Distribution of Nanomechanical Properties and Mineralization of the Osteochondral Interface in the Femoral Head

Author(s):  
Rebecca Pak ◽  
Sara E. Campbell ◽  
Rachel C. Paietta ◽  
Virginia L. Ferguson

Stiff vertebral bone and compliant hyaline articular cartilage (HAC) anchor together through a thin (∼100’s of microns) region of articular calcified cartilage (ACC). This bone–cartilage, or osteochondral (OC), interface may play a role in osteoarthritis pathogenesis through increased mineralization, disrupting loading, and damaging neighboring tissues [1,2]. Load transmission through OC regions is poorly understood, thus limiting understanding of disease progression and ability to engineer OC interface-like tissues [3].

2017 ◽  
Vol 28 (3) ◽  
pp. 272-277 ◽  
Author(s):  
Cemil Yildiz ◽  
Yusuf Erdem ◽  
Kenan Koca

Introduction: The aim of this study was to report the clinical and radiological outcomes for 21 patients (28 hips) treated for osteonecrosis of the femoral head using the lightbulb technique, a nonvascularised bone grafting technique. Methods: The study group included 14 men and 7 women, with a mean age of 33.2 (range 22-50) years, presenting with avascular necrosis of the femoral head of stage 4a or earlier, according to the Steinberg classification. Patients were treated using the nonvascularised lightbulb bone grafting technique. The primary clinical outcome was the Harris Hip Scores (HHS), while primary outcomes of treatment effectiveness and disease progression were based on radiographic evidence of disease progression and the need for total hip replacement. The rate of treatment success and failure was evaluated using the Kaplan-Meier survival analysis. Results: The mean HHS increased from 52.66 to 74.33 after treatment, with excellent-to-good outcomes obtained in 21 (75%) of the cases. Fair-to-poor results were obtained in 7 (25%) of the cases, with total hip arthroplasty subsequently required in 5 of these cases. The radiological failure rate was 50% among cases treated in Steinberg stage 1 (1/2), 42% in stage 3 (5/12), and 100% in stage 4 (2/2). Conclusions: The lightbulb technique can provide a clinically acceptable rate of successful treatment of osteonecrosis of the femoral head when used in the early stages of the disease, prior to collapse of the femoral head.


2020 ◽  
Author(s):  
CR Coveney ◽  
L Zhu ◽  
J Miotla-Zarebska ◽  
B Stott ◽  
I Parisi ◽  
...  

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.


2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Jai-Hong Cheng ◽  
Shun-Wun Jhan ◽  
Chieh-Cheng Hsu ◽  
Hung-Wen Chiu ◽  
Shan-Ling Hsu

Avascular necrosis (AVN) of the femoral head (AVNFH) is a disease caused by injury to the blood supply of the femoral head, resulting in a collapse with osteonecrosis and damage to the articular cartilage. Extracorporeal shockwave therapy (ESWT) has been demonstrated to improve AVNFH owing to its anti-inflammation activity, angiogenesis effect, and tissue regeneration in clinical treatment. However, there are still so many pieces of the jigsaw that need to be fit into place in order to ascertain the mechanism of ESWT for the treatment of AVNFH. The study demonstrated that ESWT significantly protected the trabecular bone volume fraction BV/TV ( P < 0.01 ) and the trabecular thickness ( P < 0.001 ), while in contrast, the trabecular number and trabecular separation were not significantly different after treatment as compared with AVNFH. ESWT protected the articular cartilage in animal model of AVNFH. The levels of IL1-β and IL33 were significantly induced in the AVNFH group ( P < 0.001 ) as compared with Sham and ESWT groups and reduced in ESWT group ( P < 0.001 ) as compared with AVNFH group. In addition, the expression of the receptor of IL33, ST2, was reduced in AVNFH and induced after ESWT ( P < 0.001 ). The expression of IL17A was induced in the AVNFH group ( P < 0.001 ) and reduced in the ESWT group ( P < 0.001 ). Further, the expression of the receptor of IL17A, IL17RA, was reduced in the AVNFH group ( P < 0.001 ) and improved to a normal level in the ESWT group as compared with Sham group ( P < 0.001 ). Taken together, the results of the study indicated that ESWT modulated the expression of IL1-β, pro-inflammatory cytokines IL33 and IL17A, and their receptors ST2 and IL17RA, to protect against loss of the extracellular matrix in the articular cartilage of early AVNFH.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Ludmila Mudri Hul ◽  
Adriana Mércia Guaratini Ibelli ◽  
Igor Ricardo Savoldi ◽  
Débora Ester Petry Marcelino ◽  
Lana Teixeira Fernandes ◽  
...  

AbstractLocomotor problems are among one of the main concerns in the current poultry industry, causing major economic losses and affecting animal welfare. The most common bone anomalies in the femur are dyschondroplasia, femoral head separation (FHS), and bacterial chondronecrosis with osteomyelitis (BCO), also known as femoral head necrosis (FHN). The present study aimed to identify differentially expressed (DE) genes in the articular cartilage (AC) of normal and FHS-affected broilers by RNA-Seq analysis. In the transcriptome analysis, 12,169 genes were expressed in the femur AC. Of those, 107 genes were DE (FDR < 0.05) between normal and affected chickens, of which 9 were downregulated and 98 were upregulated in the affected broilers. In the gene-set enrichment analysis using the DE genes, 79 biological processes (BP) were identified and were grouped into 12 superclusters. The main BP found were involved in the response to biotic stimulus, gas transport, cellular activation, carbohydrate-derived catabolism, multi-organism regulation, immune system, muscle contraction, multi-organism process, cytolysis, leukocytes and cell adhesion. In this study, the first transcriptome analysis of the broilers femur articular cartilage was performed, and a set of candidate genes (AvBD1, AvBD2, ANK1, EPX, ADA, RHAG) that could trigger changes in the broiler´s femoral growth plate was identified. Moreover, these results could be helpful to better understand FHN in chickens and possibly in humans.


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