Correlating chemical changes in subchondral bone mineral due to aging or defective type II collagen by Raman spectroscopy

Author(s):  
Karen A. Dehring ◽  
Blake J. Roessler ◽  
Michael D. Morris
2006 ◽  
Vol 60 (4) ◽  
pp. 366-372 ◽  
Author(s):  
Karen A. Dehring ◽  
Abigail R. Smukler ◽  
Blake J. Roessler ◽  
Michael D. Morris

2013 ◽  
Vol 2013 ◽  
pp. 1-12 ◽  
Author(s):  
Jeong-Eun Huh ◽  
Yeon-Cheol Park ◽  
Byung-Kwan Seo ◽  
Jae-Dong Lee ◽  
Yong-Hyeon Baek ◽  
...  

We sought to determine the cartilage repair capacity of WIN-34B in the collagenase-induced osteoarthritis rabbit model and in progenitor cells from subchondral bone. The cartilage protective effect of WIN-34B was measured by clinical and histological scores, cartilage area, and proteoglycan and collagen contents in the collagenase-induced osteoarthritis rabbit model. The efficacy of chondrogenic differentiation of WIN-34B was assessed by expression of CD105, CD73, type II collagen, and aggrecanin vivoand was analyzed by the surface markers of progenitor cells, the mRNA levels of chondrogenic marker genes, and the level of proteoglycan, GAG, and type II collagenin vitro. Oral administration of WIN-34B significantly increased cartilage area, and this was associated with the recovery of proteoglycan and collagen content. Moreover, WIN-34B at 200 mg/kg significantly increased the expression of CD105, CD73, type II collagen, and aggrecan compared to the vehicle group. WIN-34B markedly enhanced the chondrogenic differentiation of CD105 and type II collagen in the progenitor cells from subchondral bone. Also, we confirmed that treatment with WIN-34B strongly increased the number of SH-2(CD105) cells and expression type II collagen in subchondral progenitor cells. Moreover, WIN-34B significantly increased proteoglycan, as measured by alcian blue staining; the mRNA level of type IIα1 collagen, cartilage link protein, and aggrecan; and the inhibition of cartilage matrix molecules, such as GAG and type II collagen, in IL-1β-treated progenitor cells. These findings suggest that WIN-34B could be a potential candidate for effective anti-osteoarthritic therapy with cartilage repair as well as cartilage protection via enhancement of chondrogenic differentiation in the collagenase-induced osteoarthritis rabbit model and progenitor cells from subchondral bone.


Cartilage ◽  
2019 ◽  
pp. 194760351989075 ◽  
Author(s):  
Aswin Beck ◽  
David Wood ◽  
Christopher J. Vertullo ◽  
Jay Ebert ◽  
Greg Janes ◽  
...  

Objective To compare the histological and immunohistochemical characteristics of matrix-assisted chondrocyte implantation (MACI) grafts between patients with revision surgery and patients with total joint arthroplasty. Methods Biopsies of MACI grafts from patients with revision and total joint arthroplasty. The graft tissue characteristics and subchondral bone were examined by qualitative histology, ICRS (International Cartilage Repair Society) II scoring and semiquantitative immunohistochemistry using antibodies specific to type I and type II collagen. Results A total of 31 biopsies were available, 10 undergoing total knee arthroplasty (TKA) and 21 patients undergoing revision surgery. Patients in the clinically failed group were significantly older (46.3 years) than patients in the revision group (36.6 years) ( P = 0.007). Histologically, the predominant tissue in both groups was of fibrocartilaginous nature, although a higher percentage of specimens in the revision group contained a hyaline-like repair tissue. The percentages of type I collagen (52.9% and 61.0%) and type II collagen (66.3% and 42.2%) were not significantly different between clinically failed and revised MACI, respectively. The talar dome contained the best and patella the worst repair tissue. Subchondral bone pathology was present in all clinically failed patients and consisted of bone marrow lesions, including edema, necrosis and fibrosis, intralesional osteophyte formation, subchondral bone plate elevation, intralesional osteophyte formation, subchondral bone cyst formation, or combinations thereof. Conclusions MACI grafts in patients with revision and total joint arthroplasty were predominantly fibrocartilage in repair type, did not differ in composition and were histologically dissimilar to healthy cartilage. Clinically failed cases showed evidence of osteochondral unit failure, rather than merely cartilage repair tissue failure. The role of the subchondral bone in relation to pain and failure and the pathogenesis warrants further investigation.


2019 ◽  
Vol 2019 ◽  
pp. 1-10
Author(s):  
Shuo Wang ◽  
Yuhong Sun ◽  
Lulu Xia ◽  
Hanyue Li ◽  
Yan Xu ◽  
...  

Objective. This study investigates the effects of using a twin inclined plane device (TIPD) on the remolding and ultrastructure variation of mandibular condyle in growing rats. Materials and Methods. Forty-eight male Wistar rats (six weeks old, body weight of approximately 190–210 g) were divided into experimental group (wearing appliance, n = 32) and control group (no appliance, n = 16). Samples were collected on days 3, 14, 30, and 60. The immunohistochemical analysis for vascular endothelial growth factor (VEGF) and type II collagen was carried out. Tartrate-resistant acid phosphatase (TRAP) reaction was performed to evaluate the osteoclastic activity. Three-dimensional morphometric images were reconstructed for morphometric analysis by microcomputed tomography (micro-CT). The ultrastructure of the condylar surface was observed by scanning electron microscopy (SEM). Results. The expression of VEGF significantly increased, while the expression of type II collagen decreased in the experimental group at days 30 and 60. Furthermore, the enhanced osteoclast activity was observed under the subchondral bone, which was highest at day 30, and decreased to the lowest at day 60 in the experimental group. In addition, adaptive subchondral bone remolding in the posterior part of the condyle was observed at day 60 in the experimental group, and the SEM revealed the ultrastructure variations after installation of the TIPD. However, these changes began to reverse after 30 days. Conclusion. Condylar tissue changes point to the osteoclastic activity in the posterior region of the condyle. These adaptive changes point to bone resorption in the posterior condyle. Type II collagen and VEGF contribute to the MCC remolding induced by the TIPD. The ultrastructural changes in the posterior condylar area in response to mechanical stresses are recoverable at the initial stage.


2006 ◽  
Vol 60 (10) ◽  
pp. 1134-1141 ◽  
Author(s):  
Karen A. Dehring ◽  
Nicole J. Crane ◽  
Abigail R. Smukler ◽  
Jonathan B. McHugh ◽  
Blake J. Roessler ◽  
...  

2019 ◽  
Vol 9 (10) ◽  
pp. 1441-1447
Author(s):  
Yucheng Li ◽  
Jiang Xin ◽  
Wencai Sun

Bone marrow mesenchymal stem cells (BMSCs) have characteristics of self-renewal and multidirectional differentiation. LncRNA UCA1 regulates BMSCs differentiation. Whether LncRNA UCA1 plays a role in bone defects remains unclear. BMSCs were randomly divided into control group, radiation group (6Gy), radiation + UCA1 group followed by analysis of the expression of LncRNA UCA1, RUNX2 and OPN by real time PCR, BMSCs proliferation by MTT assay as well as ALP activity. Healthy Sprague-Dawley rats were randomly divided into control group; bone defect group; UCA1 group, in which UCA1-transfected BMSCs were infused into bone defect rats followed by analysis of bone mineral density, ALP activity as well as the formation of type II collagen by ELISA. LncRNA UCA1 expression was significantly decreased in BMSCs of irradiated group, with decreased BMSCs proliferation, reduced expression of RUNX2 and OPN as well as decreased ALP activity (P < 0.05). Transfection of UCA1 significantly up-regulated LncRNA UCA1 expression in BMSCs, promoted BMSCs proliferation, increased the expression of RUNX2 and OPN, and the activity of ALP (P < 0.05). In addition, UCA1 promoted bone mineral density, increased ALP activity and type II collagen formation in rats with bone defect. LncRNA UCA1 promotes osteogenic differentiation of BMSCs, and targeting it might be a novel approach to promote bone remodeling at the bone defect site.


1998 ◽  
Vol 78 (2) ◽  
pp. 225-228 ◽  
Author(s):  
Takagi Toshiki ◽  
Tsao Peter W. ◽  
Totsuka Ryuichi ◽  
Suzuki Tatsuo ◽  
Murata Takashi ◽  
...  

2021 ◽  
Vol 9 (1) ◽  
Author(s):  
Haixiang Liang ◽  
Spencer Stein ◽  
Pooja Swami ◽  
Henintsoa Fanjaniaina ◽  
Daniel Grande

The repair of cartilage and bone tissue post arthritis or injury in the knee joint is a challenge to the orthopedics. Both doxycycline and collagen scaffolds had been shown with positive influences on the repair of the tissue. Doxycycline inhibits catabolism related enzymes. Collagens provide tissue repair materials. In this study, the influence of doxycycline and jellyfish collagen (JFC) scaffold to the cells in vitro and tissue repair in vivo was studied. Doxycycline was found with a broad inhibition of the matrix metallopeptidases. It also had an enhancement to the progenitor chondrocytes but suppressed the maturation of chondrocytes. JFC (major type II collagen) was seen had improved both type I and type II collagen production during chondrogenesis of mesenchymal stem cells in vitro. Both doxycycline and JFC enhanced the bone formation and had synergistic effects in a late-stage during the bone repair process. However, the cartilage repair was found with no significant influence after the implantations. Overall, the control of metabolism by doxycycline and providing stimulation to collagen production by the implantation of JFC only contribute to bone growth but had little influence on cartilage repair. This indicates the growth of cartilage tissue needs more delicate regulation. The subchondral bone repair, even with some chondrocytes and proteoglycan deposition in the extracellular matrix could not convert to a repair with mature hyaluronic cartilage tissue.


Sign in / Sign up

Export Citation Format

Share Document