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This project established an in vivo method to identify and manipulate expression of markers of osteoarthritis (OA). Specifically, strategies that predictably induce joint inflammation to evaluate dietary methods of OA prevention in young horses have yet to be accomplished. Therefore, the 3 studies described herein were conducted to determine effectiveness of an intra-articular lipopolysaccharide (LPS) challenge on markers of inflammation and cartilage metabolism in young horses and potential of dietary glucosamine hydrochloride (HCl) to mitigate these alterations. In the first study, horses were challenged with 0.25 ng or 0.50 ng of intra-articular LPS solution or lactated ringer’s solution (control). Injection of LPS increased inflammation based on synovial prostaglandin E2 (PGE2) concentrations. Carboxypeptide of type II collagen (CPII), a maker of type II collagen synthesis, also increased in a dose-dependent manner. However, clinical parameters of health were not influenced and remained within normal ranges. Carpal circumference increased in response to repeated arthrocentesis. Lameness scores increased with LPS injection when compared to controls. This model of joint inflammation (0.5 ng LPS) was used in the second study to evaluate potential chondroprotective effects of oral glucosamine HCl supplementation in yearling horses. Specifically, the oral absorption of glucosamine HCl versus saline was determined by nasogastric dosing and incorporation of dietary glucosamine HCl into plasma and synovial fluid over time. Plasma and synovial fluid concentrations of glucosamine tended to increase over the 98-d period. In the third study, yearlings were challenged with intra-articular LPS to determine the potential of glucosamine HCl to mitigate inflammation when compared to contralateral joints. Injection of LPS increased synovial PGE2 and cartilage biomarkers CPII and collagenase cleavage neopeptide (C2C), a marker of type II collagen degradation. Oral glucosamine HCl decreased PGE2 and C2C concentrations, but increased levels of CPII. Results of these 3 studies provide a clearer understanding of joint inflammation and cartilage turnover in young horses and demonstrated a potential role of oral glucosamine to mitigate these effects and possibly prevent OA in horses.

Thirty-two Quarter horse mares (468 to 668 kg BW; 3 to 19 yr) were utilized in a randomized complete block design. Animals were blocked by expected foaling date and randomly assigned to treatments within block. Treatments began 110 d prior to expected foaling date and were arranged as a 2 x 2 factorial consisting of two planes of nutrition, moderate (Mod; 0.5% BW as fed grain/d) or high (High; 1% BW as fed grain/d) and two levels of L-arginine supplementation, 0.21 g/kg BW/d (Arg) or no supplemental Arg (Con; L-alanine to maintain isonitrogenous diets). Mares were housed by block, allowed ad libitum access to water and coastal bermudagrass (Cynodon dactylon) hay, and fed commercial grain twice daily in individual stalls. A modified frequent sampling i.v. glucose tolerance test (FSIGT) was performed on mares during the 11th month gestation and on foals at 5 and 30 d of age. Jugular catheters were placed 1 h before FSIGT, and horses were allowed ad libitum access to bermudagrass hay and water throughout. After a baseline plasma sample was collected, a glucose bolus of 0.3 g/kg BW was administered. Blood samples were collected at 1, 2, 3, 4, 5, 6, 7, 8, 10, 12, 14, 16, and 19 min. At minute 20, an insulin bolus of 30 mU/kg BW was administered. Blood samples continued to be collected at 22, 23, 24, 25, 27, 30, 35, 40, 50, 60, 70, 80, 90, 100, 120, 150, and 180 min. Samples were placed into tubes containing sodium heparin, immediately placed on ice, and centrifuged within 20 min. Plasma was then collected, placed in microtubes and frozen at -20 degrees C for later analysis. Glucose concentrations were analyzed using a colorimetric assay and insulin concentrations determined using a commercial RIA kit. There was no influence of dietary treatment on mare glucose area under the curve (AUCg) or peak glucose (PG) and insulin (PI) concentrations (P >= 0.55). Mare insulin area under the curve (AUCi) tended to be influenced by the interaction between nutritional plane and ARG supplementation (P <= 0.06) with HighCon mares having greater AUCi than ModCon (P <= 0.05), and HighCon mares having greater AUCi than mares fed HighArg (P <= 0.05). Foal AUCg, AUCi, and PI were not influenced by maternal diet. However, PG concentration in foals tended to be influenced by mare AA supplementation with foals from Con mares having higher concentrations compared to Arg (P <= 0.09) An influence of age was observed on foal AUCg and AUCi. Foal AUCg was greater at 5 d compared to 30 d (P <= 0.003). Foal AUCi tended to be greater at 30 d compared to 5 d (P <= 0.08). Data suggest maternal plane of nutrition and arginine supplementation can alter mare and foal glucose and insulin dynamics.

Thesis (M.Eng.)--University of Louisville, 2009. / Title and description from thesis home page (viewed May 15, 2009). Department of Industrial Engineering. Vita. "May 2009." Includes bibliographical references (p. 24-25).

Inaug.-diss.-Gottingen. / Issued also in this series. Lebenslauf. "Literaturangabe": p. [131].

Thesis (M.Sc.)--University of Hong Kong, 2005. / Includes bibliographical references (p. 81-85).

Thesis (M. Sc. Vet. Sc.)--University of Sydney, 2008. / Includes graphs and tables. Title from title screen (viewed June 11, 2009) Submitted in fulfilment of the requirements for the degree of Master of Science in Veterinary Science to the Faculty of Veterinary Science. Degree awarded 2008; thesis submitted 2007. Includes bibliography. Also available in print form.

Thesis (MSc (Veterinary Science))--University of Pretoria, 2006. / Includes bibliographical references.

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