Chondrocyte Apoptosis and Decrease of Glycosaminoglycan in Cranial Cruciate Ligament Insertion after Resection in Rabbits

Hattori, Satoshi; Sakane, Masataka; Mutsuzaki, Hirotaka; Tanaka, Junzo; Ochiai, Naoyuki; Nakajima, Hiromi

doi:10.1292/jvms.69.253

Cited by 12 publications

(30 citation statements)

References 25 publications

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“…In this study, the chondrocyte apoptosis rate in normal insertions was similar to those in previous reports of calcified cartilage layer in ACL insertion of rabbits [5] and articular cartilage of mice and rats [11]. The chondrocyte apoptosis rate in normal insertions was lower than that in the ruptured ACL group.…”

Section: Discussionsupporting

confidence: 90%

“…Previously, we reported that histological degenerative changes of the cartilage layer due to chondrocyte apoptosis in a ruptured ACL tibial insertion progress with time, particularly in the first 2 months [4]. We also reported that 2 and 4 weeks after ACL resection in rabbits, the percentages of TUNEL-positive chondrocytes were significantly higher than those in the shamoperated group, and histological changes occurred 6 weeks after the resection [5]. In our present study, we observed that approximately 30% of chondrocytes were apoptotic in ruptured ACL insertions and approximately 10% of chondrocytes in normal insertions.…”

Section: Discussionmentioning

confidence: 70%

“…We compared the percentage of TUNELpositive chondrocytes, the percentage of PCNApositive chondrocytes, the average thickness of the cartilage layer, the average thickness of the GAGstained area, and the number of chondrocytes per millimeter between the ruptured ACL group and the normal ACL group. Our histomorphometrical analysis method was described in our previous report [4,5]. The data of the ruptured ACL group and the normal ACL group were compared using unpaired Student's t test at a p < 0.05 significance value.…”

Section: Methodsmentioning

confidence: 99%

“…Moreover, we reported that 2 and 4 weeks after ACL resection in rabbits, the average percentages of TUNEL-positive chondrocytes were significantly higher than those in the sham-operated group, and histological changes occurred 6 weeks after the resection [5]. Homeostasis is achieved by balance between cell death and proliferation in tissue.…”

Section: Introductionmentioning

confidence: 99%

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Cell death and cell proliferation in cartilage layers in human anterior cruciate ligament tibial insertions after rupture

Mutsuzaki

Sakane

Honda

et al. 2010

Connective Tissue Research

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The purpose of this study is to investigate cellular responses and histological changes of cartilaginous layers in human anterior cruciate ligament (ACL) tibial insertions after rupture compared with those in normal insertions. Fully 16 tibial insertions of ruptured ACLs were obtained during primary ACL reconstructions. We also obtained 16 normal ACL tibial insertions from cadavers. Terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate-biotin nick end labeling (TUNEL) to detect apoptosis, proliferating cell nuclear antigen (PCNA) staining, and histological examination were performed. The percentage of TUNEL-positive chondrocytes in ruptured ACL insertions (30.2 +/- 15.6%) was higher than that in normal insertions (9.6 +/- 5.8%). The percentage of PCNA-positive chondrocytes was significantly different between ruptured ACL insertions (19.9 +/- 15.0%) and normal insertions (12.3 +/- 7.3%). The average thickness of the cartilage layer, the glycosaminoglycan-stained area, and the number of chondrocytes per millimeter in ruptured ACL insertions was smaller than those in normal insertions. The decrease in the number of chondrocytes owing to an imbalance between cell death and cell proliferation in the ACL insertions after rupture, as compared with normal insertions, may lead to histological changes of the cartilage layer in the insertions. An in-depth understanding of injured ACL insertion may help elucidate the etiology of histological changes and the function and significance of the existence of the cartilage layer of insertion. This understanding may help in developing optimal treatment protocols for ACL injuries if apoptosis and cell proliferation are controlled.

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Section: Discussionsupporting

confidence: 90%

Section: Discussionmentioning

confidence: 70%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Cell death and cell proliferation in cartilage layers in human anterior cruciate ligament tibial insertions after rupture

Mutsuzaki

Sakane

Honda

et al. 2010

Connective Tissue Research

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“…These studies reported that the increased apoptosis chondral tissue was related to chondral degeneration. 19,[22][23][24][25] This study has some limitations. Six weeks of follow-up is a short-term period to observe a longacting drug such as ZA.…”

Section: Discussionmentioning

confidence: 95%

Zoledronic Acid Effect on Chondrocyte Apoptosis in Degenerative Osteoarthritis Model

Uysal

Özkoç

Bolat

et al. 2016

International Surgery

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Apoptosis refers to cell death without inflammatory process, and is related to degenerative changes in joints. We hypothesized that zoledronic acid (ZA) would have a positive effect on chondrocyte viability and decreases in chondrocyte loss, which are important for the progression of degeneration. This study aimed to reveal the difference in time-dependent apoptotic changes in cartilage tissue in the anterior cruciate ligament (ACL) transection model of osteoarthritis (OA) in rat knees after treatment with zoledronic acid. We randomly divided 48 male Wistar albino rats into 6 groups. The knees of all rats except those in the control group underwent the operation for ACL transection. ZA for half of the rats and saline solution for the others was injected weekly into knees. Animals were killed at 0, 3, and 6 weeks after surgery. Apoptosis of chondrocytes were analyzed using the terminal deoxynucleotidyl transferase dUTP nick end labeling method. Comparison of groups was performed using Kruskal Wallis analysis and the Mann Whitney U test. Significant differences were observed between the groups treated with ZA and saline. ZA treatment significantly decreased the number of apoptotic cells in chondral tissue. ZA prevents time-dependent degenerative changes in chondral tissue by decreasing chondrocyte death. Intra-articular ZA may have the potential to treat and conserve chondral viability. ZA prevents chondrocyte loss and may play a therapeutic role in OA and conserving joint health. Further studies are needed to evaluate the potential of intraarticular ZA for the prevention or treatment of age-related degenerative changes.Key words: Apoptosis -Osteoarthritis -Cartilage -Zoledronic acid -Chondrocyte O steoarthritis (OA) has been considered to be, primarily, a cartilage disorder resulting from the changes in matrix composition of cartilage and the reduction of tissue cellularity. OA cartilage was initially thought to occur through loss of chondrocytes. 1 The factors that trigger the initial chondrocyte destruction still are not sufficiently apparent. OA is also associated with subchondral and periarticular bone changes.2 Increased subchondral turnover leads to changes in subchondral bone architecture.3 Apoptosis or programmed cell death represents a physiologic form of cell death that does not induce an inflammatory response. Recent studies have reported that apoptosis plays a major role in cell death in cartilage tissue. [4][5][6][7][8] In some studies, it was also suggested that osteoarthritic cartilage has shown that apoptosis has also been positively correlated with the severity of cartilage destruction and matrix depletion. [4][5][6]9 Bisphosphonates (BPs), which are the inhibitors of osteoclastic activity, show their therapeutic action by inhibition of bone remodeling. Higher rates of bone turnover is associated with progression of OA.10 BP has a protective effect against the development of osteoarthritic changes.11,12 Zoledronic acid (ZA), a third-generation BP, is the most potent form of its kind, so only smal...

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Anterior cruciate ligament insertion after partial tear: histological changes and chondrocyte turnover

Sakane

Mutsuzaki

Nakajima

et al. 2011

Knee Surg Sports Traumatol Arthrosc

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The GAG layer thicknesses in the UF and CF layers in the remaining ligament area increased up to 4 weeks and gradually decreased until 8 weeks owing to an imbalance between chondrocyte apoptosis and proliferation. If the reactions in humans are similar to those observed in the rabbits, we consider that augmentation for ligament reconstruction and partial repair should be performed within at least 1 month after injury, before insertion degeneration occurs.

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Chondrocyte Apoptosis and Decrease of Glycosaminoglycan in Cranial Cruciate Ligament Insertion after Resection in Rabbits

Cited by 12 publications

References 25 publications

Cell death and cell proliferation in cartilage layers in human anterior cruciate ligament tibial insertions after rupture

Cell death and cell proliferation in cartilage layers in human anterior cruciate ligament tibial insertions after rupture

Zoledronic Acid Effect on Chondrocyte Apoptosis in Degenerative Osteoarthritis Model

Anterior cruciate ligament insertion after partial tear: histological changes and chondrocyte turnover

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