OBJECTIVETo investigate the effect of rupture and reconstruction of the anterior cruciate ligament (ACL) on the degeneration of rabbit knee articular cartilage.

METHODS14 mature New Zealand white rabbits were divided into four groups. In group I, the ACL of the right knees in 7 rabbits was resected and immediately reconstructed, and the contralateral ACL was resected only in controll f group I. In group II, the ACL of the right knees in 7 rabbits was reconstructed 3 weeks after the ACL was resected and the contralateral joints in control group II, in which only a medial arthrotomy was performed. The rabbits were killed 8 weeks after the operation. The methods of ink straining, histology and SEM were used to analyze the changes in articular cartilage of the joints.

RESULTSThe results of ink method and HE straining were analyzed quantitatively. The degeneration of knee articular cartilage in group I was significantly weaker than that in control group I (Hc = 5.9889, P = 0.0144). The degeneration of knee articular cartilage in group II was as serious as that in control group I (Hc = 0.7143, P = 0.785).

CONCLUSIONSImmediate reconstruction of the ACL can effectively prevent articular cartilage from degeneration. Once the articular cartilage damaged moderately, delayed reconstruction of the ACL could not effectively reduce the development of degeneration. So once the ACL is ruptured, reconstruction should be performed in the early stage to restore the stability of knee joint to prevent the articular cartilage from degeneration.

Animals ; Anterior Cruciate Ligament Injuries ; Cartilage, Articular ; pathology ; Disease Models, Animal ; Knee Joint ; physiopathology ; Rabbits

Subtle changes in structure or composition can lead to degeneration of articular cartilage such as in osteoarthritis, so it is significant to study the materials attribute of the degenerating articular cartilage. A new transient ultrasonic technique was introduced into this study for measuring the swelling effects of the degenerated cartilage. The swelling-induced strain was calculated based on the measurement result, and then the uniaxial module of the articular cartilag was extracted using Narmoneva's triphasic model. The ultrasonic observation showed that the strains induced by the nonuniform swelling are depth-dependent, and the strains are small in the deep zone and big in the middle and surface zones. The uniaxial modulus also revealed that the cartilage in the deep zone (E1 = 12.20) is harder than that in surface zone (E2 = 0.15). These results suggest that the transient ultrasound technique accompanied by triphasic model provides a quantitative means to study the degeneration of articular cartilage.
Cartilage Diseases ; diagnostic imaging ; Cartilage, Articular ; diagnostic imaging ; physiopathology ; Computer Simulation ; Edema ; diagnostic imaging ; physiopathology ; Humans ; Models, Biological ; Osmotic Pressure ; Ultrasonography

BACKGROUNDQuantitative T2 mapping has been a widely used method for the evaluation of pathological cartilage properties, and the histological assessment system of osteoarthritis in the rabbit has been published recently. The aim of the study was to investigate the effectiveness of quantitative T2 mapping evaluation for articular cartilage lesions of a rabbit model of anterior cruciate ligament transection (ACLT) osteoarthritis.

METHODSTwenty New Zealand White (NZW) rabbits were divided into ACLT surgical group and sham operated group equally. The anterior cruciate ligaments of the rabbits in ACLT group were transected, while the joints were closed intactly in sham operated group. Magnetic resonance (MR) examinations were performed on 3.0T MR unit at week 0, week 6, and week 12. T2 values were computed on GE ADW4.3 workstation. All rabbits were killed at week 13, and left knees were stained with Haematoxylin and Eosin. Semiquantitative histological grading was obtained according to the osteoarthritis cartilage histopathology assessment system. Computerized image analysis was performed to quantitate the immunostained collagen type II.

RESULTSThe average MR T2 value of whole left knee cartilage in ACLT surgical group ((29.05±12.01) ms) was significantly higher than that in sham operated group ((24.52±7.97) ms) (P=0.024) at week 6. The average T2 value increased to (32.18±12.79) ms in ACLT group at week 12, but remained near the baseline level ((27.66±8.08) ms) in the sham operated group (P=0.03). The cartilage lesion level of left knee in ACLT group was significantly increased at week 6 (P=0.005) and week 12 (P<0.001). T2 values had positive correlation with histological grading scores, but inverse correlation with optical densities (OD) of type II collagen.

CONCLUSIONThis study demonstrated the reliability and practicability of quantitative T2 mapping for the cartilage injury of rabbit ACLT osteoarthritis model.

Animals ; Anterior Cruciate Ligament ; metabolism ; physiopathology ; Cartilage, Articular ; metabolism ; physiopathology ; Collagen Type II ; metabolism ; Magnetic Resonance Imaging ; Male ; Osteoarthritis ; metabolism ; physiopathology ; Rabbits

Undifferentiated spondyloarthropathy (USpA) includes the forms that do not meet criteria for the established categories of spondyloarthropathy. The clinical spectrum of USpA is therefore wide and few studies have been published on USpA, especially peripheral arthritis. A total of 107 patients fulfilling the European Spondyloarthropathy Study Group criteria for SpA were studied retrospectively by a chart review and interview by a rheumatologist. Peripheral arthritis, excluding hip and shoulder involvement, occurred in 97 of the 107 patients (91%). Joint involvement tended to be monoarticular or pauciarticular, and most frequently developed in peripheral joints including the knee and ankle. Among the 97 patients with peripheral arthritis, only 37 (35%) had a persistent arthritis. HLA-B27 was detected in 80 patients (78%). Peripheral arthritis was found in the lower extremities regardless of symmetry or asymmetry and tended to run a benign course with only a few patients having persistent arthritis
Adult ; Arthritis/diagnosis/metabolism/*physiopathology ; Cartilage, Articular/physiopathology ; Female ; HLA-B27 Antigen/metabolism ; Humans ; Korea ; Male ; Prognosis ; Retrospective Studies ; Sex Factors

Osteotomies were performed through post-lateral approach under the base of femoral neck on 60 New Zealand white rabbits. The changes of the thickness and biomechanical properties of acetabular cartilage following the cartilage degeneration and the relationship to the postoperative time 2, 4, 6, 8, 12, 16 weeks later were measured respectively. The cartilage specimens were harvested and measured by the automated creep indentation apparatus to obtain the thickness and biomechanical properties. The cartilage became thicker within 6 weeks after operation, cartilage degeneration developed critically from the surface with the lost of the biomechanical properties. The degeneration progressed till the eartilage became thinner and thinner and the to be torn out into pieces at last. The matrix of articular cartilage degraded markedly for the absence of normal stress load following the femoral neck fracture, led to the decline of the biomechanical properties and kept the degeneration progress to osteoarthritis.
Animals ; Biomechanical Phenomena ; Cartilage, Articular ; pathology ; physiopathology ; Disease Models, Animal ; Elasticity ; Female ; Femoral Neck Fractures ; pathology ; physiopathology ; Male ; Rabbits ; Stress, Mechanical ; Time Factors

Nitric oxide (NO) has been considered as an important mediator in inflammatory phases and in loss of cartilage. In inflammatory arthritis, NO levels are correlated with disease activity and articular cartilage is able to produce large amounts of NO with the appropriate inducing factor such as cytokines. The old animals are shown to have a greater sensitivity to NO than young animals. This study evaluated the basal production of NO in normal and OA-affected chondroyctes from young and old patients and compared the levels of NO formation in response to IL-1beta. The results showed that the basal levels were 7-fold higher in old chondrocytes than those of young cells. However, the IL-1beta induced NO production was seen to decrease with age. Aminoguianidine (AG), a competitive inhibitor of iNOS, inhibited NO formation completely in both chondrocytes from young and old individuals. However, at the same concentration of AG it caused partial inhibition of NO and iNOS formation in chondrocytes from OA-affected individuals. In addition, although the IL-1beta induced NO production was much lesser than that of young chondrocytes, the inhibition of collagen production by IL-1beta was prominent in old chondrocytes and OA-affected chondrocytes. These results suggest that age-related differences in the regulation of NO production and collagen production, which may affect the ageing cells and osteoarthritic changes in some way.
Aging/*physiology ; Cartilage, Articular/*physiopathology ; Cells, Cultured ; Chondrocytes/*metabolism ; Collagen Type II/metabolism ; Enzyme Inhibitors/pharmacology ; Guanidines/pharmacology ; Human ; Interleukin-1/pharmacology ; Nitric Oxide/*biosynthesis ; Osteoarthritis/*metabolism

Nitric oxide (NO) has been considered as an important mediator in inflammatory phases and in loss of cartilage. In inflammatory arthritis, NO levels are correlated with disease activity and articular cartilage is able to produce large amounts of NO with the appropriate inducing factor such as cytokines. The old animals are shown to have a greater sensitivity to NO than young animals. This study evaluated the basal production of NO in normal and OA-affected chondroyctes from young and old patients and compared the levels of NO formation in response to IL-1beta. The results showed that the basal levels were 7-fold higher in old chondrocytes than those of young cells. However, the IL-1beta induced NO production was seen to decrease with age. Aminoguianidine (AG), a competitive inhibitor of iNOS, inhibited NO formation completely in both chondrocytes from young and old individuals. However, at the same concentration of AG it caused partial inhibition of NO and iNOS formation in chondrocytes from OA-affected individuals. In addition, although the IL-1beta induced NO production was much lesser than that of young chondrocytes, the inhibition of collagen production by IL-1beta was prominent in old chondrocytes and OA-affected chondrocytes. These results suggest that age-related differences in the regulation of NO production and collagen production, which may affect the ageing cells and osteoarthritic changes in some way.
Aging/*physiology ; Cartilage, Articular/*physiopathology ; Cells, Cultured ; Chondrocytes/*metabolism ; Collagen Type II/metabolism ; Enzyme Inhibitors/pharmacology ; Guanidines/pharmacology ; Human ; Interleukin-1/pharmacology ; Nitric Oxide/*biosynthesis ; Osteoarthritis/*metabolism

OBJECTIVETo evaluate the compositional variation of fibrous callus in the fracture site and the joint cavity and joint cartilage after being transplanted in the muscle pouch.

METHODSThirty 2 month old New Zealand white rabbits (weighing 1-1.5 kg) were randomly divided into two groups: a callus transplantation group (Group A, n=15) and a cartilage transplantation group (Group B, n=15). In Group A, closed radius fracture was made and the autologous fibrous callus was transplanted in the right knee joint cavity at 12 days postoperatively. In Group B, the right knee joint cartilage of the animals was transplanted in the autologous back muscle pouches under anesthesia. Then all the animals were killed by overdose anesthetic 3 weeks after transplantation. And the transplanted fibrous callus, the healed bones in the fracture sites and the transplanted joint cartilage were obtained for assessment of compositional variation.

RESULTSPure fibrous composition was found in the callus at the fracture sites in Group A at 12 days postoperatively. And for 11 out of the 15 animals, the fibrous callus was transformed into cartilaginous tissues after 3 weeks of transplantation, but the fibrous callus was absent in the other 4 animals. The fibrous calluses at the original site and the fracture locus were differentiated into bony tissues. Bony tissue transformation was found in the transplanted joint cartilages in the muscle pouch of all the animals in Group B.

CONCLUSIONSThe fracture sites or joint cavity may facilitate callus differentiation in different ways: the former is helpful for osteogenesis while the latter for the development and maintenance of cartilages, and the muscle pouch is inclined to induce the osteogenic phenotype for cartilages.

Animals ; Bony Callus ; cytology ; transplantation ; Cartilage, Articular ; cytology ; transplantation ; Cell Differentiation ; Fracture Healing ; physiology ; Knee Joint ; Male ; Muscle, Skeletal ; Rabbits ; Radius Fractures ; physiopathology

OBJECTIVETo investigate chondrocyte apoptosis and expression of Fas and inducible nitric oxide synthase (iNOS) in articular cartilage in the pathogenesis of Kashin-beck disease (KBD) and primary osteoarthritis (OA).

METHODSThe collected samples of articular cartilage were divided into three groups: normal control (15 cases), KBD adults (15 cases) and OA (15 cases). Chondrocyte apoptosis was detected by terminal deoxynucleotidyl transferase biotin-dUTP nick end labeling method, and Fas and iNOS in articular cartilage were stained by immunohistochemistry.

RESULTSThe positive percentages of chondrocyte apoptosis stained in articular cartilage of KBD and OA were significantly higher than that of the control (P < 0.01), and the positive percentage of chondrocytes apoptosis in the eroded areas of articular cartilage were significantly higher than in the non-eroded areas in articular cartilage of the same patient with KBD and OA (P < 0.05). There was no significant difference in positive percentage of chondrocytes apoptosis between KBD and OA. The positive percentages of Fas and iNOS in chondrocytes were significantly higher in KBD and OA than in control (P < 0.01). Significant differences in Fas and iNOS expression between the eroded areas and non-eroded areas were seen in articular cartilage of patients with KBD and OA (P < 0.05), but such difference did not exist between KBD and OA.

CONCLUSIONCell apoptosis seems to be associated with the pathogenesis of both KBD and OA. Fas and iNOS might mediate chondrocyte apoptosis.

Adult ; Apoptosis ; Cartilage, Articular ; pathology ; Chondrocytes ; cytology ; Endemic Diseases ; Female ; Humans ; In Situ Nick-End Labeling ; Male ; Nitric Oxide Synthase ; metabolism ; Osteoarthritis ; pathology ; physiopathology ; Osteoarthritis, Knee ; pathology ; physiopathology ; fas Receptor ; metabolism

OBJECTIVETo investigate chondrocyte apoptosis and the expression of biochemical markers associated with apoptosis in Kashin-Beck disease (KBD) and in an established T-2 toxin- and selenium (Se) deficiency-induced rat model.

METHODSCartilages were collected from the hand phalanges of five patients with KBD and five healthy children. Sprague-Dawley rats were administered a selenium-deficient diet for 4 weeks prior to T-2 toxin exposure. The apoptotic chondrocytes were observed by terminal deoxynucleotidyl transferase dUTP nick end labeling staining. Caspase-3, p53, Bcl-2, and Bax proteins in the cartilages were visualized by immunohistochemistry, their protein levels were determined by Western blotting, and mRNA levels were determined by real-time reverse transcription polymerase chain reaction.

RESULTSIncreased chondrocyte apoptosis was observed in the cartilages of children with KBD. Increased apoptotic and caspase-3-stained cells were observed in the cartilages of rats fed with normal and Se-deficient diets plus T-2 toxin exposure compared to those in rats fed with normal and Se-deficient diets. Caspase-3, p53, and Bax proteins and mRNA levels were higher, whereas Bcl-2 levels were lower in rats fed with normal or Se-deficiency diets supplemented with T-2 toxin than the corresponding levels in rats fed with normal diet.

CONCLUSIONT-2 toxin under a selenium-deficient nutritional status induces chondrocyte death, which emphasizes the role of chondrocyte apoptosis in cartilage damage and progression of KBD.

Adolescent ; Animals ; Apoptosis ; drug effects ; Biomarkers ; Cartilage, Articular ; physiopathology ; Child ; Chondrocytes ; physiology ; Female ; Humans ; Kashin-Beck Disease ; etiology ; physiopathology ; Male ; Matrilin Proteins ; genetics ; metabolism ; Models, Animal ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Selenium ; deficiency ; T-2 Toxin ; pharmacology