Effects of in vivo cyclic compressive loading on the distribution of local Col2 and superficial lubricin in rat knee cartilage

This study aimed to examine the effects of an episode of in vivo cyclic loading on rat knee articular cartilage (AC) under medium‐term observation, while also investigating relevant factors associated with the progression of post‐traumatic osteoarthritis (PTOA). Twelve‐week‐old Wistar rats underwent...

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Published inJournal of orthopaedic research Vol. 39; no. 3; pp. 543 - 552
Main Authors Ji, Xiang, Ito, Akira, Nakahata, Akihiro, Nishitani, Kohei, Kuroki, Hiroshi, Aoyama, Tomoki
Format Journal Article
LanguageEnglish
Published United States 01.03.2021
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ISSN0736-0266
1554-527X
1554-527X
DOI10.1002/jor.24812

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Abstract This study aimed to examine the effects of an episode of in vivo cyclic loading on rat knee articular cartilage (AC) under medium‐term observation, while also investigating relevant factors associated with the progression of post‐traumatic osteoarthritis (PTOA). Twelve‐week‐old Wistar rats underwent one episode comprising 60 cycles of 20 N or 50 N dynamic compression on the right knee joint. Spatiotemporal changes in the AC after loading were evaluated using histology and immunohistochemistry at 3 days and 1, 2, 4, and 8 weeks after loading (n = 6 for each condition). Chondrocyte vitality was assessed at 1, 3, 6, and 12 hours after loading (n = 2 for each condition). A localized AC lesion on the lateral femoral condyle was confirmed in all subjects. The surface and intermediate cartilage in the affected area degenerated after loading, but the calcified cartilage remained intact. Expression of type II collagen in the lesion cartilage was upregulated after loading, whereas the superficial lubricin layer was eroded in response to cyclic compression. However, the distribution of superficial lubricin gradually recovered to the normal level 4 weeks after loading‐induced injury. We confirmed that 60 repetitions of cyclic loading exceeding 20 N could result in cartilage damage in the rat knee. Endogenous repairs in well‐structured joints work well to rebuild protective layers on the lesion cartilage surface, which may be the latent factor delaying the progression of PTOA. This study investigated the appropriate cyclic compression loading approach associated with the progression of post‐traumatic osteoarthritis on Rat model, and newly found localized type II collagen upregulated within 3 days after loading and superficial lubricin decreased immediately after damage yet recovered gradually to the normal level.
AbstractList This study aimed to examine the effects of an episode of in vivo cyclic loading on rat knee articular cartilage (AC) under medium‐term observation, while also investigating relevant factors associated with the progression of post‐traumatic osteoarthritis (PTOA). Twelve‐week‐old Wistar rats underwent one episode comprising 60 cycles of 20 N or 50 N dynamic compression on the right knee joint. Spatiotemporal changes in the AC after loading were evaluated using histology and immunohistochemistry at 3 days and 1, 2, 4, and 8 weeks after loading (n = 6 for each condition). Chondrocyte vitality was assessed at 1, 3, 6, and 12 hours after loading (n = 2 for each condition). A localized AC lesion on the lateral femoral condyle was confirmed in all subjects. The surface and intermediate cartilage in the affected area degenerated after loading, but the calcified cartilage remained intact. Expression of type II collagen in the lesion cartilage was upregulated after loading, whereas the superficial lubricin layer was eroded in response to cyclic compression. However, the distribution of superficial lubricin gradually recovered to the normal level 4 weeks after loading‐induced injury. We confirmed that 60 repetitions of cyclic loading exceeding 20 N could result in cartilage damage in the rat knee. Endogenous repairs in well‐structured joints work well to rebuild protective layers on the lesion cartilage surface, which may be the latent factor delaying the progression of PTOA. This study investigated the appropriate cyclic compression loading approach associated with the progression of post‐traumatic osteoarthritis on Rat model, and newly found localized type II collagen upregulated within 3 days after loading and superficial lubricin decreased immediately after damage yet recovered gradually to the normal level.
This study aimed to examine the effects of an episode of in vivo cyclic loading on rat knee articular cartilage (AC) under medium-term observation, while also investigating relevant factors associated with the progression of post-traumatic osteoarthritis (PTOA). Twelve-week-old Wistar rats underwent one episode comprising 60 cycles of 20 N or 50 N dynamic compression on the right knee joint. Spatiotemporal changes in the AC after loading were evaluated using histology and immunohistochemistry at 3 days and 1, 2, 4, and 8 weeks after loading (n = 6 for each condition). Chondrocyte vitality was assessed at 1, 3, 6, and 12 hours after loading (n = 2 for each condition). A localized AC lesion on the lateral femoral condyle was confirmed in all subjects. The surface and intermediate cartilage in the affected area degenerated after loading, but the calcified cartilage remained intact. Expression of type II collagen in the lesion cartilage was upregulated after loading, whereas the superficial lubricin layer was eroded in response to cyclic compression. However, the distribution of superficial lubricin gradually recovered to the normal level 4 weeks after loading-induced injury. We confirmed that 60 repetitions of cyclic loading exceeding 20 N could result in cartilage damage in the rat knee. Endogenous repairs in well-structured joints work well to rebuild protective layers on the lesion cartilage surface, which may be the latent factor delaying the progression of PTOA.
This study aimed to examine the effects of an episode of in vivo cyclic loading on rat knee articular cartilage (AC) under medium-term observation, while also investigating relevant factors associated with the progression of post-traumatic osteoarthritis (PTOA). Twelve-week-old Wistar rats underwent one episode comprising 60 cycles of 20 N or 50 N dynamic compression on the right knee joint. Spatiotemporal changes in the AC after loading were evaluated using histology and immunohistochemistry at 3 days and 1, 2, 4, and 8 weeks after loading (n = 6 for each condition). Chondrocyte vitality was assessed at 1, 3, 6, and 12 hours after loading (n = 2 for each condition). A localized AC lesion on the lateral femoral condyle was confirmed in all subjects. The surface and intermediate cartilage in the affected area degenerated after loading, but the calcified cartilage remained intact. Expression of type II collagen in the lesion cartilage was upregulated after loading, whereas the superficial lubricin layer was eroded in response to cyclic compression. However, the distribution of superficial lubricin gradually recovered to the normal level 4 weeks after loading-induced injury. We confirmed that 60 repetitions of cyclic loading exceeding 20 N could result in cartilage damage in the rat knee. Endogenous repairs in well-structured joints work well to rebuild protective layers on the lesion cartilage surface, which may be the latent factor delaying the progression of PTOA.This study aimed to examine the effects of an episode of in vivo cyclic loading on rat knee articular cartilage (AC) under medium-term observation, while also investigating relevant factors associated with the progression of post-traumatic osteoarthritis (PTOA). Twelve-week-old Wistar rats underwent one episode comprising 60 cycles of 20 N or 50 N dynamic compression on the right knee joint. Spatiotemporal changes in the AC after loading were evaluated using histology and immunohistochemistry at 3 days and 1, 2, 4, and 8 weeks after loading (n = 6 for each condition). Chondrocyte vitality was assessed at 1, 3, 6, and 12 hours after loading (n = 2 for each condition). A localized AC lesion on the lateral femoral condyle was confirmed in all subjects. The surface and intermediate cartilage in the affected area degenerated after loading, but the calcified cartilage remained intact. Expression of type II collagen in the lesion cartilage was upregulated after loading, whereas the superficial lubricin layer was eroded in response to cyclic compression. However, the distribution of superficial lubricin gradually recovered to the normal level 4 weeks after loading-induced injury. We confirmed that 60 repetitions of cyclic loading exceeding 20 N could result in cartilage damage in the rat knee. Endogenous repairs in well-structured joints work well to rebuild protective layers on the lesion cartilage surface, which may be the latent factor delaying the progression of PTOA.
Author Nishitani, Kohei
Aoyama, Tomoki
Nakahata, Akihiro
Ji, Xiang
Kuroki, Hiroshi
Ito, Akira
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Issue 3
Keywords type II collagen
cartilage degeneration
rat model
post-traumatic osteoarthritis
in vivo cyclic compression
superficial lubricin
Language English
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Snippet This study aimed to examine the effects of an episode of in vivo cyclic loading on rat knee articular cartilage (AC) under medium‐term observation, while also...
This study aimed to examine the effects of an episode of in vivo cyclic loading on rat knee articular cartilage (AC) under medium-term observation, while also...
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SubjectTerms ADAMTS5 Protein - metabolism
Animals
cartilage degeneration
Cartilage, Articular - physiology
Chondrocytes - physiology
Collagen Type II - metabolism
in vivo cyclic compression
Knee Joint - physiology
Male
Matrix Metalloproteinase 13 - metabolism
post‐traumatic osteoarthritis
Proteoglycans - metabolism
Random Allocation
rat model
Rats
Rats, Wistar
superficial lubricin
type II collagen
Weight-Bearing
Title Effects of in vivo cyclic compressive loading on the distribution of local Col2 and superficial lubricin in rat knee cartilage
URI https://onlinelibrary.wiley.com/doi/abs/10.1002%2Fjor.24812
https://www.ncbi.nlm.nih.gov/pubmed/32716572
https://www.proquest.com/docview/2427518049
Volume 39
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