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Kevin C. Baker - One of the best experts on this subject based on the ideXlab platform.
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traumatic joint injury induces acute catabolic bone turnover concurrent with Articular Cartilage Damage in a rat model of post traumatic osteoarthritis
Journal of Orthopaedic Research, 2020Co-Authors: Tristan Maerz, Michael D. Newton, Mackenzie M. Fleischer, Samantha E. Hartner, Karissa Gawronski, Lucas Junginger, Kevin C. BakerAbstract:Assess acute alterations in bone turnover, microstructure, and histomorphometry following noninvasive anterior cruciate ligament rupture (ACLR). Twelve female Lewis rats were randomized to receive noninvasive ACLR or Sham loading (n = 6/group). In vivo μCT was performed at 3, 7, 10, and 14 days postinjury to quantify compartment-dependent subchondral (SCB) and epiphyseal trabecular bone remodeling. Near-infrared (NIR) molecular imaging was used to measure in vivo bone anabolism (800 CW BoneTag) and catabolism (Cat K 680 FAST). Metaphyseal bone remodeling and Articular Cartilage morphology was quantified using ex vivo μCT and contrast-enhanced µCT, respectively. Calcein-based dynamic histomorphometry was used to quantify bone formation. OARSI scoring was used to assess joint degeneration, and osteoclast number was quantified on TRAP stained-sections. ACLR induced acute catabolic bone remodeling in subchondral, epiphyseal, and metaphyseal compartments. Thinning of medial femoral condyle (MFC) SCB was observed as early as 7 days postinjury, while lateral femoral condyles (LFCs) exhibited SCB gains. Trabecular thinning was observed in MFC epiphyseal bone, with minimal changes to LFC. NIR imaging demonstrated immediate and sustained reduction of bone anabolism (~15%-20%), and a ~32% increase in bone catabolism at 14 days, compared to contralateral limbs. These findings were corroborated by reduced bone formation rate and increased osteoclast numbers, observed histologically. ACLR-injured femora had significantly elevated OARSI score, Cartilage thickness, and Cartilage surface deviation. ACL rupture induces immediate and sustained reduction of bone anabolism and overactivation of bone catabolism, with mild-to-moderate Articular Cartilage Damage at 14 days postinjury.
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Traumatic Joint Injury Induces Acute Catabolic Bone Turnover Concurrent with Articular Cartilage Damage in a Rat Model of Post-Traumatic Osteoarthritis
2020Co-Authors: Tristan Maerz, Michael D. Newton, Mackenzie M. Fleischer, Samantha E. Hartner, Karissa Gawronski, Lucas Junginger, Kevin C. BakerAbstract:Objective: Assess acute alterations in bone turnover, microstructure, and histomorphometry following noninvasive anterior cruciate ligament rupture (ACLR). Methods: Twelve female Lewis rats were randomized to receive noninvasive ACLR or Sham loading (n=6/group). In vivo microCT was performed at 3, 7, 10, and 14 days post-injury to quantify compartment-dependent subchondral (SCB) and epiphyseal trabecular bone remodeling. Near-infrared (NIR) molecular imaging was used to measure in vivo bone anabolism (800 CW BoneTag) and catabolism (Cat K 680 FAST). Metaphyseal bone remodeling and Articular Cartilage morphology was quantified using ex vivo microCT and contrast-enhanced microCT, respectively. Calcein-based dynamic histomorphometry was used to quantify bone formation. OARSI scoring was used to assess joint degeneration, and osteoclast number was quantified on TRAP stained-sections. Results: ACLR induced acute catabolic bone remodeling in subchondral, epiphyseal, and metaphyseal compartments. Thinning of medial femoral condyle (MFC) SCB was observed as early as 7 days post-injury, while lateral femoral condyles (LFC) exhibited SCB gains. Trabecular thinning was observed in MFC epiphyseal bone, with minimal changes to LFC. NIR imaging demonstrated immediate and sustained reduction of bone anabolism (~15-20%), and a ~32% increase in bone catabolism at 14 days, compared to contralateral limbs. These findings were corroborated by reduced bone formation rate and increased osteoclast numbers, observed histologically. ACLR-injured femora had significantly elevated OARSI score, Cartilage thickness, and Cartilage surface deviation. Conclusion: ACL rupture induces immediate and sustained reduction of bone anabolism and overactivation of bone catabolism, with mild-to-moderate Articular Cartilage Damage at 14 days post-injury.
Tristan Maerz - One of the best experts on this subject based on the ideXlab platform.
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traumatic joint injury induces acute catabolic bone turnover concurrent with Articular Cartilage Damage in a rat model of post traumatic osteoarthritis
Journal of Orthopaedic Research, 2020Co-Authors: Tristan Maerz, Michael D. Newton, Mackenzie M. Fleischer, Samantha E. Hartner, Karissa Gawronski, Lucas Junginger, Kevin C. BakerAbstract:Assess acute alterations in bone turnover, microstructure, and histomorphometry following noninvasive anterior cruciate ligament rupture (ACLR). Twelve female Lewis rats were randomized to receive noninvasive ACLR or Sham loading (n = 6/group). In vivo μCT was performed at 3, 7, 10, and 14 days postinjury to quantify compartment-dependent subchondral (SCB) and epiphyseal trabecular bone remodeling. Near-infrared (NIR) molecular imaging was used to measure in vivo bone anabolism (800 CW BoneTag) and catabolism (Cat K 680 FAST). Metaphyseal bone remodeling and Articular Cartilage morphology was quantified using ex vivo μCT and contrast-enhanced µCT, respectively. Calcein-based dynamic histomorphometry was used to quantify bone formation. OARSI scoring was used to assess joint degeneration, and osteoclast number was quantified on TRAP stained-sections. ACLR induced acute catabolic bone remodeling in subchondral, epiphyseal, and metaphyseal compartments. Thinning of medial femoral condyle (MFC) SCB was observed as early as 7 days postinjury, while lateral femoral condyles (LFCs) exhibited SCB gains. Trabecular thinning was observed in MFC epiphyseal bone, with minimal changes to LFC. NIR imaging demonstrated immediate and sustained reduction of bone anabolism (~15%-20%), and a ~32% increase in bone catabolism at 14 days, compared to contralateral limbs. These findings were corroborated by reduced bone formation rate and increased osteoclast numbers, observed histologically. ACLR-injured femora had significantly elevated OARSI score, Cartilage thickness, and Cartilage surface deviation. ACL rupture induces immediate and sustained reduction of bone anabolism and overactivation of bone catabolism, with mild-to-moderate Articular Cartilage Damage at 14 days postinjury.
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Traumatic Joint Injury Induces Acute Catabolic Bone Turnover Concurrent with Articular Cartilage Damage in a Rat Model of Post-Traumatic Osteoarthritis
2020Co-Authors: Tristan Maerz, Michael D. Newton, Mackenzie M. Fleischer, Samantha E. Hartner, Karissa Gawronski, Lucas Junginger, Kevin C. BakerAbstract:Objective: Assess acute alterations in bone turnover, microstructure, and histomorphometry following noninvasive anterior cruciate ligament rupture (ACLR). Methods: Twelve female Lewis rats were randomized to receive noninvasive ACLR or Sham loading (n=6/group). In vivo microCT was performed at 3, 7, 10, and 14 days post-injury to quantify compartment-dependent subchondral (SCB) and epiphyseal trabecular bone remodeling. Near-infrared (NIR) molecular imaging was used to measure in vivo bone anabolism (800 CW BoneTag) and catabolism (Cat K 680 FAST). Metaphyseal bone remodeling and Articular Cartilage morphology was quantified using ex vivo microCT and contrast-enhanced microCT, respectively. Calcein-based dynamic histomorphometry was used to quantify bone formation. OARSI scoring was used to assess joint degeneration, and osteoclast number was quantified on TRAP stained-sections. Results: ACLR induced acute catabolic bone remodeling in subchondral, epiphyseal, and metaphyseal compartments. Thinning of medial femoral condyle (MFC) SCB was observed as early as 7 days post-injury, while lateral femoral condyles (LFC) exhibited SCB gains. Trabecular thinning was observed in MFC epiphyseal bone, with minimal changes to LFC. NIR imaging demonstrated immediate and sustained reduction of bone anabolism (~15-20%), and a ~32% increase in bone catabolism at 14 days, compared to contralateral limbs. These findings were corroborated by reduced bone formation rate and increased osteoclast numbers, observed histologically. ACLR-injured femora had significantly elevated OARSI score, Cartilage thickness, and Cartilage surface deviation. Conclusion: ACL rupture induces immediate and sustained reduction of bone anabolism and overactivation of bone catabolism, with mild-to-moderate Articular Cartilage Damage at 14 days post-injury.
Annemarie Uel - One of the best experts on this subject based on the ideXlab platform.
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no effect of risedronate on Articular Cartilage Damage in the dunkin hartley guinea pig model of osteoarthritis
Scandinavian Journal of Rheumatology, 2013Co-Authors: Jesper Skovhus Thomse, T S Straarup, Carl Christia Danielse, Hans Oxlund, Annemarie UelAbstract:Objectives: To investigate whether treatment with a bisphosphonate would influence the subchondral bone plate stiffness and the development of Cartilage Damage in Dunkin Hartley guinea pigs, which develop osteoarthritis (OA) spontaneously.Method: Fifty-six 3-month-old male Dunkin Hartley guinea pigs were randomized into a baseline group and six groups receiving either the bisphosphonate risedronate (30 µg/kg) or vehicle five times a week for 6, 12, or 24 weeks. The medial condyle of the right stifle joint was investigated by histology, using the Osteoarthritis Research Society International (OARSI) score, along with static and dynamic histomorphometry. The subchondral bone plate of the left tibia was tested mechanically with indentation testing. Degradation products of C-terminal telopeptides of type II collagen (CTX-II) were measured in serum.Results: The OARSI score did not differ between risedronate-treated and control animals at any time point. The fraction of bone surfaces covered with osteoclasts (O...
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relationship between Articular Cartilage Damage and subchondral bone properties and meniscal ossification in the dunkin hartley guinea pig model of osteoarthritis
Scandinavian Journal of Rheumatology, 2011Co-Authors: Jesper Skovhus Thomse, T S Straarup, Carl Christia Danielse, Hans Oxlund, Annemarie UelAbstract:Objectives: To describe the age-related changes of Articular Cartilage, subchondral bone morphology, and stiffness. Furthermore, to investigate whether subchondral bone histological and mechanical properties and meniscal histological properties are related to Articular Cartilage Damage in the Dunkin Hartley guinea pig model of osteoarthritis (OA).Methods: Forty male Dunkin Hartley guinea pigs aged 2, 6, 9, and 12 months were studied. The right stifle joints and the left menisci were embedded undecalcified and the tibial Articular Cartilage and subchondral bone and the menisci were examined using histology. The stiffness of the left tibial subchondral bone was determined with indentation testing.Results: The Osteoarthritis Research Society International (OARSI) grade of the osteoarthritic Cartilage lesions of the medial (p < 0.001) and lateral (p < 0.001) condyle and the ossification of the medial (p < 0.001) and lateral (p < 0.001) meniscus increased significantly with age and was significantly more prono...
Michael D. Newton - One of the best experts on this subject based on the ideXlab platform.
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traumatic joint injury induces acute catabolic bone turnover concurrent with Articular Cartilage Damage in a rat model of post traumatic osteoarthritis
Journal of Orthopaedic Research, 2020Co-Authors: Tristan Maerz, Michael D. Newton, Mackenzie M. Fleischer, Samantha E. Hartner, Karissa Gawronski, Lucas Junginger, Kevin C. BakerAbstract:Assess acute alterations in bone turnover, microstructure, and histomorphometry following noninvasive anterior cruciate ligament rupture (ACLR). Twelve female Lewis rats were randomized to receive noninvasive ACLR or Sham loading (n = 6/group). In vivo μCT was performed at 3, 7, 10, and 14 days postinjury to quantify compartment-dependent subchondral (SCB) and epiphyseal trabecular bone remodeling. Near-infrared (NIR) molecular imaging was used to measure in vivo bone anabolism (800 CW BoneTag) and catabolism (Cat K 680 FAST). Metaphyseal bone remodeling and Articular Cartilage morphology was quantified using ex vivo μCT and contrast-enhanced µCT, respectively. Calcein-based dynamic histomorphometry was used to quantify bone formation. OARSI scoring was used to assess joint degeneration, and osteoclast number was quantified on TRAP stained-sections. ACLR induced acute catabolic bone remodeling in subchondral, epiphyseal, and metaphyseal compartments. Thinning of medial femoral condyle (MFC) SCB was observed as early as 7 days postinjury, while lateral femoral condyles (LFCs) exhibited SCB gains. Trabecular thinning was observed in MFC epiphyseal bone, with minimal changes to LFC. NIR imaging demonstrated immediate and sustained reduction of bone anabolism (~15%-20%), and a ~32% increase in bone catabolism at 14 days, compared to contralateral limbs. These findings were corroborated by reduced bone formation rate and increased osteoclast numbers, observed histologically. ACLR-injured femora had significantly elevated OARSI score, Cartilage thickness, and Cartilage surface deviation. ACL rupture induces immediate and sustained reduction of bone anabolism and overactivation of bone catabolism, with mild-to-moderate Articular Cartilage Damage at 14 days postinjury.
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Traumatic Joint Injury Induces Acute Catabolic Bone Turnover Concurrent with Articular Cartilage Damage in a Rat Model of Post-Traumatic Osteoarthritis
2020Co-Authors: Tristan Maerz, Michael D. Newton, Mackenzie M. Fleischer, Samantha E. Hartner, Karissa Gawronski, Lucas Junginger, Kevin C. BakerAbstract:Objective: Assess acute alterations in bone turnover, microstructure, and histomorphometry following noninvasive anterior cruciate ligament rupture (ACLR). Methods: Twelve female Lewis rats were randomized to receive noninvasive ACLR or Sham loading (n=6/group). In vivo microCT was performed at 3, 7, 10, and 14 days post-injury to quantify compartment-dependent subchondral (SCB) and epiphyseal trabecular bone remodeling. Near-infrared (NIR) molecular imaging was used to measure in vivo bone anabolism (800 CW BoneTag) and catabolism (Cat K 680 FAST). Metaphyseal bone remodeling and Articular Cartilage morphology was quantified using ex vivo microCT and contrast-enhanced microCT, respectively. Calcein-based dynamic histomorphometry was used to quantify bone formation. OARSI scoring was used to assess joint degeneration, and osteoclast number was quantified on TRAP stained-sections. Results: ACLR induced acute catabolic bone remodeling in subchondral, epiphyseal, and metaphyseal compartments. Thinning of medial femoral condyle (MFC) SCB was observed as early as 7 days post-injury, while lateral femoral condyles (LFC) exhibited SCB gains. Trabecular thinning was observed in MFC epiphyseal bone, with minimal changes to LFC. NIR imaging demonstrated immediate and sustained reduction of bone anabolism (~15-20%), and a ~32% increase in bone catabolism at 14 days, compared to contralateral limbs. These findings were corroborated by reduced bone formation rate and increased osteoclast numbers, observed histologically. ACLR-injured femora had significantly elevated OARSI score, Cartilage thickness, and Cartilage surface deviation. Conclusion: ACL rupture induces immediate and sustained reduction of bone anabolism and overactivation of bone catabolism, with mild-to-moderate Articular Cartilage Damage at 14 days post-injury.
Mackenzie M. Fleischer - One of the best experts on this subject based on the ideXlab platform.
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traumatic joint injury induces acute catabolic bone turnover concurrent with Articular Cartilage Damage in a rat model of post traumatic osteoarthritis
Journal of Orthopaedic Research, 2020Co-Authors: Tristan Maerz, Michael D. Newton, Mackenzie M. Fleischer, Samantha E. Hartner, Karissa Gawronski, Lucas Junginger, Kevin C. BakerAbstract:Assess acute alterations in bone turnover, microstructure, and histomorphometry following noninvasive anterior cruciate ligament rupture (ACLR). Twelve female Lewis rats were randomized to receive noninvasive ACLR or Sham loading (n = 6/group). In vivo μCT was performed at 3, 7, 10, and 14 days postinjury to quantify compartment-dependent subchondral (SCB) and epiphyseal trabecular bone remodeling. Near-infrared (NIR) molecular imaging was used to measure in vivo bone anabolism (800 CW BoneTag) and catabolism (Cat K 680 FAST). Metaphyseal bone remodeling and Articular Cartilage morphology was quantified using ex vivo μCT and contrast-enhanced µCT, respectively. Calcein-based dynamic histomorphometry was used to quantify bone formation. OARSI scoring was used to assess joint degeneration, and osteoclast number was quantified on TRAP stained-sections. ACLR induced acute catabolic bone remodeling in subchondral, epiphyseal, and metaphyseal compartments. Thinning of medial femoral condyle (MFC) SCB was observed as early as 7 days postinjury, while lateral femoral condyles (LFCs) exhibited SCB gains. Trabecular thinning was observed in MFC epiphyseal bone, with minimal changes to LFC. NIR imaging demonstrated immediate and sustained reduction of bone anabolism (~15%-20%), and a ~32% increase in bone catabolism at 14 days, compared to contralateral limbs. These findings were corroborated by reduced bone formation rate and increased osteoclast numbers, observed histologically. ACLR-injured femora had significantly elevated OARSI score, Cartilage thickness, and Cartilage surface deviation. ACL rupture induces immediate and sustained reduction of bone anabolism and overactivation of bone catabolism, with mild-to-moderate Articular Cartilage Damage at 14 days postinjury.
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Traumatic Joint Injury Induces Acute Catabolic Bone Turnover Concurrent with Articular Cartilage Damage in a Rat Model of Post-Traumatic Osteoarthritis
2020Co-Authors: Tristan Maerz, Michael D. Newton, Mackenzie M. Fleischer, Samantha E. Hartner, Karissa Gawronski, Lucas Junginger, Kevin C. BakerAbstract:Objective: Assess acute alterations in bone turnover, microstructure, and histomorphometry following noninvasive anterior cruciate ligament rupture (ACLR). Methods: Twelve female Lewis rats were randomized to receive noninvasive ACLR or Sham loading (n=6/group). In vivo microCT was performed at 3, 7, 10, and 14 days post-injury to quantify compartment-dependent subchondral (SCB) and epiphyseal trabecular bone remodeling. Near-infrared (NIR) molecular imaging was used to measure in vivo bone anabolism (800 CW BoneTag) and catabolism (Cat K 680 FAST). Metaphyseal bone remodeling and Articular Cartilage morphology was quantified using ex vivo microCT and contrast-enhanced microCT, respectively. Calcein-based dynamic histomorphometry was used to quantify bone formation. OARSI scoring was used to assess joint degeneration, and osteoclast number was quantified on TRAP stained-sections. Results: ACLR induced acute catabolic bone remodeling in subchondral, epiphyseal, and metaphyseal compartments. Thinning of medial femoral condyle (MFC) SCB was observed as early as 7 days post-injury, while lateral femoral condyles (LFC) exhibited SCB gains. Trabecular thinning was observed in MFC epiphyseal bone, with minimal changes to LFC. NIR imaging demonstrated immediate and sustained reduction of bone anabolism (~15-20%), and a ~32% increase in bone catabolism at 14 days, compared to contralateral limbs. These findings were corroborated by reduced bone formation rate and increased osteoclast numbers, observed histologically. ACLR-injured femora had significantly elevated OARSI score, Cartilage thickness, and Cartilage surface deviation. Conclusion: ACL rupture induces immediate and sustained reduction of bone anabolism and overactivation of bone catabolism, with mild-to-moderate Articular Cartilage Damage at 14 days post-injury.
