Publications by authors named "Janet M Anderson-Mackenzie"

There is increasing recognition that osteoarthritis (OA) is a complex disease involving the whole synovial joint, rather than the articular cartilage alone, however its aetiology and pathogenesis is not understood. Our initial studies revealed elevated turnover of bone and ligament collagen in human and mouse OA, respectively. To investigate the relative appearance of pathology in cartilage, bone and ligament, we studied the progression of spontaneous OA in the Dunkin-Hartley (DH) guinea pig knee, and compared with age-matched control Bristol Strain 2 (BS2) knees.

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Objective: The influence of the cruciate ligaments in spontaneous osteoarthritis (OA) is not understood, although ligament rupture is known to cause secondary OA. Additionally, femoral notch narrowing at the anterior cruciate ligament (ACL) insertion site is associated with disease severity, but it is unknown whether ligament deterioration precedes or follows osteophyte formation. We examined cruciate ligament mechanics and metabolism and the intercondylar notch width in OA-prone Dunkin-Hartley (DH) guinea pigs at ages up to and including the age at OA onset (24 weeks), and compared the data with those in age-matched controls (Bristol strain 2 [BS2] guinea pigs).

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There is a need for a reliable assay for the quantification of collagen type I synthesis in the guinea pig, an important model for many connective tissue diseases. Procollagen type I C-terminal propeptide (PICP) is the established marker of type I collagen synthesis but, to date, no assay has been developed to measure PICP in guinea pig tissue extracts. A monoclonal antibody, known to cross-react with intact guinea pig procollagen type I (anti-PICP), was tested for its ability to bind soluble guinea pig PICP in crude skin extracts using a biosensor.

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Osteoarthritis has an unknown aetiology, and tissue samples from early stage human osteoarthritis tissue cannot be reliably obtained. Therefore understanding the development of OA relies on using animal models: such as the spontaneous changes seen in the Dunkin-Hartley guinea pig strain, which are biochemically, histologically and radiologically similar to human OA. We investigated the role of bone change in early OA development using the non-OA developing Bristol strain-2 as control from 3 to 36 weeks by standard microfocal X-ray imaging and histological techniques.

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