Management of severe tracheal anomalies remains a clinical challenge. Tissue engineering offers new hope in trachea reconstruction surgery. However to date no optimal technique achieved in the formation of human or animal trachea. The main problem lies on the biomaterial used and the complex city of forming trachea in vivo. This study was aimed at creating tissue-engineered trachea cartilage from easily accessible human and animal nasal septum cartilage using internal scaffold and biodegradable human and animal fibrin.
Absorbable Implants ; Chondrocytes/pathology ; Chondrocytes/*transplantation ; Mice, Nude ; Polyethylene ; *Tissue Engineering ; Trachea/pathology ; Trachea/*surgery

OBJECTIVETo study the evaluation of bipolar radiofrequency (RFE) chondroplasty to cartilage injure.

METHODSSixteen goats underwent resection of anterior cruciate and medial meniscus to create cartilage injured model. Bipolar frequency energy chondroplasty were performed on injured articular cartilage 3 months after operation. The left knee was regarded as sham-operated control. The zero time effects and later changes of radiofrequency on cartilage surface and chondrocytes were observed.

RESULTSAt zero time, the rough injured surface became smooth, and clefts were melted. Some chondrocytes were dead in the superficial layer, cells in deeper layer remained alive. Three months later, the surface of the articular was smoother than the sham-operated side. The histological modified Mankin' s score of cartilage was significantly higher than the sham-operated side (operated side 12 +/- 4; sham-operated side 14 +/- 5, P < 0.01). The result of Fluorescence-activated cell sorter (FACs) showed that there were no obvious difference of dead chondrocyte between operated side and sham-operated side, (24 +/- 10)% and (12 +/- 1)% (P > 0.05).

CONCLUSIONSBipolar radiofrequency energy (1 grade) does not create more chondrocyte death than the sham-operated side. Bipolar radiofrequency chondroplasty is an appropriate method to treat articular cartilage injury.

Animals ; Cartilage, Articular ; injuries ; pathology ; surgery ; Catheter Ablation ; Chondrocytes ; pathology ; Disease Models, Animal ; Female ; Goats ; Male

OBJECTIVETo trace the pathological changes of the cultured autologous chondrocytes mass after implanted in cartilage defects and investigate the pathophysiological mechanisms of the antologous chondrocytes mass transplantation in the repair of cartilage defects.

METHODSTwenty-four New Zealand white rabbits of 4 to 6 month-old and weighing more than 3.0 kg (female and male was unrestricted) were randomly divided into experiment group and the control group. For 12 rabbits of experiment group, the cartilage defects were repaired with the autologous chondrocytes mass and sealed with one piece of periosteum. Firstly, cartilage tissue of 10 to 30 mg was obtained from the shoulder of the rabbits after anaesthetized by 1 mg/kg 20% sumianxin. Then, chondrocytes were isolated from the cartilage tissue with 0.2% type II collagenase digestion and were cultured in DMEM/F-12 supplemented with 20% fetal bovine serum (FBS), 50 microg/ml ascorbic acid-2-phosphate, 0.4 mM proline, 5 microg/ml insulin and 1 mM non-essential amino acids (NEAA) in flasks in vitro. The cells were harvested until a thin film of the cells covered the bottom of the flask could be seen with naked eyes. Then the film was collected with a curled glass stick and formed a solid mass. On this time, the animal was anaesthetized again and the full-thickness cartilage square defect of 4.0 mm x 6.0 mm was fabricated in the patellar grove of distal femur, and then the cellular mass was transplanted into the defect covered by one piece of periosteum which obtained from the upper anterior of tibia and sealed with the femoral condyles. For 12 rabbits of the control group, the defects were sealed with one piece of periosteum only. The animals were sacrificed in the 1st, 3rd, 6th and 12th weeks after the operation respectively. The histologic sections were stained with safranin O-fast green, hematoxylin-eosin (H&E) and picric acid-Sirius red and immunostained for type II collagen and aggrecan.

RESULTSIn the 1st week, the transplanted cells oriented to articular surface differentiated to matured hyaline chondrocytes and excrete large amount cartilage matrix. In the 3rd week, the trend was more obvious and the periosteum was union to the cell mass. In the 12th week, the defects were repaired with hyaline-like cartilage tissue, and in the 24th week, the repair tissue turned to matured hyaline cartilage. In the control group, the defects were repaired with fibrocartilage tissues.

CONCLUSIONIt was evidenced that the defects were repaired by the autologous chondrocytes mass transplantation. The procedure was gradual and initialed from up toward joint to down to the deep of the defect.

Animals ; Cartilage, Articular ; pathology ; surgery ; Chondrocytes ; transplantation ; Female ; Knee Joint ; pathology ; surgery ; Male ; Rabbits ; Transplantation, Autologous

The Wnt signaling exists in every kinds of species and regulates a variety of biological processes including cell fate, proliferation and function, immunity, stress, apoptosis and so on. During the researching, Wnt signaling also plays an important role in chondrocyte differentiation and maturation. So it has been the new spot in pathogenesis of osteoarthritis study.
Animals ; Chondrocytes ; metabolism ; pathology ; Humans ; Osteoarthritis ; metabolism ; pathology ; Signal Transduction ; Wnt Proteins ; metabolism

Osteoarthritis (OA) is a prevalent degenerative joint disease characterized by cartilage loss and accounts for a major source of pain and disability worldwide. However, effective strategies for cartilage repair are lacking, and patients with advanced OA usually need joint replacement. Better comprehending OA pathogenesis may lead to transformative therapeutics. Recently studies have reported that exosomes act as a new means of cell-to-cell communication by delivering multiple bioactive molecules to create a particular microenvironment that tunes cartilage behavior. Specifically, exosome cargos, such as noncoding RNAs (ncRNAs) and proteins, play a crucial role in OA progression by regulating the proliferation, apoptosis, autophagy, and inflammatory response of joint cells, rendering them promising candidates for OA monitoring and treatment. This review systematically summarizes the current insight regarding the biogenesis and function of exosomes and their potential as therapeutic tools targeting cell-to-cell communication in OA, suggesting new realms to improve OA management.
Apoptosis ; Cartilage/pathology* ; Cartilage, Articular/metabolism* ; Cell Communication ; Chondrocytes/metabolism* ; Exosomes/pathology* ; Humans ; Osteoarthritis/therapy*

OBJECTIVETo investigate the gene expression and potential functions of transforming growth factor-beta1 in osteophyte development.

METHODSA total of 25 specimens were obtained from individuals undergoing total knee arthroplasty due to severe primary osteoarthritis. Tissue samples were embedded in paraffin wax and made into sections. Hematoxylin and eosin and toluidine blue stainings were performed. The expressions of collagen I, IIa, IIb, and X were detected by immunohistochemistry. Based on the histomorphology of cellularity and matrix abundance, the glycosaminoglycans content, and the differential expressions of collagen I, IIa, IIb, and X, the osteophytic tissues were classified. For each different type of osteophyte, expressions of transforming growth factor-beta1 were detected by immunohistochemistry and in situ hybridization, and results were analyzed using the image analysis system.

RESULTSFive different types of osteophytes were identified as type I, type II, type III, type IV, and type V. Transforming growth factor-beta1 mRNA was more and intensely expressed in chondrocytes of type II and III osteophytes, and was less in other types of osteophytes. The difference was significant (P<0.05, P<0.01).

CONCLUSIONTransforming growth factor-beta1 mRNA is mainly expressed in early-mid stages of osteophytes and may play an important role in promoting the proliferation and differentiation of chondrocytes in the early stages of osteophyte development.

Chondrocytes ; metabolism ; pathology ; Humans ; Osteoarthritis, Knee ; metabolism ; pathology ; Osteophyte ; metabolism ; pathology ; RNA, Messenger ; biosynthesis ; Transforming Growth Factor beta1 ; biosynthesis ; genetics

The progressive destruction of condylar cartilage is a hallmark of the temporomandibular joint (TMJ) osteoarthritis (OA); however, its mechanism is incompletely understood. Here, we show that Kindlin-2, a key focal adhesion protein, is strongly detected in cells of mandibular condylar cartilage in mice. We find that genetic ablation of Kindlin-2 in aggrecan-expressing condylar chondrocytes induces multiple spontaneous osteoarthritic lesions, including progressive cartilage loss and deformation, surface fissures, and ectopic cartilage and bone formation in TMJ. Kindlin-2 loss significantly downregulates the expression of aggrecan, Col2a1 and Proteoglycan 4 (Prg4), all anabolic extracellular matrix proteins, and promotes catabolic metabolism in TMJ cartilage by inducing expression of Runx2 and Mmp13 in condylar chondrocytes. Kindlin-2 loss decreases TMJ chondrocyte proliferation in condylar cartilages. Furthermore, Kindlin-2 loss promotes the release of cytochrome c as well as caspase 3 activation, and accelerates chondrocyte apoptosis in vitro and TMJ. Collectively, these findings reveal a crucial role of Kindlin-2 in condylar chondrocytes to maintain TMJ homeostasis.
Aggrecans/metabolism* ; Animals ; Cartilage, Articular/metabolism* ; Chondrocytes/pathology* ; Cytoskeletal Proteins/metabolism* ; Mice ; Muscle Proteins/metabolism* ; Osteoarthritis/pathology* ; Temporomandibular Joint/pathology*

OBJECTIVETo assess the value of magnetic resonance imaging (MRI) T2 mapping in quantitative evaluation of cartilage repair following matrix-associated autologous chondrocyte transplantation (MACT).

METHODSSix patients (with 9 plug cartilages) following MACT underwent MRI on a 3.0 Tesla MR scan system at 3, 6 and 12 months after the surgery. The full-thickness and zonal areas (deep and superficial layers) T2 values were calculated for the repaired cartilage and control cartilage.

RESULTSThe mean T2 values of the repaired cartilage after MACT were significantly higher than that of the control cartilages at 3 and 6 months (P<0.05), but not at 12 months (P=0.063). At 6 and 12 months, the T2 values of the superficial layers were significantly higher than those of the deep layers in the repaired cartilages (P<0.05). The zonal (deep and superficial layers) T2 values of the repaired cartilages decreased significantly over time at 6 and 12 months as compared to those at 3 months after the surgery (P<0.05).

CONCLUSIONMRI T2 mapping can serve as an important modality for assessing the repair of the articular cartilage following MACT.

Cartilage, Articular ; pathology ; Chondrocytes ; transplantation ; Humans ; Magnetic Resonance Imaging ; Transplantation, Autologous

OBJECTIVETo estimate zonal variation of GAG content in reparative cartilage after matrix associated autologous chondrocyte implantation (MACI) using delayed gadolinium-enhanced magnetic resonance imaging of the cartilage (dGEMRIC).

METHODSSeven patients (14 cartilage defects) undergoing MACI were recruited for examination with dGEMRIC at 3, 6, and 12 months after the procedure to calculate global and zonal longitudinal relaxivity (Δ R1) of the normal cartilage and reparative cartilage.

RESULTSThe mean Δ R1 values of normal cartilage were significantly lower than those of reparative cartilage after MACI. A significant decrease was noted in the mean Δ R1 values from the deep layer to the superficial layer in the reparative cartilage at the 3 examinations. The Δ R1 values of the reparative cartilage showed no significant variation between 3 months and 6 months, but a significant decrease in the Δ R1 values occurred at 12 months.

CONCLUSIONSdGEMRIC is feasible to assess cartilage repair noninvasively following MACI.

Cartilage ; pathology ; Chondrocytes ; transplantation ; Gadolinium ; Humans ; Magnetic Resonance Imaging ; Orthopedic Procedures

This study determined the effects of selenium on the growth of Fusarium strains and the effects of products extracted from the fungal cultures on relevant indicators of chondrocytes injury. The results showed that selenium supplementation resulted in differential effects on the mycelial growth of the strains. Levels of the chondrocyte injury indicators, including cell viability, proteoglycan and type II collagen contents and their mRNA expressions, were all reduced to varying degrees when the chondrocytes were incubated with fermentation extracts, the inhibitory effect varied depending on selenium content supplemented to fungal culture media. The results indicated that certain chain relations existed between the content of selenium in the environment, the production of some metabolites by fungi, and the occurrence of chondrocyte damage. The extent of this relationship and the role it plays in Kaschin-Beck disease pathogenesis merit further study.
Animals ; Cell Survival ; Cells, Cultured ; Chondrocytes ; pathology ; Fermentation ; Fusarium ; drug effects ; physiology ; Rabbits ; Selenium ; pharmacology