To review the structure and function of the calcified cartilage zone and its role in the pathogenesis of osteoarthritis (OA). Methods Recent l iterature about calcified zone was reviewed and analyzed in terms of architecture, composition, biomechanics, and biological function. Results Calcified zone has particular structure and material properties, and functions as a semi permeable membrane; chondrocytes in the calcified zone retain some characteristics of growth plate cells, which play a crucial role in cartilage function maintenance and pathogenesis of OA. Therefore, reconstructionof the calcified zone at osteochondral conjunction has become one of the hot research in the fields of interface tissue engineering. Conclusion It is necessary to pay more attention to calcified cartilage zone, which is important for both the treatment of OA and the preparation of tissue engineered osteochondral composite.
To investigate the pathologic characteristics of the articular cartilage and subchondral bone from osteoarthritic knees, and to compare the structural parameters of articular cartilage and subchondral bone between the medial and lateral tibial plateau, so as to determine the role of calcified zone and subchondral bone in the pathogenesis of osteoarthritis (OA). Methods The tibial plateaus were taken from 30 patients undergoing total knee arthroplasty between October 2009 and May 2011. The subjects included 11 males and 19 females with an average age of 65.1 years (range, 55-78years). The mean disease duration was 16.6 years (range, 10-25 years); the mean varus angle of the diseased knee was 9.3° (range, 1-23°). After gross observation, the cartilage-bone samples were taken out from the most weight-bearing regions in the internal areas of the medial and lateral plateaus. The decalcified paraffin-embedded sections were prepared and stained with HE and Safranin O/fast green for cartilage assessment (Mankin score), staging, and bone histomorphometry; the pathologic features of the cartilage and subchondral bone were also observed. The thickness of total articular cartilage (TAC), articular calcified cartilage (ACC), subchondral bone plate (SCP), and the trabecular bone volume (BV/TV) were measured by Image Pro Plus 6.0 imaging system, then the ratio of ACC/TAC was calculated. Results Macroscopic results showed that articular cartilage degeneration was more severe in the medial plateau than in the lateral plateau; Mankin score of the medial plateau (12.4 ± 1.1) was significantly higher than that of the lateral plateau (8.3 ± 1.6) (t=12.173, P=0.000). In the 60 samples, 14 samples were at stage I, characterisd by fissures within the superficial zone, dupl icated tidemark, and thickend subchondral bone; 19 samples were at stage II, characterisd by fissures extending into the deep zone, multiple subchondral bone resorption pits, and obviously thickend subchondral bone; and 27 samples were at stage III, characterisd by full-thickness cartilage defects, endochondral ossification, and eburnated subchondral bone. The bone histomorphometric study showed that TAC thickness of the medial plateau was significantly lower than that of the lateral plateau (P lt; 0.05); the ratios of ACC/TAC, BV/TV, and SCP thickness of the medial plateau were significantly higher than those of the lateral plateau (P lt; 0.05). However, there was no significantdifference in the ACC thickness between the medial and lateral plateaus (P gt; 0.05). Conclusion The calcified zone andsubchondral bone may play an important role in the initiation and progression of OA.
Objective To review the progress of mechanism of parathyroid hormone (PTH) and parathyroid hormone-related protein (PTHrP) on normal and osteoarthritis (OA) cartilage and subchondral bones. Methods Recent 1iterature about the effects of PTH and PTHrP on normal and OA cartilage was reviewed. Results PTH and PTHrP can repress the hypertrophic differentiation and apoptosis of chondrocytes and promote their prol iferation, which has a protection effect on chondrocytes of OA; osteoblasts from subchondral bone of OA show a decreased reaction to PTH. Conclusion PTHand PTHrP may delay and protect the progression of OA, which involves in regulating cartilage degeneration and subchondral bone remodl ing through many kinds of signal pathway.
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.
Objective To investigate the effects of xianl inggubao (XLGB) on subchondral bone and articular cartilage in the rat osteoarthritis model induced by anterior cruciate l igament transection (ACLT). Methods Twentyfour 3-month-old female SD rats were divided randomly into 3 groups (n=8): Sham group (group A), ACLT group (group B) and XLGB group (group C). The osteoarthritis model was made by ACLT in groups B and C, the joint cave was sutured after exposure of ACL in group A. After 4 days, XLGB was given at 250 mg/(kg·d) in group C and the equivalent amount of sal ine was given in groups A and B. After 12 weeks, the gross appearance of femoral condyles was observed, the degree of cartilagedegeneration was scored by Mankin scoring system. The immunostaining for MMP-13 was performed to investigate the effect of XLGB on prevention of cartilage matrix loss. The bone mineral density (BMD) measurement and bone histomorphometric analysis were done in subchondral bone of right distal femur and proximal tibia after 12 weeks. Results The gross appearance of femoral condyles showed that ulcer in the group C was smaller than that in group B after 12 weeks. The Mankin’s scale and IA value for MMP-13 in group C were markedly lower than those in group B (P lt; 0.05). BMD of the subchondral bone in the group B was significantly lower than those in the groups A and C (P lt; 0.05). The bone mass in group C were significantly higher than that in group B (P lt; 0.05). Conclusion Oral administration of XLGB (250 mg/ kg per day) for 12 weeks could prevent the cartilage degeneration of rats after ACLT, down-regulating MMP-13 and increasing subchondral bone mass might participate in this process.
Objective To review the effect of calcitonin on cartilage and subchondral bone of osteoarthritis. Methods Recent l iteratures about the effect of calcitonin on osteoarthritis was reviewed. Results Calcitonin could promotethe synthesis of important cartilage matrix such as proteoglycans and collagen II, propell ing the regeneration of cartilage and subchondral bone. Conclusion Calcitonin can protect articular cartilage through promoting the synthesis of cartilage and inhibiting its degradation.
ObjectiveTo review the current treatment status of osteochondral defects (OCD) of the knee joint. MethodsRecent literature concerning treatment of OCD of the knee joint was extensively reviewed and summarized. ResultsOCD affect both the articular cartilage and the underlying subchondral bone, whereas OCD caused by different etiologies require various treatments. OCD repair is available by conventional clinical methods or the advanced tissue engineering strategies. Current clinical treatment outcomes remain uncertain; tissue engineering has emerged as a potential option as it can be efficiently applied to regenerate bone, cartilage, and the bone-cartilage interface, as well as effectively restore normal function and mechanical properties of the cartilage and subchondral bone. ConclusionOCD management and repair remain a great challenge in orthopedic surgery, thus cartilage and subchondral bone should be promoted as an interdependent functional unit considering treatment strategies to provide the best solution for the treatment of osteochondral defects.
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 explore the relationship between subchondral bone reconstruction and articular cartilage regeneration in a rabbit model of spontaneous osteochondral repair. MethodsTwenty-four 6-month-old New Zealand white rabbits were included. The osteochondral defects (4 mm in diameter and 3 mm in depth) were created in the trochlear groove of the unilateral femur, which penetrated the subchondral bone without any treatment. The rabbits were sacrificed at 1, 4, 12, and 24 weeks after operation, respectively. The specimens were obtained for macroscopic, histological, and immunohistochemical observations. According to the International Cartilage Repair Society (ICRS) histological scoring, the effect of cartilage repair was assessed. The histomorphometrical parameters of subchondral bone were analyzed by micro-CT scan and reconstruction, and the relationship between cartilage repair and the histomorphometrical parameters of the subchondral bone were also analyzed. ResultsOsteochondral defects could be repaired spontaneously in rabbit model. With time, defect was gradually filled with repaired tissue, subchondral bone plate under the defect region gradually migrated upward. Bone mineral density, bone volume fraction, tissue mineralized density, trabecula number, and trabecula thickness were increased, while trabecula spacing was decreased. Significant difference was found in the other parameters between different time points (P<0.05) except for trabecula thickness between at 4 and 12 weeks after operation (P>0.05). Histological examination showed that fibrous repair was predominant with rare hyaline cartilage. With time, ICRS scores increased gradually, showing significant differences between other time points (P<0.05) except for between at 4 and 12 weeks after operation (P>0.05). Among the histomorphometrical parameters of subchondral bone, the trabecula spacing was negatively correlated with ICRS score (r=-0.584, P=0.039), and the other histomorphometrical parameters were positively correlated with ICRS score (r=0.680-0.891). ConclusionThere is relevant correlation as well as independent process between cartilage regeneration and subchondral bone reconstruction in the rabbit model of spontaneous osteochondral repair, and fast subchondral bone remodeling may adversely affect articular cartilage repair.
ObjectiveTo review the role of vertebral subchondral bone in maintaining normal physiological function of the intervertebral disc and in the intervertebral disc degeneration in light of bone anatomy, microstructure, histopathological features, and MRI imaging features. MethodsThe related home and abroad literature concerning vertebral subchondral bone and intervertebral disc degeneration was extensively reviewed and comprehensively analyzed. ResultsVertebral subchondral bone is part of the vertebral endplate and is defined as the vascularized cortical and trabecular bone layer located between the cartilage endplate and vertebral body. It not only plays a cushion shocks role in terms of conducting stress and effectively resists the hydrostatic nucleus, but also ensures the normal supply of disc nutrition. Subchondral bone sclerosis caused by bone remodeling abnormality severely decreases the ability of subchondral bone stress absorption and protective function of disc, which finally leads to increased inflammatory factors locally and hindered nutrition pathway of disc and enhanced disc degeneration. ConclusionTo further strengthen the knowledge and understanding of the vertebral subchondral bone will play a positive role in the study on the pathogenesis of intervertebral disc degeneration.