"January 2003" / Errata slip inserted inside front cover. / Includes bibliographical references (leaves 282-313) / xxx, 313 leaves : ill. ; 30 cm. / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / Thesis (Ph.D.)--University of Adelaide, Dept. of Pathology, 2003

With increasing rates of obesity, research has begun to focus of co-morbidities of obesity such as osteoarthritis. The majority of existing research has focused on older adults as the group most likely to suffer from osteoarthritis. The purpose of this study was to determine if overweight and obese young adults exhibit biomechanical risk factors for knee osteoarthritis, and to determine if young adults with biomechanical risk factors of osteoarthritis can modify these with instruction. This purpose was divided into two separate studies. Study 1: Thirty adults between 18-35 years old were recruited into three groups according to body mass index: normal, overweight, and obese. Participants walked through the lab while we collected 3-d kinematic and kinetic data. Overweight and obese young adults walked with similar gait compared to normal weight young adults. Study 2: Nine young adults between 18-35 years were recruited who walked with stiff-knee gait. Baseline measures of gait were collected in the form of 3-d kinematics and kinetics as participants walked through the laboratory. They then completed the gait instruction program which consisted of four blocks of training. Each block included ten single steps where the participant was provided feedback, followed by 100 practice steps around the laboratory. Participants were successful in increasing sagittal plane kinematics and kinetics of interest in the study. Conclusion: Identifying individuals who had biomechanical risk factors of osteoarthritis according to body mass index was not possible. According to the results of our study, obese and overweight young adults are not at increased risk of osteoarthritis compared to normal weight young adults. Individuals who may be at increased risk due to stiff-knee gait were able to improve their gait following instruction.

Thesis (Ph.D.)--University of Delaware, 2006. / Principal faculty advisor: Lynn Snyder-Mackler, Dept. of Physical Therapy. Includes bibliographical references.

<p>This scientific paper is about the changes in the skeleton caused by the diseases osteoarthritis and osteoporosis. Six males and one female from Banken 1, S:ta Gertrud  and S:t Hans in Visby were chosen for an osteological analysis. All individuals are adults and dates back to the middle ages. One male suffered from both osteoporosis and osteoarthritis and one female and three males suffered from osteoarthritis. One male might have been in the beginning faze of osteoarthritis, and one male shows no sign of any of the diseases. In addition to osteoarthritis and osteoporosis, some of the individuals suffer from other pathological conditions. Some of the bones from most of the individuals were x-rayed at Visby hospital, to see if medical technique could show some additional information to the osteological analysis. The x-rays were interpreted by doctor Staffan Jennerholm from Visby hospital, but other doctors have also participated. The x-rays confirmed results from the osteological analysis in most cases, although it showed new information in several cases. Some bones from three individuals were taken to Roland Alvarssons` Doctor Practice in Visby to measure the bone density, to check if any of the individuals had osteoporosis. The result confirmed that one male had osteoporosis, as expected from the osteological analysis.</p> / Noen steder i oppgaven står det "osteoartrithis", men det skal stå "osteoarthritis"

The first objective of my work was to use the ank/ank (progressive ankylosis) mutant mice, which have a deficiency in inorganic pyrophosphate transport, to address the role of Ank in joint ankylosis. I observed the presence of hypertrophic chondrocytes in the uncalcified ank/ank mice articular cartilage. This novel phenotype is likely due to a dysregulation of chondrocyte maturation as these chondrocytes expressed hypertrophic chondrocyte markers (collagen type X and tissue non-specific alkaline phosphatase). I also showed by immunohistochemical staining that beta-catenin expression was upregulated and localized in the nuclei of articular ank/ank chondrocytes, suggesting activation of Wnt/beta-catenin signaling in these chondrocytes. The second objective was to use ank/ank mice as an informative model for understanding ankylosis mechanisms in human ankylosing spondylitis (AS) patients, as WNT/beta-catenin signaling plays an important role in ankylosis in AS patients. We attempted rescue of joint ankylosis in ank/ank mice by gene transfer of noggin, an antagonist of BMP signaling. Paradoxically, noggin-treated ank/ank mice had accelerated ankylosis, as evidenced by joint pathology and IHC staining of beta-catenin showed more intense signals in the spinal chondrocytes of the treated mice. As noggin and sclerostin (an antagonist of beta-catenin signaling) form a mutually inhibitory complex, we hypothesize that the formation of this complex results in relieving suppression of both beta-catenin and BMP signaling, leading to more severe ankylosis in ank/ank mice. By quantitative molecular imaging, I have demonstrated that ankylosis in these mutant mice developed simultaneously in distal and axial joint, instead of being a centripetal process. In summary, I have made three original observations in the ank/ank mice: the hypertrophic chondrocyte phenotype; activation of beta-catenin signaling and the simultaneous development of ankylosis in distal and axial joints. These mutant mice serve as valuable model for pre-clinical studies which enable modeling and testing of novel anti-ankylosis treatments.

Osteoarthritis is a disease that causes decreases in hand function in the elderly adult and can lead to full disability of the hand. There is no clear cause of osteoarthritis of the hand, although injury and overuse can contribute to development of the disease. Traditional treatments include splinting, paraffin therapy, medications and, in severe cases, joint replacement. Nontraditional therapies include mobility training, therapeutic touch, acupuncture and exercise. The purpose of this study was to explore the non-traditional treatment of hand-strengthening exercise as a way to improve hand function. Specifically, this study evaluated the effects of an eightweek hand exercise program utilizing Hand Exercisers and FlexBars on hand grip strength and dexterity in 13 elderly women aged 70-85 (M=80.4, SD= +/- 4.25) who showed signs and symptoms of hand osteoarthritis, which are pain, stiffness and swelling.. Participants were evaluated before and after the exercise intervention for grip strength, pinch strength, range of motion of the trapeziometacarpal, metacarpophalangeal, interphalangeal and wrist joints, and were timed on a hand dexterity test that involved putting on and buttoning a shirt with ten 3/8th inch buttons. A repeated measures ANOVA was the mode of data analysis. Hand strength significantly improved (p<0.05), as both grip (19%) and pinch (26%) strength showed improvements. In range of motion testing, palmar flexion (12%), interphalangeal flexion (46%), metacarpophalangeal flexion (39%) and wrist extension (11%) showed significant improvements while palmar abduction (12%) and wrist flexion (8%) did not. Hand dexterity also improved as evidenced by a 24% decrease in the amount of time to button a shirt. Pain, stiffness and disability, as measured by the AUSCAN, also decreased significantly, with a 17.3% decrease in means. The results indicate that hand exercise programs can be used to increase hand function while decreasing the signs and symptoms in patients with hand osteoarthritis. / Thesis (M.Ed.)--Wichita State University, College of Education, Dept. of Kinesiology and Sport Studies. / "July 2006." / Includes bibliographic references (leaves 33-37).

The first objective of my work was to use the ank/ank (progressive ankylosis) mutant mice, which have a deficiency in inorganic pyrophosphate transport, to address the role of Ank in joint ankylosis. I observed the presence of hypertrophic chondrocytes in the uncalcified ank/ank mice articular cartilage. This novel phenotype is likely due to a dysregulation of chondrocyte maturation as these chondrocytes expressed hypertrophic chondrocyte markers (collagen type X and tissue non-specific alkaline phosphatase). I also showed by immunohistochemical staining that beta-catenin expression was upregulated and localized in the nuclei of articular ank/ank chondrocytes, suggesting activation of Wnt/beta-catenin signaling in these chondrocytes. The second objective was to use ank/ank mice as an informative model for understanding ankylosis mechanisms in human ankylosing spondylitis (AS) patients, as WNT/beta-catenin signaling plays an important role in ankylosis in AS patients. We attempted rescue of joint ankylosis in ank/ank mice by gene transfer of noggin, an antagonist of BMP signaling. Paradoxically, noggin-treated ank/ank mice had accelerated ankylosis, as evidenced by joint pathology and IHC staining of beta-catenin showed more intense signals in the spinal chondrocytes of the treated mice. As noggin and sclerostin (an antagonist of beta-catenin signaling) form a mutually inhibitory complex, we hypothesize that the formation of this complex results in relieving suppression of both beta-catenin and BMP signaling, leading to more severe ankylosis in ank/ank mice. By quantitative molecular imaging, I have demonstrated that ankylosis in these mutant mice developed simultaneously in distal and axial joint, instead of being a centripetal process. In summary, I have made three original observations in the ank/ank mice: the hypertrophic chondrocyte phenotype; activation of beta-catenin signaling and the simultaneous development of ankylosis in distal and axial joints. These mutant mice serve as valuable model for pre-clinical studies which enable modeling and testing of novel anti-ankylosis treatments.

One of the most poorly understood co-morbidities associated with obesity is the pathway to osteoarthritis of the knee. To implement appropriate preventative strategies, it is important to explore how obesity is a causal factor for osteoarthritis. The present research compared the kinematics and kinetics of a group of young obese, but otherwise healthy, adults to a group of young, healthy-weight adults, in an attempt to identify mechanical abnormalities at the knee during walking that may predispose the obese to osteoarthritis of the knee. Optotrak motion capture (Northern Digital Inc. Waterloo, Ontario) and a forceplate (AMTI OR6-7, Advanced Mechanical Technology Inc, Watertown, MA) were used to measure ground reaction forces and moments of 16 participants – 8 obese and 8 sex-, age- and height-matched healthy-weight – to analyze knee joint kinematics and kinetics at three walking speeds. Participants wore an accelerometer (ActiGraph GT3X, Fort Walton Beach, USA) for seven days to measure daily steps counts. Dependent t-tests were performed to determine group differences in ground reaction forces, knee angles and knee moments, as well as knee adduction moment impulse and cumulative knee adductor load (CKAL). The obese group walked at a significantly slower self-selected speed (p=0.013). While not statistically significant, the obese group did present with a more valgus mean dynamic knee alignment than the health-weight group. A significantly greater maximum abduction angle (p=0.009) and smaller minimum knee flexion angle at heel contact (p=0.001) was found in the obese group. A significant difference was found in the peak medial rotation moment in the transverse plane (p=0.003). A greater stance duration lead to a significantly greater knee adduction moment impulse (p=0.049) in the obese group. While significant group differences were not found in the steps per day, the obese group had a significantly greater CKAL (p=0.025). Obese young adults with healthy knees demonstrated a gait pattern of reduced medial knee joint compartment loading through greater knee abduction, medial knee rotation and a slower walking speed compared to matched controls. The ramifications of gait modifications on long-term musculoskeletal health remain unknown, but compensations may lead to increased risk of osteoarthritis of the knee.

Thesis (Ph. D.)--University of Missouri--Columbia, 2003. / Typescript. Vita. Includes bibliographical references.

Thesis (Ph. D.)--University of Missouri--Columbia, 2003. / "May 2003." Typescript. Vita. Includes bibliographical references.