliferation is not known. It has been hypothesised however, that chondrocytes adjacent to the 'zone of necrosis' may have been exposed to increased concentrations of 'survival factors' causing their proliferative response (Walker et al, 2000). In addition, cells within this zone o f proliferation appear to up-regulate their expression of the integrin subunits, a5…”

Section: Articular Cartilage Injuriesmentioning

confidence: 99%

Novel strategies for enhancing tissue integration in cartilage repair

Davies

Caterson

Duance

2004

Int J Experimental Path

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Introduction Articular cartilage is unable to initiate a spontaneous repair response when injured due to its avascular and aneural properties. Within adult cartilage, chondrocytes are entrapped within an extensive extracellular matrix and are unable to migrate to sights of injury to regulate tissue repair. Injury to this tissue therefore inevitably leads to degeneration of the cartilage and the development of degenerative diseases such as osteoarthritis. The surgical technique of autologous chondrocyte transplantation (ACT) was developed for the treatment of full‐thickness cartilage defects (Brittberg et al. 1994). Implantation of chondrocytes into the defect site repairs the injury site with a mixture of fibrocartilaginous and hyaline‐like tissue that poorly integrates with the existing cartilage and frequently degenerates with time. In this current study, we have developed an in vitro model to investigate methods for enhancing this integration and the development of a more biomechanically stable repair tissue. Materials and methods Bovine articular cartilage explants from the metacarpalphalangeal joint were experimentally injured using a stainless steel trephine and cultured for a period of 28 days. Autologous chondrocytes in an agarose suspension were injected into the interface region at the injury site. Media was collected and analysed for proteoglycan and collagen content using the DMMB and hydroxyproline assays, respectively. Matrix metalloproteinase (MMP) expression was also analysed using zymography and an adapted collagen fibril assay. Results Morphological analyses indicate attempts at repair and integration within both control and experimental treatment groups, although the presence of autologous chondrocytes appeared to amplify this repair response. Although not statistically significant, considerable differences in proteoglycan release between injured explants and the intact control group were seen. Collagen release into the media was only seen at day 28 within experimental cultures. An up‐regulation of MMP‐2 and MMP‐9 was seen within the experimental cultures compared to the controls. Preliminary data also suggest up‐regulation of collagenases in the experimental group when compared to controls. Discussion As seen with clinical ACT treatment, the presence of autologous chondrocytes appears to enhance repair and integration attempts; however, morphologically, this repair tissue appears to be fibrocartilaginous. Further analysis will establish whether the repair tissue is true hyaline cartilage and monitor the synthesis and turnover of macromolecules within the established culture system.

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Cellular Responses of Embryonic Hyaline Cartilage to Experimental Wounding In Vitro

Cited by 13 publications

References 0 publications

Development of partial thickness articular cartilage injury in an ovine model

Development of partial thickness articular cartilage injury in an ovine model

Development of Partial-thickness Articular Cartilage Injury in a Rabbit Model

Novel strategies for enhancing tissue integration in cartilage repair

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