Objective To review the recent research progress on relationshi p between subchondral bone and cartilage degeneration in osteoarthritis (OA), and to predict future research directions. Methods Recent l iteratures about the pathological changes of subchondral bone in OA were reviewed and analyzed in terms of biomechanics, bone remodel ingand biological factors. Results Subchondral bone sclerosis or softening was the result of osteoarthritis and also closely related to the occurrence and development of OA. Inhibiting the bone metabol ism of subchondral bone could slow the degeneration of articular cartilage. Conclusion For the treatment of OA, it is necessary to pay close attention to cartilage changes and the prevention of subchondral bone degeneration.
In order to observe the histological changes of the autogenous perichondrium graft from rib in the repair of injured articular cartilage of the condylar process of mandible, 50 rabbits were used, in which 15 were served as control. The articular cartilage with its subchondral bone were resected and an autogenous graft of costal perichondrium was sutured onto the raw surface of the condylar process, and in the controls, only the articular portion of the condylar process was resected without the application of autogenous costal perichondrium graft. The morphological changes of the newly formed cartilage during the process of its development were investigated by hiostological and autoradiog aphic techniques. The result revealed that 10 days after operation, the graft had increased in thickness and was richly populated form the proliferation of mesenchyme-like cells. Twenty to thirty days later, the chondrocytes were matured and the newly formed cartilage had covered the bony surface of mandibular condyle. At 60 days, the newly formed cartilagenous joint surface became glossy, and the morphology and arrangement of cells tended to be regular simulating the morphology of normal articular cartilage. From the experiment, it could be concluded that (1) The autogenous perichondrium graft placed on the condylar surface of mandible could form new articular cartilage which was similar in tissue morphology to the normal condylar cartilage. (2) The process of development of newly formed cartilage was similar to that of the normal cartilage. (3) The motion and loading on the joint could promote the formation of new cartilage and undergo biological reformation, gradually resulting in normal joint morphology. On this basis, the clinical application of autogenous perichondrium graft to repair injured cartilage of the condylar process of the mandible was feasible.
The repair of defects of articular cartilage has continued to be a difficult problem. This article provided a collective review from literature pertaining to the advances gained in the repair of cartilaginous defects. In the spontaneous repair, if the defect of the cartilage was less than 3 mm, might result in complete or partial repair, but in those the diameter was more than 3 mm, the defect could not be repaired by normal cartilage. Although the cartilaginous autograft could give good result, but it could not be widely applied because short of supply of the autogenous cartilage. Cartilagious allograft could not be taken to repair cartilaginous defect because of reaction from tissue rejection. The transplantation of periosteal or perichondral graft had been tried but was eventually abandoned because of poor long-term result. The transplantation of free chondrocytes might be a method of hope. In general, transplantation of free chondrocytes into the cartilaginous defect will be lost. The supply of autogenous chondrocytes was very limited, and the heterogenous chondrocytes would inflict immunoreaction after being transplanted. In late of 1980, a new concept of tissue engineering was proposed. The problem that a scaffold of appropriate material which could hold the free chondrocytes in place from being lost might undergo proliferation and differentiation into new cartilage was far from being solved. Although tissue engineering still had various problems needed further investigation, but it will probably be the main direction of development in this field.
ObjectiveTo observe the feasibility of acellular cartilage extracellular matrix (ACECM) oriented scaffold combined with chondrocytes to construct tissue engineered cartilage.MethodsChondrocytes from the healthy articular cartilage tissue of pig were isolated, cultured, and passaged. The 3rd passage chondrocytes were labeled by PKH26. After MTT demonstrated that PKH26 had no influence on the biological activity of chondrocytes, labeled and unlabeled chondrocytes were seeded on ACECM oriented scaffold and cultivated. The adhesion, growth, and distribution were evaluated by gross observation, inverted microscope, and fluorescence microscope. Scanning electron microscope was used to observe the cellular morphology after cultivation for 3 days. Type Ⅱ collagen immunofluorescent staining was used to check the secretion of extracellular matrix. In addition, the complex of labeled chondrocytes and ACECM oriented scaffold (cell-scaffold complex) was transplanted into the subcutaneous tissue of nude mouse. After transplantation, general physical conditions of nude mouse were observed, and the growth of cell-scaffold complex was observed by molecular fluorescent living imaging system. After 4 weeks, the neotissue was harvested to analyze the properties of articular cartilage tissue by gross morphology and histological staining (Safranin O staining, toluidine blue staining, and typeⅡcollagen immunohistochemical staining).ResultsAfter chondrocytes that were mainly polygon and cobblestone like shape were seeded and cultured on ACECM oriented scaffold for 7 days, the neotissue was translucency and tenacious and cells grew along the oriented scaffold well by inverted microscope and fluorescence microscope. In the subcutaneous microenvironment, the cell-scaffold complex was cartilage-like tissue and abundant cartilage extracellular matrix (typeⅡcollagen) was observed by histological staining and typeⅡcollagen immunohistochemical staining.ConclusionACECM oriented scaffold is benefit to the cell adhesion, proliferation, and oriented growth and successfully constructes the tissue engineered cartilage in nude mouse model, which demonstrates that the ACECM oriented scaffold is promise to be applied in cartilage tissue engineering.
ObjectiveTo explore the anthropometric changes of the auricle after auricular cartilage unfolding in moderate concha-type microtia patients, so as to provide the basis to help evaluate surgical timing and prognostic.MethodsA total of 33 children with moderate concha-type microtia, who were treated with auricular cartilage unfolding between October 2016 and September 2018 and met the inclusive criteria, were included in the study. There were 24 boys and 9 girls with an average age of 1.4 years (range, 1-3 years). Sixteen cases were left ears and 17 cases were right ears. The follow-up time was 12-23 months (mean, 17.5 months). The affected auricular detailed structures were observed and quantitatively analyzed before operation and at immediate after operation. The width, length, and perimeter of auricle before operation and at immediate after operation and at last follow-up were noted with three dimensional-scanning technology. The normal auricle was noted as control.ResultsThere were (7.5±1.0) and (11.3±0.8) structures of the affected auricle at pre- and post-operation, respectively, showing significant difference between pre- and post-operation (t=23.279, P=0.000). The length, width, and perimeter of the affected auricle constantly increased after operation, and there were significant differences between pre-operation and immediately after operation and between immediately after operation and last follow-up (P<0.05). The differences of length, width, and perimeter of the affected auricle between immediately after operation and last follow-up were (3.13±1.44), (2.44±0.92), and (8.50±3.76) mm, respectively. And the differences of length, width, and perimeter of the normal auricle between pre-operation and last follow-up were (3.16±1.54), (2.35±0.86), and (9.79±4.60) mm, respectively. There was no significant difference in the differences of length, width, and perimeter between the affected auricle and the normal auricle (P>0.05).ConclusionThe auricular cartilage unfolding in treatment of the moderate concha-type microtia can receive more ear structures and increase auricle sizes, which make it possible for free composite tissue transplantation. In addition, the affected and the contralateral normal auricles have a very similar growth rate and it offers the theoretical foundation for the early treatment for moderate concha-type microtia.
ObjectiveTo study the feasibility of acellular matrix materials prepared from deer antler cartilage and its biological compatibility so as to search for a new member of the extracellular matrix family for cartilage regeneration. MethodsThe deer antler mesenchymal (M) layer tissue was harvested and treated through decellular process to prepare M layer acellular matrix; histologic observation and detection of M layer acellular matrix DNA content were carried out. The antler stem cells [antlerogenic periosteum (AP) cells] at 2nd passage were labelled by fluorescent stains and by PKH26. Subsequently, the M layer acellular matrix and the AP cells at 2nd passage were co-cultured for 7 days; then the samples were transplanted into nude mice to study the tissue compatibility of M layer acellular matrix in the living animals. ResultsHE and DAPI staining confirmed that the M layer acellular matrix did not contain nucleus; the DNA content of the M layer acellular matrix was (19.367±5.254) ng/mg, which was significantly lower than that of the normal M layer tissue [(3 805.500±519.119) ng/mg](t=12.630, P=0.000). In vitro co-culture experiments showed that AP cells could adhere to or even embedded in the M layer acellular matrix. Nude mice transplantation experiments showed that the introduced AP cells could proliferate and induce angiogenesis in the M layer acellular matrix. ConclusionThe deer antler cartilage acellular matrix is successfully prepared. The M layer acellular matrix is suitable for adhesion and proliferation of AP cells in vitro and in vivo, and it has the function of stimulating angiogenesis. This model for deer antler cartilage acellular matrix can be applied in cartilage tissue engineering in the future.
Objective To review the research progress of in-situ three dimensional (3D) bio-printing technology in the repair of bone and cartilage injuries. Methods Literature on the application of in-situ 3D bio-printing technology to repair bone and cartilage injuries at home and abroad in recent years was reviewed, analyzed, and summarized. Results As a new tissue engineering technology, in-situ 3D bio-printing technology is mainly applied to repair bone, cartilage, and skin tissue injuries. By combining biomaterials, bioactive substances, and cells, tissue is printed directly at the site of injury or defect. At present, the research on the technology mainly focuses on printing mode, bio-ink, and printing technology; the application research in the field of bone and cartilage mainly focuses on pre-vascularization, adjusting the composition of bio-ink, improving scaffold structure, printing technology, loading drugs, cells, and bioactive factors, so as to promote tissue injury repair. Conclusion Multiple animal experiments have confirmed that in-situ 3D bio-printing technology can construct bone and cartilage tissue grafts in a real-time, rapid, and minimally invasive manner. In the future, it is necessary to continue to develop bio-inks suitable for specific tissue grafts, as well as combine with robotics, fusion imaging, and computer-aided medicine to improve printing efficiency.
Superficial cartilage defect is an important factor that causes osteoarthritis. Therefore, it is very important to investigate the influence of superficial cartilage defects on its surface morphology and mechanical properties. In this study, the knee joint cartilage samples of adult pig were prepared, which were treated by enzymolysis with chymotrypsin and physical removal with electric friction pen, respectively. Normal cartilage and surface treated cartilage were divided into five groups: control group (normal cartilage group), chymotrypsin immersion group, chymotrypsin wiping group, removal 10% group with electric friction pen, and removal 20% group with electric friction pen. The surface morphology and structure of five groups of samples were characterized by laser spectrum confocal microscopy and environmental field scanning electron microscopy, and the mechanical properties of each group of samples were evaluated by tensile tests. The results show that the surface arithmetic mean height and fracture strength of the control group were the smallest, and the fracture strain was the largest. The surface arithmetic mean height and fracture strength of the removal 20% group with electric friction pen were the largest, and the fracture strain was the smallest. The surface arithmetic mean height, fracture strength and fracture strain values of the other three groups were all between the above two groups, but the surface arithmetic mean height and fracture strength of the removal 10% group with electric friction pen, the chymotrypsin wiping group and the chymotrypsin soaking group decreased successively, and the fracture strain increased successively. In addition, we carried out a study on the elastic modulus of different groups, and the results showed that the elastic modulus of the control group was the smallest, and the elastic modulus of the removal 20% group with electric friction pen was the largest. The above study revealed that the defect of the superficial area of cartilage changed its surface morphology and structure, and reduced its mechanical properties. The research results are of great significance for the prevention and repair of cartilage injury.
ObjectiveTo investigate whether subchondral bone microstructural parameters are related to cartilage repair during large osteochondral defect repairing based on three-dimensional (3-D) printing technique. MethodsBiomimetic biphasic osteochondral composite scaffolds were fabricated by using 3-D printing technique. The right trochlea critical sized defects (4.8 mm in diameter, 7.5 mm in depth) were created in 40 New Zealand white rabbits (aged 6 months, weighing 2.5-3.5 kg). Biomimetic biphasic osteochondral composite scaffolds were implanted into the defects in the experimental group (n=35), and no composite scaffolds implantation served as control group (n=5); the left side had no defect as sham-operation group. Animals of experimental and sham-operation groups were euthanized at 1, 2, 4, 8, 16, 24, and 52 weeks after operation, while animals of control group were sampled at 24 weeks. Subchondral bone microstructural parameters and cartilage repair were quantitatively analyzed using Micro-CT and Wayne scoring system. Correlation analysis and regression analysis were applied to reveal the relationship between subchondral bone parameters and cartilage repair. The subchondral bone parameters included bone volume fraction (BV/TV), bone surface area fraction (BSA/BV), trabecular thickness (Tb.Th), trabecular number (Tb.N), and trabecular spacing (Tb.Sp). ResultsIn the experimental group, articular cartilage repair was significantly improved at 52 weeks postoperatively, which was dominated by hyaline cartilage tissue, and tidal line formed. Wayne scores at 24 and 52 weeks were significantly higher than that at 16 weeks in the experimental group (P<0.05), but no significant difference was found between at 24 and 52 weeks (P>0.05); the scores of experimental group were significantly lower than those of sham-operation group at all time points (P<0.05). In the experimental group, new subchondral bone migrated from the surrounding defect to the centre, and subchondral bony plate formed at 24 and 52 weeks. The microstructural parameters of repaired subchondral bone followed a "twin peaks" like discipline to which BV/TV, BSA/BV, and Tb.N increased at 2 and 16 weeks, and then they returned to normal level. The Tb.Sp showed reversed discipline compared to the former 3 parameters, no significant change was found for Tb.Th during the repair process. Correlation analysis showed that BV/TV, BSA/BV, Tb.Th, Tb.N, and Tb.Sp were all related with gross appearance score and histology score of repaired cartilage. ConclusionSubchondral bone parameters are related with cartilage repair in critical size osteochondral repair in vivo. Microstructural parameters of repaired subchondral bone follow a "twin peaks" like discipline (osteoplasia-remodeling-osteoplasia-remodeling) to achieve reconstruction, 2nd week and 16th week are critical time points for subchondral bone functional restoration.
ObjectiveTo review the pathological effects of cellular senescence in the occurrence and development of osteoarthritis (OA) and potential therapeutic targets.MethodsThe role of chondrocyte senescence, synovial cell senescence, mesenchymal stem cells senescence in OA, and the biological mechanism and progress of chondrocyte senescence were summarized by consulting relevant domestic and abroad literature.ResultsThe existing evidence has basically made clear that chondrocyte senescence, mesenchymal stem cells senescence, and cartilage repair abnormalities, and the occurrence and development of OA have a certain causal relationship, and the role of the senescence of synovial cells, especially synovial macrophages in OA is still unclear. Transcription factors and epigenetics are the main mechanisms that regulate the upstream pathways of cellular senescence. Signal communication between cells can promote the appearance of senescent phenotypes in healthy cells. Targeted elimination of senescent cells and promotion of mesenchymal stem cells rejuvenation can effectively delay the progress of OA.ConclusionCellular senescence is an important biological phenomenon and potential therapeutic target in the occurrence and development of OA. In-depth study of its biological mechanism is helpful to the early prevention and treatment of OA.