Intraoperative hyperspectral imaging (HSI) as a new diagnostic tool for the detection of cartilage degeneration

To investigate, whether hyperspectral imaging (HSI) is able to reliably differentiate between healthy and damaged cartilage tissue. A prospective diagnostic study was performed including 21 patients undergoing open knee surgery. HSI data were acquired during surgery, and the joint surface’s cartilage was assessed according to the ICRS cartilage injury score. The HSI system records light spectra from 500 to 1000 nm and generates several parameters including tissue water index (TWI) and the absorbance at 960 nm and 540 nm. Receiver operating characteristic curves were calculated to assess test parameters for threshold values of HSI. Areas with a cartilage defect ICRS grade ≥ 3 showed a significantly lower TWI (p = 0.026) and higher values for 540 nm (p < 0.001). No difference was seen for 960 nm (p = 0.244). For a threshold of 540 nm > 0.74, a cartilage defect ICRS grade ≥ 3 could be detected with a sensitivity of 0.81 and a specificity of 0.81. TWI was not suitable for cartilage defect detection. HSI can provide reliable parameters to differentiate healthy and damaged cartilage. Our data clearly suggest that the difference in absorbance at 540 nm would be the best parameter to achieve accurate identification of damaged cartilage.

Effect of Type 1 Collagen Bioactive Material Scaffold on the Recovery of Sports-Caused Cartilage Injury

This study was aim to investigate the effect of type 1 collagen (Col I) bioactive scaffold on regeneration and repair of motor cartilage injury. Fifteen New Zealand rabbits were randomly divided into sham operation group (Sham group, only cartilage was exposed, no defect was made), model group Focal cortical dysplasias (FCD) group, cartilage defect model], and treatment group (Col I group, cartilage defect + Col I bioactive scaffold treatment). The cartilage tissue of each group was detected 16 weeks after the operation. Immunohistochemistry and Western Blot were adopted to detect the expression of cartilage related proteins in each group. The results showed that Col I bioactive scaffold could repair the gross morphology of cartilage defect, promote the regeneration and repair of chondrocytes in defect area, and reduce the mast cells in defect area. Western Blot detection of the expression of signal pathway marker proteins showed that expression of Wnt protein, β-catenin protein, and phosphofructokinase-1 (PFK-1) protein in the FCD group were significantly reduced than Sham group (P < 0.05), while the expression of phosphoenolpyruvate carboxykinase 1 (PEPCK1) protein was significantly increased (P < 0.05). Expression of Wnt protein, β-catenin protein, and PFK-1 protein in Col I group increased significantly versus FCD group (P < 0.05), while the expression of PEPCK1 protein significantly decreased (P < 0.05). In conclusion, Col I bioactive scaffolds could regenerate and repair cartilage defects, and the mechanism may be related to Wnt signaling pathway and glycolysis/gluconeogenesis pathway.

Mussel inspired injectable chitosan hydrogel modified with catechol for cell adhesion and cartilage defect repair

Repairing articular cartilage defect is a great challenge due to the poor self-regenerative capability of cartilage. Hydrogel-based tissue engineering has been considered as an effective strategy. In this study, inspired...

Time Matters: Knee Cartilage Defect Expansion and High-Grade Lesion Formation while Awaiting Autologous Chondrocyte Implantation

Objective The objective of this study was to assess potential risk factors, including time delay until implantation, for knee cartilage defect expansion or new high-grade defect formation between biopsy and Autologous Chondrocyte Implantation (ACI) or Matrix Autologous Chondrocyte Implantation (MACI). Study design Consecutive knee ACI and MACI cases by a single surgeon ( n = 111) were reviewed. The relationship between time between biopsy and staged implantation and (1) progression in primary cartilage defect size and (2) development of a new high-grade (Outerbridge grade ≥3) cartilage defect were determined with adjustment for demographics, body mass index, smoking status, coronal alignment, initial cartilage status, and prior surgery. Results Average size of the primary defect at time of biopsy was 4.50 cm2. Mean time to chondrocyte implantation was 155 days. Defect expansion increased 0.11 cm2 (standard error = 0.03) per month delay to implantation ( P = 0.001). Independent predictors of defect expansion were male sex, smaller initial defect size, and delay to implantation (adjusted mean = 0.15 cm2 expansion per month). A total of 16.2% of patients ( n = 18/111) developed a new high-grade defect. Independent predictors of a new secondary defect were Outerbridge grade 2 changes (vs. 0-1) on the surface opposing the index defect and delayed implantation (per month increase, adjusted odds ratio = 1.21, 95% confidence interval: 1.01-1.44; P = 0.036). Conclusions Patients undergoing 2-stage cell-based cartilage restoration with either ACI or MACI demonstrated long delays between stages of surgery, placing them at risk for expanding defects and development of new high-grade cartilage defects. Patients who were male, had smaller initial defect size, and longer time between surgeries were at greater risk for defect expansion. Level of Evidence III, retrospective comparative study.

Zonal-Layered Chondrocyte Sheets for Repairment of Full-Thickness Articular Cartilage Defect: A Mini-Pig Model

The cell sheet technique is a promising approach for tissue engineering, and the present study is aimed to determine a better configuration of cell sheets for cartilage repair. For stratified chondrocyte sheets (S-CS), articular chondrocytes isolated from superficial, middle, and deep zones were stacked accordingly. Heterogeneous chondrocyte sheets (H-CS) were obtained by mixing zonal chondrocytes. The expressions of chondrocytes, cytokine markers, and glycosaminoglycan (GAG) production were assessed in an in vitro assay. The curative effect was investigated in an in vivo porcine osteochondral defect model. The S-CS showed a higher cell viability, proliferation rate, expression of chondrogenic markers, secretion of tissue inhibitor of metalloproteinase, and GAG production level than the H-CS group. The expressions of ECM destruction enzyme and proinflammatory cytokines were lower in the S-CS group. In the mini-pigs articular cartilage defect model, the S-CS group had a higher International Cartilage Repair Society (ICRS) macroscopic score and displayed a zonal structure that more closely resembled the native cartilage than those implanted with the H-CS. Our study demonstrated that the application of the S-CS increased the hyaline cartilage formation and improved the surgical outcome of chondrocyte implication, offering a better tissue engineering strategy for treating articular cartilage defects.

A New Method to Develop the Primate Model of Knee Osteoarthritis With Focal Cartilage Defect

Objective: Osteoarthritis (OA) is a common degenerative joint disease, and animal models have proven pivotal in investigating this disease. This study aimed to develop a primate model of OA that may be more relevant to research studies on OA in humans.Method: Twelve female rhesus macaques were randomly divided into three groups. Four animals were untreated (Control group); four were subjected to the modified Hulth method, involving cutting of the anterior and posterior cruciate ligaments, and transecting the meniscus (Hulth group); and four were subjected to the modified Hulth method combined with cartilage defect (MHCD group). Each primate was subjected to motor ability tests, and underwent arthroscopic, radiographic, morphological, and pathological observation of the knee joints at various times for up to 180 days.Results: Motor ability on Day 180 was significantly lower in the MHCD group than in the Control (p＜0.01) and Hulth (p＜0.05) groups. Radiographic and morphological examination showed that the severity of knee joint deformity and articular cartilage injury were greater in the MHCD group than in the other groups. Pathological examination showed that cartilage thickness was significantly lower in the MHCD group than in the other groups at the same time points. The Mankin score on Day 180 was markedly higher in the MHCD group than in the Hulth (p＜0.05) and Control (p＜0.001) groups.Conclusion: The MHCD model of OA closely resembles the pathophysiological processes of spontaneous knee OA in humans. The time required to develop knee OA is shorter using the MHCD model than using the Hulth method.

Hyaluronic acid hydrogel encapsulated BMP-14-modified ADSCs accelerate cartilage defect repair in rabbits

Background Cartilage defect has a limited capacity to heal. In this context, we hypothesized that hyaluronic acid (HA) hydrogel encapsulated BMP-14-modified adipose-derived mesenchymal stem cells (ADSCs) could accelerate cartilage defect repair in rabbits. Methods ADSCs were isolated and identified by flow cytometry. ADSCs were treated with adenovirus vector encoding BMP-14 (Ad-BMP-14) or adenovirus vector encoding control (Ad-ctrl). Real-time PCR (RT-PCR) and western blot assay was performed to verify the transfection efficacy and chondrogenic differentiation markers (ACAN, Collagen II and SOX9). Rabbit cartilage defect model was performed and randomly divided into following groups: control group, HA hydrogel + ADSCs, ADSCs, HA hydrogel + BMP-14 transfected ADSCs, HA hydrogel + BMP-14 transfected ADSCs. At 6, 9 and 12 weeks after surgery, scanning electron microscopy, hematoxylin–eosin, Safranin-O/Fast Green and immunohistochemical staining for Collagen II were performed to determine the role of HA hydrogel encapsulated BMP-14-modified ADSCs in cartilage repair in vivo. Results ADSCs were successfully isolated and positively expressed CD29, CD44 and CD90. Transfection efficacy of Ad-BMP-14 was verified by RT-PCR and western blot assay. Moreover, Ad-BMP-14 could significantly increased chondrogenic differentiation markers (ACAN, Collagen II and SOX9). The LV-BMP-14-ADSCs and HA hydrogel + LV-BMP-14-ADSCs groups revealed smoother surface cartilage repair that was level with the surrounding cartilage and almost complete border integration. Conclusions HA hydrogel encapsulated BMP-14-modified ADSCs accelerate cartilage defect repair in rabbits. We need to further validate the specific mechanism of action of HA hydrogel encapsulated LV-BMP-14-ADSCs involved in the repairing cartilage damage in vivo.