Electronic Thesis and Dissertation Repository

Thesis Format

Monograph

Degree

Master of Science

Program

Physiology and Pharmacology

Supervisor

Beier, Frank

Abstract

Post-traumatic Osteoarthritis (PTOA) is a degenerative joint disease, leading to articular cartilage breakdown, osteophytes, and synovitis, caused by an initial joint trauma. Pro-inflammatory cytokines increase catabolic activity and may perpetuate inflammation following joint trauma. Interleukin-15 (IL-15), a pro-inflammatory cytokine, is increased in OA patients, although its exact role in the disease pathology is unknown. Using Il15 deficientrats, this study investigated the role of IL-15 in PTOA pathogenesis in an injury-induced model of OA. Semi-quantitative scoring of the articular cartilage, subchondral bone, and osteophyte formation reveals no significant difference between Il15 deficient rats and wild-type rats, following PTOA-induction. Similarly, synovitis scoring across 6 parameters found no significant difference between genetic variants. Overall, IL-15 does not appear to play a key role in PTOA pathogenesis in this model.

Summary for Lay Audience

Post-traumatic Osteoarthritis (PTOA) is a degenerative joint disease, leading to cartilage breakdown and changes to the surrounding tissue, caused by an initial joint injury. Pro-inflammatory cytokines may increase joint damage and cause chronic inflammation following joint trauma. Interluekin-15 (IL-15), a pro-inflammatory cytokine, is increased in OA patients, although its exact role in the disease is unknown. Using Il15 deficient rats, this study investigated the role of IL-15 in PTOA progression in an injury-induced model of OA. The cartilage, bone, and joint capsule were analyzed to assess PTOA damage. Examination of the joint tissue reveals no significant difference between Il15 deficient rats and control rats, following PTOA-induction. Overall, IL-15 does not appear to play a key role in PTOA progression in this model.

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