Calcified cartilage zone and its dimensional relationship to the articular cartilage in the human temporomandibular joint of elderly individuals

1993 ◽  
Vol 51 (3) ◽  
pp. 183-191 ◽  
Author(s):  
Lennart Flygare ◽  
Bjorn Klinge ◽  
Madeleine Rohlin ◽  
Sigvard Akerman ◽  
Jan Lanke
Keyword(s):  
Articular Cartilage ◽  
Temporomandibular Joint ◽  
Elderly Individuals ◽  
Calcified Cartilage

MORPHOLOGICAL FEATURES OF THE ARTICULAR CARTILAGE OF THE TEMPOROMANDIBULAR JOINT

2017 ◽  
Vol 19 (8) ◽  
pp. 164-165
Author(s):  
I.R. Gubaydullin ◽  
◽  
M.I. Astakhova ◽  
L.I. Kuznetsova ◽  
N.S. Kuznetsova ◽  
...  
Keyword(s):  
Articular Cartilage ◽  
Temporomandibular Joint ◽  
Morphological Features

scholarly journals The ciliary protein IFT88 controls post-natal cartilage thickness and influences development of osteoarthritis

2020 ◽  
Author(s):  
CR Coveney ◽  
L Zhu ◽  
J Miotla-Zarebska ◽  
B Stott ◽  
I Parisi ◽  
...  
Keyword(s):  
Articular Cartilage ◽  
Cell Biology ◽  
Articular Chondrocytes ◽  
Skeletal Development ◽  
Cartilage Degradation ◽  
Cartilage Thickness ◽  
Tissue Growth ◽  
Calcified Cartilage ◽  
Health And Disease

AbstractMechanical forces are known to drive cellular signalling programmes in cartilage development, health, and disease. Proteins of the primary cilium, implicated in mechanoregulation, control cartilage formation during skeletal development, but their role in post-natal cartilage is unknown. Ift88fl/fl and AggrecanCreERT2 mice were crossed to create a cartilage specific inducible knockout mouse AggrecanCreERT2;Ift88fl/fl. Tibial articular cartilage thickness was assessed, through adolescence and adulthood, by histomorphometry and integrity by OARSI score. In situ cell biology was investigated by immunohistochemistry (IHC) and qPCR of micro-dissected cartilage. OA was induced by destabilisation of the medial meniscus (DMM). Some mice were provided with exercise wheels in their cage. Deletion of IFT88 resulted in a reduction in medial articular cartilage thickness (atrophy) during adolescence from 102.57μm, 95% CI [94.30, 119.80] in control (Ift88fl/fl) to 87.36μm 95% CI [81.35, 90.97] in AggrecanCreERT2;Ift88fl/fl by 8-weeks p<0.01, and adulthood (104.00μm, 95% CI [100.30, 110.50] in Ift88fl/fl to 89.42μm 95% CI [84.00, 93.49] in AggrecanCreERT2;Ift88fl/fl, 34-weeks, p<0.0001) through a reduction in calcified cartilage. Thinning in adulthood was associated with spontaneous cartilage degradation. Following DMM, AggrecanCreERT2;Ift88fl/fl mice had increased OA (OARSI scores at 12 weeks Ift88fl/fl = 22.08 +/− 9.30, and AggrecanCreERT2;Ift88fl/fl = 29.83 +/− 7.69). Atrophy was not associated with aggrecanase-mediated destruction or chondrocyte hypertrophy. Ift88 expression positively correlated with Tcf7l2 and connective tissue growth factor. Cartilage thickness was restored in AggrecanCreERT2;Ift88fl/fl by voluntary wheel exercise. Our results demonstrate that ciliary IFT88 regulates cartilage thickness and is chondroprotective, potentially through modulating mechanotransduction pathways in articular chondrocytes.

Effect of functional lateral shift of the mandible on hyaluronic acid metabolism related to lubrication of temporomandibular joint in growing rats

2020 ◽  
Vol 42 (6) ◽  
pp. 658-663
Author(s):  
Xiyuan Guo ◽  
Ippei Watari ◽  
Yuhei Ikeda ◽  
Wu Yang ◽  
Takashi Ono
Keyword(s):  
Hyaluronic Acid ◽  
Articular Cartilage ◽  
Temporomandibular Joint ◽  
Experimental Period ◽  
Lateral Shift ◽  
Control Group ◽  
Condylar Cartilage ◽  
Growing Rats ◽  
Shift Group ◽  
Recovery Group

Summary Background Hyaluronic acid (HA) is a major molecular component of the articular cartilage of the temporomandibular joint (TMJ) influencing joint lubrication. Functional lateral shift of the mandible (FLSM) can lead to malocclusion. This study investigated the effects of FLSM on HA metabolism and lubrication of the TMJ in growing rats. Methods Thirty 5-week-old male Wistar rats were divided into shift, recovery, and control groups. Rats in the shift and recovery groups were fitted with guiding plates to produce a 2-mm FLSM which were removed from the rats in the recovery group 14 days later. Animals were sacrificed at 14 and 28 days after the appliances were attached. Immunohistochemistry of HA-binding protein (HABP), hyaluronan synthase (HAS), and hyaluronoglucosaminidases (HYALs) was examined. Results The thickness of HABP-positively stained areas in the lateral regions in the bilateral condyle was reduced during the experimental period in the shift group compared with that in the control group. The proportion of HAS2-stained areas was bilaterally decreased in different regions of condylar cartilage during the experimental period in the shift group. The reduction of the HYAL2-stained area proportion in the condylar cartilage was more significant than that of HYAL1 at 14 days after appliance attachment in the shift group. HAS2 staining was not recovered in the recovery group. Limitations This research was based on animal experiments with a limited experimental period. Conclusion FLSM altered lubrication related HA metabolism in the articular cartilage of the TMJ in growing rats.

Automated Indentation Demonstrates Structural Stiffness of Femoral Articular Cartilage and Temporomandibular Joint Mandibular Condylar Cartilage Is Altered in FgF2KO Mice

Cartilage ◽  
2020 ◽  
pp. 194760352096256
Author(s):  
Paige S. Woods ◽  
Alyssa A. Morin ◽  
Po-Jung Chen ◽  
Sarah Mahonski ◽  
Liping Xiao ◽  
...  
Keyword(s):  
Articular Cartilage ◽  
Temporomandibular Joint ◽  
Functional Characterization ◽  
Structural Stiffness ◽  
Motion Controller ◽  
Condylar Cartilage ◽  
Spatially Resolved ◽  
Mandibular Condylar Cartilage ◽  
Fgf2 Expression ◽  
Health And Disease

Objective Employ an automated indentation technique, using a commercially available machine, to assess the effect of fibroblast growth factor 2 (FGF2) expression on structural stiffness over the surface of both murine femoral articular cartilage (AC) and temporomandibular joint (TMJ) mandibular condylar cartilage (MCC). Design Experiments were performed using 3-month-old female homozygote Fgf2KO mice with wild type (WT) littermates. After euthanization, isolated mandibles and hindlimbs were either processed for histology or subjected to automated indentation on a Biomomentum Mach-1 v500csst with a 3-axis motion controller in a phosphate buffered saline bath using a 0.3 mm spherical tip indenter. The effect of indentation depth on normal force was characterized, then structural stiffness was calculated and mapped at multiple positions on the AC and MCC. Results Automated indentation of the AC and TMJ MCC was successfully completed and was able to demonstrate both regional variation in structural stiffness and differences between WT and Fgf2KO mice. Structural stiffness values for Fgf2KO AC were significantly smaller than WT at both the medial/anterior ( P < 0.05) and medial/posterior ( P < 0.05) positions. Global Fgf2KO also lead to a decrease in MCC thickness of the TMJ compared with WT ( P < 0.05) and increased structural stiffness values for Fgf2KO at both the posterior and anterior location ( P < 0.05). Conclusions Automated indentation spatially resolved differences in structural stiffness between WT and Fgf2KO tissue, demonstrating FGF2 expression affects femoral AC and TMJ MCC. This quantitative method will provide a valuable approach for functional characterization of cartilage tissues in murine models relevant to knee joint and TMJ health and disease.

scholarly journals Alterations in periarticular bone and cross talk between subchondral bone and articular cartilage in osteoarthritis

2012 ◽  
Vol 4 (4) ◽  
pp. 249-258 ◽  
Author(s):  
Steven R. Goldring
Keyword(s):  
Articular Cartilage ◽  
Subchondral Bone ◽  
Therapeutic Interventions ◽  
Bone Thickness ◽  
Intimate Contact ◽  
Skeletal Changes ◽  
Calcified Cartilage ◽  
Diarthrodial Joint ◽  
Composition Structure ◽  
And Function

The articular cartilage and the subchondral bone form a biocomposite that is uniquely adapted to the transfer of loads across the diarthrodial joint. During the evolution of the osteoarthritic process biomechanical and biological processes result in alterations in the composition, structure and functional properties of these tissues. Given the intimate contact between the cartilage and bone, alterations of either tissue will modulate the properties and function of the other joint component. The changes in periarticular bone tend to occur very early in the development of OA. Although chondrocytes also have the capacity to modulate their functional state in response to loading, the capacity of these cells to repair and modify their surrounding extracellular matrix is relatively limited in comparison to the adjacent subchondral bone. This differential adaptive capacity likely underlies the more rapid appearance of detectable skeletal changes in OA in comparison to the articular cartilage. The OA changes in periarticular bone include increases in subchondral cortical bone thickness, gradual decreases in subchondral trabeular bone mass, formation of marginal joint osteophytes, development of bone cysts and advancement of the zone of calcified cartilage between the articular cartilage and subchondral bone. The expansion of the zone of calcified cartilage contributes to overall thinning of the articular cartilage. The mechanisms involved in this process include the release of soluble mediators from chondrocytes in the deep zones of the articular cartilage and/or the influences of microcracks that have initiated focal remodeling in the calcified cartilage and subchondral bone in an attempt to repair the microdamage. There is the need for further studies to define the pathophysiological mechanisms involved in the interaction between subchondral bone and articular cartilage and for applying this information to the development of therapeutic interventions to improve the outcomes in patients with OA.

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