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Full-thickness cartilage defects are repaired via a microfracture technique and intraarticular injection of the small-molecule compound kartogenin.

Xu X, Shi D, Shen Y, Xu Z, Dai J, Chen D, Teng H, Jiang Q - Arthritis Res. Ther. (2015)

Bottom Line: At 4 weeks, group 1 showed better defect filling and a greater number of chondrocyte-like cells compared with group 2.At 12 weeks, group 1 showed statistically significantly higher ICRS scores and modified O'Driscoll scores compared with group 2.More hyaline cartilage-like tissue was found in the defects of group 1 at 12 weeks.

View Article: PubMed Central - PubMed

Affiliation: The Center of Diagnosis and Treatment for Joint Disease, Drum Tower Hospital, Medical School, Nanjing University, Zhongshan Road 321, Nanjing, 210008, Jiangsu, China. xuxingquan12345@163.com.

ABSTRACT

Introduction: Microfracture does not properly repair full-thickness cartilage defects. The purpose of this study was to evaluate the effect of intraarticular injection of the small-molecule compound kartogenin (KGN) on the restoration of a full-thickness cartilage defect treated with microfracture in a rabbit model.

Methods: Full-thickness cartilage defects (3.5 mm in diameter and 3 mm in depth) were created in the patellar groove of the right femurs of 24 female New Zealand White rabbits. The rabbits were divided into two groups (12 in each group) based on postsurgery treatment differences, as follows: microfracture plus weekly intraarticular injection of KGN (group 1) and microfracture plus dimethyl sulfoxide (group 2). Six rabbits from each group were illed at 4 and 12 weeks after surgery, and their knees were harvested. The outcome was assessed both macroscopically, by using the International Cartilage Repair Society (ICRS) macroscopic evaluation system, and histologically, by using the modified O'Driscoll histologic scoring system. Immunohistochemistry for type II and I collagen was also conducted.

Results: At 4 weeks, group 1 showed better defect filling and a greater number of chondrocyte-like cells compared with group 2. At 12 weeks, group 1 showed statistically significantly higher ICRS scores and modified O'Driscoll scores compared with group 2. More hyaline cartilage-like tissue was found in the defects of group 1 at 12 weeks.

Conclusions: Intraarticular injection of KGN enhances the quality of full-thickness cartilage defects repair after microfracture, with better defect filling and increased hyaline-like cartilage formation.

No MeSH data available.


Related in: MedlinePlus

Best, mean and worst results of safranin O staining in experimental (A, C and E) and control group (B, D and F) at 12 weeks. (A) The repair tissue showed homogenous intense safranin O staining. Tidemark formation was observed, and subchondral bone formation was good. The surface was not smooth, with fibrous tissue existing. (C) The staining of the repair tissue was homogenously intense. No fissues or cracks were seen. But, no tidemark formation was observed. (E) Subchondral bone formation was poor with a large crack in the center of the repair tissue. But, safranin O staining was still intense in the extracellular matrix (ECM) of the repair tissue. No tidemark formation was found. (B) The ECM of the repair tissue was stained slightly and heterogeneously. The surface was not regular. No tidemark formation was seen. Subchondral bone formation was not good. (D) The repair tissue was stained negatively. No tidemark formation was seen, and subchondral bone formation was poor. (F) Little subchondral bone was seen. Safranin O staining was negative in the ECM of the repair tissue. All the magnification was 20X.
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Fig4: Best, mean and worst results of safranin O staining in experimental (A, C and E) and control group (B, D and F) at 12 weeks. (A) The repair tissue showed homogenous intense safranin O staining. Tidemark formation was observed, and subchondral bone formation was good. The surface was not smooth, with fibrous tissue existing. (C) The staining of the repair tissue was homogenously intense. No fissues or cracks were seen. But, no tidemark formation was observed. (E) Subchondral bone formation was poor with a large crack in the center of the repair tissue. But, safranin O staining was still intense in the extracellular matrix (ECM) of the repair tissue. No tidemark formation was found. (B) The ECM of the repair tissue was stained slightly and heterogeneously. The surface was not regular. No tidemark formation was seen. Subchondral bone formation was not good. (D) The repair tissue was stained negatively. No tidemark formation was seen, and subchondral bone formation was poor. (F) Little subchondral bone was seen. Safranin O staining was negative in the ECM of the repair tissue. All the magnification was 20X.

Mentions: Histological analysis of the repair tissue in group 1 showed the formation of hyaline cartilage-like tissue. At 4 weeks, Toluidine blue staining revealed a larger amount of positively stained repair tissue in the defects in group 1 than in group 2 (Figure 2A, C). At 12 weeks, Toluidine blue staining (Figure 3) and Safranin O staining (Figure 4A, C and E) were used to assess the proteoglycans content in the repair tissue and showed three grades of intensity. Intense homogeneous staining of Toluidine blue and Safranin O at 12 weeks demonstrated that the defects in the majority of the specimens (5 of 6) were almost completely reconstructed (Figure 3; Figure 4A, C and E). Both the lateral and basal integration were satisfactory, and the subchondral bone was properly formed. In addition, well organized repair tissue was observed in the best repaired specimen (1 of 6) with nearly complete tidemark formation and nearly normal cell distribution. However, a penetrating crack was still detected in the repair tissue of the least repaired specimen (1 of 6).Figure 2


Full-thickness cartilage defects are repaired via a microfracture technique and intraarticular injection of the small-molecule compound kartogenin.

Xu X, Shi D, Shen Y, Xu Z, Dai J, Chen D, Teng H, Jiang Q - Arthritis Res. Ther. (2015)

Best, mean and worst results of safranin O staining in experimental (A, C and E) and control group (B, D and F) at 12 weeks. (A) The repair tissue showed homogenous intense safranin O staining. Tidemark formation was observed, and subchondral bone formation was good. The surface was not smooth, with fibrous tissue existing. (C) The staining of the repair tissue was homogenously intense. No fissues or cracks were seen. But, no tidemark formation was observed. (E) Subchondral bone formation was poor with a large crack in the center of the repair tissue. But, safranin O staining was still intense in the extracellular matrix (ECM) of the repair tissue. No tidemark formation was found. (B) The ECM of the repair tissue was stained slightly and heterogeneously. The surface was not regular. No tidemark formation was seen. Subchondral bone formation was not good. (D) The repair tissue was stained negatively. No tidemark formation was seen, and subchondral bone formation was poor. (F) Little subchondral bone was seen. Safranin O staining was negative in the ECM of the repair tissue. All the magnification was 20X.
© Copyright Policy - open-access
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4376363&req=5

Fig4: Best, mean and worst results of safranin O staining in experimental (A, C and E) and control group (B, D and F) at 12 weeks. (A) The repair tissue showed homogenous intense safranin O staining. Tidemark formation was observed, and subchondral bone formation was good. The surface was not smooth, with fibrous tissue existing. (C) The staining of the repair tissue was homogenously intense. No fissues or cracks were seen. But, no tidemark formation was observed. (E) Subchondral bone formation was poor with a large crack in the center of the repair tissue. But, safranin O staining was still intense in the extracellular matrix (ECM) of the repair tissue. No tidemark formation was found. (B) The ECM of the repair tissue was stained slightly and heterogeneously. The surface was not regular. No tidemark formation was seen. Subchondral bone formation was not good. (D) The repair tissue was stained negatively. No tidemark formation was seen, and subchondral bone formation was poor. (F) Little subchondral bone was seen. Safranin O staining was negative in the ECM of the repair tissue. All the magnification was 20X.
Mentions: Histological analysis of the repair tissue in group 1 showed the formation of hyaline cartilage-like tissue. At 4 weeks, Toluidine blue staining revealed a larger amount of positively stained repair tissue in the defects in group 1 than in group 2 (Figure 2A, C). At 12 weeks, Toluidine blue staining (Figure 3) and Safranin O staining (Figure 4A, C and E) were used to assess the proteoglycans content in the repair tissue and showed three grades of intensity. Intense homogeneous staining of Toluidine blue and Safranin O at 12 weeks demonstrated that the defects in the majority of the specimens (5 of 6) were almost completely reconstructed (Figure 3; Figure 4A, C and E). Both the lateral and basal integration were satisfactory, and the subchondral bone was properly formed. In addition, well organized repair tissue was observed in the best repaired specimen (1 of 6) with nearly complete tidemark formation and nearly normal cell distribution. However, a penetrating crack was still detected in the repair tissue of the least repaired specimen (1 of 6).Figure 2

Bottom Line: At 4 weeks, group 1 showed better defect filling and a greater number of chondrocyte-like cells compared with group 2.At 12 weeks, group 1 showed statistically significantly higher ICRS scores and modified O'Driscoll scores compared with group 2.More hyaline cartilage-like tissue was found in the defects of group 1 at 12 weeks.

View Article: PubMed Central - PubMed

Affiliation: The Center of Diagnosis and Treatment for Joint Disease, Drum Tower Hospital, Medical School, Nanjing University, Zhongshan Road 321, Nanjing, 210008, Jiangsu, China. xuxingquan12345@163.com.

ABSTRACT

Introduction: Microfracture does not properly repair full-thickness cartilage defects. The purpose of this study was to evaluate the effect of intraarticular injection of the small-molecule compound kartogenin (KGN) on the restoration of a full-thickness cartilage defect treated with microfracture in a rabbit model.

Methods: Full-thickness cartilage defects (3.5 mm in diameter and 3 mm in depth) were created in the patellar groove of the right femurs of 24 female New Zealand White rabbits. The rabbits were divided into two groups (12 in each group) based on postsurgery treatment differences, as follows: microfracture plus weekly intraarticular injection of KGN (group 1) and microfracture plus dimethyl sulfoxide (group 2). Six rabbits from each group were illed at 4 and 12 weeks after surgery, and their knees were harvested. The outcome was assessed both macroscopically, by using the International Cartilage Repair Society (ICRS) macroscopic evaluation system, and histologically, by using the modified O'Driscoll histologic scoring system. Immunohistochemistry for type II and I collagen was also conducted.

Results: At 4 weeks, group 1 showed better defect filling and a greater number of chondrocyte-like cells compared with group 2. At 12 weeks, group 1 showed statistically significantly higher ICRS scores and modified O'Driscoll scores compared with group 2. More hyaline cartilage-like tissue was found in the defects of group 1 at 12 weeks.

Conclusions: Intraarticular injection of KGN enhances the quality of full-thickness cartilage defects repair after microfracture, with better defect filling and increased hyaline-like cartilage formation.

No MeSH data available.


Related in: MedlinePlus